Abstract
The cardiovascular apparatus supplies blood to the body’s organs and responds to sudden changes in demand for nutrients according to the organism’s activity. Blood velocity and pressure can be associated with kinetic and potential energy, respectively.
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Notes
- 1.
Coronary perfusion can be modeled using a poroelastic model for the myocardial microcirculation and a Darcy solver using the arbitrary Lagrangian–Eulerian (ALE) formulation.
- 2.
A semi-implicit coupling scheme that exhibits a good stability has been proposed [4]. The pressure stress is implicitly coupled with the structure to ensure stability; remaining terms are explicitly treated. The implicit–explicit splitting can be conveniently performed using a Chorin–Temam projection scheme. A stabilized explicit coupling scheme based on Nitsche’s method can be used, stability being independent of the fluid–structure density ratio [5].
- 3.
Heart valve motions rely on a multibody contact problem with attachment constraints due to chordæ tendinæ [7]. The fluid and immersed valve meshes do not match; the kinematic continuity is imposed using Lagrange multipliers. The method relies on a fictitious domain, which allows very large displacements, combined with the ALE formalism to manage both elastic valve and wall motions. A partitioned fluid–structure algorithm associates independent fluid and structure solvers.
- 4.
Valve cusps do not evert into the atrium during the ventricular systole by contraction of the papillary muscles, which are related to ventricular myocardium.
- 5.
In 1895, Frank found that under isovolumetric conditions, the larger the EDV, the greater the developed tension and pressure. Starling’s later experiments demonstrated that the heart intrinsically responds to venous return (to EDV) increases by increasing the stroke volume (heart autoregulation). The relationship between EDV and stroke volume is associated with the relationship between sarcomere length and calcium ion influx and sensitivity. Myofilament length-dependent activation is explained by the separation distance between actin and myosin along the sarcomeric filament axis. The intrinsic ability of the heart to develop greater tension at longer myocardial fiber lengths over a finite range of fiber lengths is due to sliding filament arrangement in cardiomyocytes, with increase of cross-bridge number between actin and myosin filaments. The Frank–Starling mechanism refers to the heart’s intrinsic capability of increasing inotropy and stroke volume in response to venous-return increase. The Frank–Starling effect describes static filling mechanisms in an isolated motionless heart. It works for high filling pressure and low flow rate (cardiac failure); however, cardiac functioning is an unsteady phenomenon.
- 6.
This frequency-dependent enhanced contractility helps to offset the decreased ventricular filling time at higher cardiac frequencies by shortening the systole time duration, thereby increasing the time available for diastole.
- 7.
Positive chronotropy (C+) induces positive inotropy (I+).
- 8.
During systole, the heart moves downward.
- 9.
The mitral annulus descends about 1.3 cm during the left ventricular ejection phase in normal subjects [16].
- 10.
Cardiac β-myosin is a mechanoenzyme that converts the energy from ATP hydrolysis for muscle contraction. Two cardiac myosin heavy chains (α MHC–β MHC) have different levels of ATPase activity. The β MHC and α MHC subtypes are predominantly expressed in late fetal life and adults, respectively. The former is encoded by the MYH7 gene.
- 11.
The resting transmembrane potential is higher (less negative) in cardiofibroblasts than that of cardiomyocytes. During action potential upstroke, the transmembrane potential of cardiomyocytes becomes higher than that of cardiofibroblasts, which then can act as current sinks, which slows down cardiomyocyte activation and can attenuate maximum upstroke velocity and peak amplitude of the action potential [18].
- 12.
The conduction velocity generally increases initially and then decreases when cardiofibroblast density and/or coupling increase.
- 13.
\(\updelta \upupsilon \upalpha \varsigma\): couple, pair, binary number.
- 14.
In the myocardium, a diad means that a T tubule is associated with a single terminal cisterna. On the other hand, in the skeletal muscle, a triad is formed by a T tubule flanked on either side by the junctional sarcoplasmic reticulum, at the level of the Z line.
- 15.
The principal cardiac pore-forming α subunit isoform NaV1.5 preferentially localizes to intercalated discs, whereas the brain-type α subunit isoforms NaV1.1, NaV1.3, and NaV1.6 reside in transverse tubules [26]. They contribute to the coupling of sarcolemmal depolarization to contraction. On the other hand, NaV1.5 in intercalated discs is primarily responsible for action potential conduction between cardiomyocytes.
- 16.
Cardiac inward rectifier K + currents (i K1) through channels of the KIR2 category participate in the maintenance of resting membrane potential as well as late phase repolarization. In rabbits, KIR2.1 and KIR2.2, which lodge in T tubules, but not KIR2.3, are synthesized in ventriculomyocytes [27]. Current i K1 is predominantly due to KIR2.1–KIR2.2 heterotetramers. In mice, i K1 also crosses KIR2.1–KIR2.2 heterotetramers. In guinea pigs, KIR2.1, KIR2.2, and KIR2.3, but not KIR2.4 are produced in ventriculomyocytes [28]. Three different inward rectifier conductances are linked to KIR2.1, KIR2.2, and KIR2.3 homotetrameric channels, intermediate-conductance KIR2.1 and large-conductanceIR2.2 being the primary determinants of i K1 current with little contribution from low-conductance KIR2.3 channel [28]. In humans, KIR2.1 resides in ventriculomyocytes, KIR2.1 and KIR2.2 in atrial cells, and KIR2.3 in ventricular cells (cells including not only cardiomyocytes, but also endotheliocytes, vascular smooth myocytes, cardiofibroblasts, and neurons, among others). In the guinea pig heart, KIR2.1, KIR2.2, and KIR2.3 are expressed in both cardiomyocytes and capillary endotheliocytes. Subunit KIR2.4 is restricted to cardiac parasympathetic and postganglionic sympathetic neurons as well as sensory nerve fibers [28].
- 17.
The lumen of T tubules varies within a given mammalian species. Using confocal microscopy, it was assessed to be about 400 nm in humans [22]. However, stimulated emission depletion (STED) imaging that has a better spatial resolution detects a lower caliber.
- 18.
Although the volume density of the T-tubule network is only 1 to 3%, it represents about one-third of the entire plasma membrane area [22]. Transverse tubule density varies among ventriculomyocytes from different animal species.
- 19.
P110αPI3K and P110βPI3K are required for the maintenance of the organized network of T tubules, as they regulate junctophilin-2 localization [30]. The 4 junctophilins tether the plasma membrane to the endoplasmic reticulum in excitable cells. The major cardiac junctophilin isoform JP2 has a C-terminal transmembrane domain that anchors the protein in the SR membrane and 8 N-terminal membrane occupation and recognition nexus (MORN) motifs that interact with the plasma membrane to stabilize the junction between the plasma and SR membrane.
- 20.
A.k.a. mortalin Mot2, peptide-binding protein PBP74, mitochondrial stress protein-70, 75-kDa mitochondrial heat shock protein mtHSP75, and 75-kDa glucose-regulated protein GRP75.
- 21.
Reactive oxygen species comprise free radicals with an unpaired electron (e.g., membrane-impermeable O2 •−, and extremely short lifetime OH •) and nonradical derivatives (e.g., more stable, membrane-permeable H2O2). The main reactive nitrogen species is the free radical NO •.
- 22.
Only Nox1, Nox2, and Nox4 isoforms are synthesized in the heart. Among them, Nox2 localized to T tubules is the predominant isoform in the adult cardiomyocyte.
- 23.
Subtype NOS3 preferentially lodges in caveolae of the sarcolemma at T tubules and crests. Isoform NOS2 resides in caveolae and SR membrane.
- 24.
Calcium ion signaling ability derives almost entirely from its binding to and unbinding from target proteins and its fluxes through permeable carriers that depolarize the plasma membrane. The cyclic rise and fall of intracellular Ca 2+ concentration engages and disengages the molecular machinery of contractile myofilaments.
- 25.
During restoration, cytosolic Ca 2+ ions reenter the sarcoplasmic reticulum through sarco(endo)plasmic reticulum Ca 2+ ATPase (SERCA) and is extruded to the extracellular space by sarcolemmal Na +–Ca 2+ exchanger (NCX) and plasma membrane Ca 2+ ATPase (PMCA).
- 26.
Myokinase converts ATP and AMP into 2 ADP molecules.
- 27.
Oxidation of NADH at ETCcomplex-I is indirectly coupled to ATP production. Oxidation of FADH2 bypasses ETCcomplex-I, thereby pumping fewer H + across the inner mitochondrial membrane. Therefore, in addition to a greater oxygen requirement than that using glucose as input substrate, fatty acids are less efficient for the generation of ATP than glucose [38].
- 28.
Most exogenous triacylglycerols derive from chylomicrons; a minor part originates from VLDL particles. A significant proportion of fatty acids from VLDLs is taken up by cardiac VLDL–apoE receptors. VLDL-derived fatty acids are equally distributed between β-oxidation and deposition into intramyocardial lipids.
- 29.
Concentration of FFAs can vary from very low values in the fetal circulation to more than 2 mmol during myocardial ischemia and uncontrolled diabetes [38]. Activated sympathetic nervous system can rapidly increase circulating FFA concentration, primarily via stimulation by β-adrenoceptors of hormone-sensitive lipase in adipose tissue. Lipoprotein lipase is responsible for most FFAs from chylomicrons used for fatty acid β-oxidation.
- 30.
Uncoupling proteins (UCP1–UCP5) are mitochondrial transport proteins that serve for the reentry of protons from the intermembrane space to the mitochondrial matrix uncoupled to ATP synthesis. Subtype UCP1 is highly expressed in brown adipose tissue, but not in the heart. Ubiquitous UCP2 minimizes generation of mitochondrion-derived reactive oxygen species. Isoform UCP3, a fatty acid anion transporter, is highly produced in the heart, skeletal muscle, and brown adipose tissue.
- 31.
Fatty acid anions are also generated in the cytosol during hydrolysis of cytosolic fatty acylCoA by cytosolic thioesterases.
- 32.
Pyruvate dehydrogenase is phosphorylated (inactivated) by pyruvate dehydrogenase kinase (PDHK) and dephosphorylated (activated) by pyruvate dehydrogenase phosphatase (PDHP). Among the 4 isoforms (PDHK1–PDHK4), PDHK4 is the predominant cardiac isoform. Pyruvate dehydrogenase kinase is inhibited by pyruvate and reduced acetylCoA/CoA and NADH/NAD + ratios [38]. A high level of circulating free fatty acids and intracellular accumulation of long-chain fatty acids support NR1c1-mediated PDHK4 synthesis. Pyruvate dehydrogenase phosphatase is activited by Ca 2+ and Mg 2+ ions.
- 33.
Pyruvate is the usual mitochondrial fuel produced by glycolysis.
- 34.
Mutations in the OPA1 gene cause autosomal dominant type-1 optic atrophy. Optic atrophy protein OPA1, a.k.a. mitochondrial genome maintenance protein MGM1 and mitochondrial nucleoid protein, contains a mitochondrial targeting signal, hence localizing to mitochondria.
- 35.
Methyltransferases of the NOL1–NOP2–SUn (Sad1P [Schizosaccharomyces pombe] and Unc84 [Caenorhabditis elegans)] domain-containing protein family catalyzes the methylation of cytosine to 5-methylcytosine. The proteic domain refers to ribosomal RNA methyltransferase nucleolar protein homolog NoL1, also called NoP2 and NSun1, which is found in archaeal, bacterial, and eukaryotic proteins.
- 36.
Subunit Med13 is also targeted by miR208a and other muscle-specific miRNAs encoded by introns of myosin heavy-chain genes.
- 37.
Pyruvate dehydrogenase enables entry from glycolysis to oxidative phosphorylation. Glycogen processing by glycogen phosphorylase is the early metabolic response to cardiac work change.
- 38.
Adenine nucleotide transport occurs as an electroneutral divalent exchange of MgATP 2− for HPO4 2− anion. In biology, phosphorus is found as a free phosphate ion in solution and is called inorganic phosphate (generally denoted P i ) to distinguish it from phosphates bound in various phosphate compounds, especially adenosine phosphates (AMP, ADP, and ATP). In a dilute aqueous solution, phosphate exists in 4 forms. The phosphate ion (PO4 3−) is the conjugate base of the hydrogen phosphate divalent ion (HPO4 2−) that is the conjugate base of the dihydrogen phosphate monovalent ion (H2PO4 −), which in turn is the conjugate base of phosphoric acid (H3PO4). In humans, H +- and Na +-dependent renal type-2a sodium–phosphate cotransporter also has a preferential affinity for the inorganic phosphate species HPO4 2− [52].
- 39.
Electrogenic ATP 4−–ADP 3− exchange. The charge imbalance associated with the adenine nucleotide carrier leads to a large difference in the ATP/ADP ratio between the mitochondrial matrix space and cytosol. The transport of ATP, ADP, and phosphate across the inner mitochondrial membrane costs additional energy (about 1/3 of the minimum required for ATP synthesis within the mitochondrial matrix) supplied by the respiratory chain.
- 40.
I.e., ONOO − reacts nucleophilically with carbon dioxide. In vivo, the concentration of CO2 is about 1 mmol; its reaction with ONOO − occurs quickly to form nitrosoperoxycarbonate (ONOOCO2 −).
- 41.
An adduct (Latin adductus: strict) is a product of a direct addition of at least 2 distinct molecules forming a single reaction product that contains all atoms of all components.
- 42.
Dissociation of a molecule generating 2 free radicals.
- 43.
In chemistry, the cage effect describes influence of its surroundings on properties of a molecule. In a solvent, a molecule is often supposed existing in a cage of solvent molecules, the so-called solvent cage. Reactions occur when a molecule occasionally exits and meets another molecule.
- 44.
Hydrogen peroxide carries out a 2-electron oxidation of heme-peroxidase produced compound-1 (obtained by monovalent reaction from NO2 − into NO2 •) and compound 2 (result of another NO2 • molecule forming a second molecule of NO2 •). Nitrogen dioxide can promote nitration of free and protein tyrosine, performing Tyr oxidation to tyrosine, followed by the addition of a second NO2 • molecule [58]. However, nitrogen dioxide alone is an inefficient nitrating catalyst, as 2 NO2 • molecules are needed to nitrate one tyrosine and because NO2 •-mediated oxidation of tyrosine is slow w.r.t. oxidation of thiols.
- 45.
SCOT-knockout mice develop hyperketonemic hypoglycemia and die within 48 h of extrauterine life [71].
- 46.
D3-Hydroxy[3-14C]butyrate is incorporated into lipid in lactating mammary glands of rats, a major site of ketone body utilization. This incorporation decreases in short-term insulin deficiency (2 h) and starvation (24 h), but increases again on refeeding (2 h) [72]. The activity of cytosolic acetoacetylCoA synthase follows changes in nutritional state, but is not affected by short-term insulin deficiency.
- 47.
β-Oxidation is the sequential derivation of 2 carbon units in the form of acetylCoA from fatty acyl chains. It mainly occurs within the mitochondrial matrix and sometimes in peroxisomes.
- 48.
I.e., synthesis of new lipids from acetylCoA using acetylCoA carboxylase and fatty acid synthase.
- 49.
In obesity, lipolysis is deregulated. The basal lipolysis rate rises. The concentration of circulating free fatty acids augments, hence provoking insulin resistance. Stimulation of lipolysis by catecholamines as well as its inhibition by insulin are precluded.
- 50.
Nicotinic acid, also termed niacin, vitamin-B3, and vitamin-PP, is used in the treatment of dyslipidemia. It increases the concentration of high-density lipoproteins and decreases that of very-low-density and low-density lipoproteins [73]. Nicotinic acid also lowers plasma concentrations of free fatty acids and triglycerides. It decreases lipolysis in adipocytes, as it impedes cAMP accumulation via the Gi–ACase axis and hormone-sensitive triglyceride lipase [74].
- 51.
Two subtypes of GPR109 exist (GPR109a–GPR109b) that are also called nicotinic acid and niacin receptor-1 and -2 (NiacR1–NiacR2) as well as protein upregulated in macrophages by interferon-γ (PUMaγ) in mice and HM74a and HM74b (HM74) in humans. NiacR1 and NiacR2 are high- and low-affinity receptor for nicotinic acid, respectively [73]. Receptor NiacR1 is highly expressed in adipose tissue and spleen. In fact, NiacR1 is also detected in the lung and trachea, whereas NiacR2 resides in the lung, adipose tissue, and spleen, as well as leukocytes. The ligand-inducible nuclear receptor NR1c3 (or PPARγ) is necessary and sufficient for adipogenesis, as it controls the differentiation, maintenance, and function of adipocytes. It also regulates numerous genes of the adipocytic phenotype, such as those involved in lipid uptake (e.g., lipoprotein lipase, scavenger receptor ScaRb3, and oxidized LDL receptor) and synthesis, lipid storage and lipid droplet stabilization (e.g., perilipin), glycerol and fatty acid recycling (i.e., reesterification of fatty acids and glycerol to triglycerides), and fatty acid oxidation [75]. The transcription factor NR1c3 has 2 isoforms, NR1c3a (PPARγ1) and NR1c3b (PPARγ2). The latter that has a longer N-terminus is restricted to adipocytes. The former is more widely distributed (e.g., adipocytes, enterocytes, monocytes, and macrophages). Polyunsaturated fatty acids and eicosanoids activate NR1c3 factor. Factor NR1c3 heterodimerizes with retinoic acid X receptors (NR2b) and binds to PPAR-responsive elements (PPREs). The human antilipolytic G-protein-coupled receptors comprise GPR81, GPR109a, and human-specific GPR109b. The genes that possess a NR1c–NR2b-binding site in their promoter, such as those encoding GPR81, GPR109a, and GPR109b, contribute to the reduction of circulating free fatty acids [75]. The Gpr81, Gpr109A, and Gpr109B genes colocalize in chromosome 12q24.31. In addition, certain aromatic Damino acids, including Dphenylalanine, Dtryptophan, and the metabolite of the latter, Dkynurenine, connect to GPR109b, which abounds in human neutrophils, but not GPR109a [76]. DIsomers may operate as hormonal, antibacterial, or modulatory peptides of immunity, or neuropeptides. They serves as chemoattractants for neutrophils via activated GPR109b. They diminish the activity of adenylate cyclase and elicit a transient influx of calcium ions. The potent chemotactic factor for eosinophils and neutrophils, 5-oxo-eicosatetraenoic acid, links to GPR48 receptor, which has high sequence similarity to GPR109b. Other chemotactic GPCRs comprise GPCRs for leukocyte chemoattractants CXCL8, C5a, Nformyl methionyl-leucyl-phenylalanine (fMLP), platelet-activating factor, and leukotriene-B4), as well as human, neutrophil-specific, Gi/o- and Gq-coupled GPR43 receptor for short chain fatty acids, such as sodium acetate and sodium propionate, which are by-products of anaerobic bacteria.
- 52.
Acetate is rapidly taken up by cells and is transformed to acetylCoA in both the cytosol and mitochondria by acetylCoA synthase. AcetylCoA is a common metabolic intermediate for synthesis of cholesterol and fatty acids, which are incorporated into membranes. In mitochondria, acetylCoA is also oxidized in the tricarboxylic acid cycle to carbon dioxide and water. The radiochemical acetate is used as a positron emission tomography (PET) tracer for studying myocardial oxidative metabolism and regional myocardial blood flow.
- 53.
In tumoral cells, overexpressed fatty acid synthase converts most of the acetate into fatty acids that are incorporated into intracellular phosphatidylcholine-based membrane nanodomains.
- 54.
A.k.a. ankyrin-R, R standing for restricted expression and RBC-related isoform.
- 55.
A.k.a. ankyrin-B referring to broad expression and brain-related isoform.
- 56.
A.k.a. ankyrin-G (general expression).
- 57.
Interacting proteins include PKA, CamK2, methylase, cytosolic protein Tyr phosphatase PTPn3, glycerol-3-phosphate dehydrogenase 1-like protein (GPD1L), α-actinin, ankyrin-3, calcium ion, calmodulin, caveolin-3, N-cadherin, connexin-43, disc large homolog DLg1, fibroblast growth factor FGF12, Nedd4-2 ubiquitin ligase, plakophilin-2, RanGRF, syntrophin-α1, -β1, -β2, and -γ2, telethonin, and 14-3-3η [89]. N-glycosylation of NaV1.5 associated with glycogenes (i.e., glycosyltransferases, glycosidases, and sugar nucleotide synthesis and transporters) modulates its electrical signaling. It is phosphorylated by PKA, PKC, CamK2, Fyn, and dephosphorylated by PTPn3 [89].
- 58.
In addition to SucnR1, extracellular succinate is actively transported through sodium–dicarboxylate cotransporters. These cotransporters are not produced in the heart.
- 59.
Current models use local tensors representing electrical conductivity and mechanical stiffness parameters in 3 orthogonal directions (myofiber, in-sheet transverse, and sheet-normal axis) in few parietal layers.
- 60.
Typically, it consists of a periodic train of brief pulses (duration 1 ms; magnitude ∼ twice the amplitude required to excite fully recovered tissue).
- 61.
The mean arterial pressure is underestimated using 0.333 as a multiplier rather than 0.412 [121]:
$$\mathrm{mAP} = p_{\mathtt{d}} + 0.412(p_{\mathtt{s}} - p_{\mathtt{d}}).$$ - 62.
Acetylcholine primes vasodilation of both local and regional arterioles and arteries.
- 63.
Subtype PKG1 is the predominant vascular isoform.
- 64.
A major subtype in smooth myocytes.
- 65.
On the other hand, PKG activated by the NO-cGMP axis phosphorylates numerous ion carriers, thereby reducing the cytosolic Ca 2+ level as well as causing a membrane hyperpolarization, hence a relaxation of arterial smooth myocytes.
- 66.
The hydrostatic pressure decreases with height at a rate of ∼ 100 Pa/cm for an arterial (p a) and venous (p v) pressure and ∼ 0.1 Pa/cm for an alveolar pressure (p A).
- 67.
Four MLCK types exist: skeletal (skMLCK), cardiac (cMLCK), and smooth muscle (smMLCK) isoforms encoded by the MYLK2, MYLK3, and MYLK1 genes, respectively, as well as nonmuscle MLCK (nmMLCK) with 4 high-molecular-weight isoforms (MLCK1–MLCK4) that are splice variants translated from the MYLK1 gene. Isoforms MLCK1 and MLCK2 are the most highly expressed subtypes in the vascular endothelium.
- 68.
Glycosaminoglycans are linear heteropolysaccharides, combination of which create different GAG types, such as heparan (50% of the total GAG pool at the endothelial surface), chondroitin, and dermatan sulfate, and hyaluronic acid or hyaluronan. Membrane-bound glypicans with their heparan sulfate chains localize to caveolae. Transmembrane syndecans cluster in the outer edge of caveolae. They connect to the cytoskeleton. Hyaluronan is a very long glycosaminoglycans that is not sulfated. It is not attached to a core protein. Transmembrane epican, or heparan sulfate proteoglycan, can contain chondroitin and heparan sulfate as well as oligosaccharides. It localizes to caveolae.
- 69.
A glycoprotein has short oligosaccharide branched chains. Glycoproteins encompass many receptors on the cell surface, such as integrins, selectins, and members of the immunoglobulin superfamily.
- 70.
After removal of the glycocalyx by heparinase, cultured endotheliocytes do not align in the streamwise direction and can proliferate after 1 d of experiencing flow.
- 71.
The skin and skeletal muscles jointly contain around two-thirds of the extracellular fluid.
- 72.
Chaperone HSP90 binds to both NOS3 and sGC and facilitates their interaction, stabilizing sGC and enhancing cGMP production.
- 73.
Isoform VEGFa, or VEGF, is synthesized in almost all cells subjected to hypoxia or other stress types. These proteins signals upon binding to their cognate receptors, in particular VEGFR1 to VEGFR3, once they homo- and heterodimerize. They operate as a potent (but not very powerful) endothelial growth factor, a powerful vascular permeabilizing agent, and a potent vasodilator.
- 74.
In cultured endothelial monolayers most often stimulated by thrombin as an acute inflammatory stimulus, paracellular gap formation is blocked upon inhibition of RoCK or MLCK, but not in situ. Thrombin launches an active cell RhoA-dependent contraction that creates large gap formation and, hence, an acute increase in endothelial barrier permeability. Some of the effects of thrombin on vascular permeability result from the release of other inflammatory mediators from mastocytes or neurons. Thrombin primes a contraction-dependent increase in permeability [150]. On the other hand, platelet-activating factor rises endothelial permeability in a cell contraction-independent manner in inflamed rat mesentery venules. In addition, thrombin activates platelets that contribute to elevated endothelial permeability.
- 75.
A.k.a. synectin-binding RhoA exchange factor (Syx).
- 76.
In Drosophila melanogaster, the Crumbs polarity complex includes: (1) type-1 transmembrane Crumbs (Crb) and (2) Stardust (Sdt), a scaffold protein of the MAGUK (membrane-associated guanylate kinase) family. In humans, it comprises: (1) Crumbs homologs (Crb1–Crb3) encoded by 3 genes and (2) members of the P55-like (P55 Stardust) MAGUK subfamily, or membrane protein, palmitoylated (MMP1–MMP7), among which MPP5, or protein associated with Lin7 PALS1, is most similar to Stardust; (3) protein (PALS1) associated with tight junctions (PATJ) and its related molecule multiPDZ domain-containing protein MuPP1; and (4) Lin7 homolog-C (Lin7a–Lin7c; Abnormal cell lineage Lin7 in Caenorhabditis elegans) encoded by 3 genes.
- 77.
Macromolecular transport is not always coupled with water flows. Furthermore, capillaries without large pores exist.
- 78.
The CSNK1D and CSNK1E genes encode casein kinases CK1δ and CK1ε, respectively.
- 79.
The circadian clock in the suprachiasmatic nucleus (Bmal1-based oscillator) is entrained by light. Another circadian clock in the dorsomedial nucleus of the hypothalamus (also Bmal1-based oscillator) is primed by food [173].
- 80.
Fibrinolytic activity falls during early morning hours.
- 81.
Several proteins encoded by these genes tune lipogenesis and lipolysis, as well as lipid droplet stability (e.g., adiponutrin, 1-acylglycerol-3-phosphate O-acyltransferase, and diacylglycerol O-acyltransferase-2 that are involved in lipogenesis) on the one hand, and glycogenolysis and glycolysis (e.g., protein kinase-A, protein phosphatase-1, and phosphofructokinase) [179]. Moreover, the transcriptional activity of peroxisome proliferator-activated receptors PPARα (NR1c1) that activates genes for fatty acid oxidation is controlled by the circadian clock of the cardiomyocyte.
- 82.
Metabolomics technology relies on method coupling (mass spectrometry, gas and liquid chromatography, and capillary electrophoresis. Hepatic lipase mRNA in the mouse liver has a peak expression slightly before that of lysophosphatidylcoline [171].
- 83.
Image-guided radiofrequency ablation treats cancers particularly localized to the liver, kidney, and adrenal glands by heating. One or more radiofrequency needles are inserted into the tumor. Cryotherapy uses gas-refrigerated cryoprobes, which are inserted inside the tumor, initiating the formation of ice balls to destroy cancerous cells by freezing and thawing processes. One of the main difficulties is the determination of the optimal position of the probes and treatment duration for complete destruction of cancerous cells without damaging too many surrounding normal cells. Another kind of tumor therapy consists of thermal and mechanical exposure to high-frequency focused ultrasound (HIFU). Tumor antigens and other compounds released from destroyed cells can stimulate antitumoral immunity. The optimal exposure time is an important parameter to avoid damage of normal cells, especially walls of neighboring blood vessels.
- 84.
Pennes underestimated the magnitudes of the conduction and convection terms in the energy balance, using inappropriate values of tissue thermal conductivity and tissue perfusion rate.
- 85.
Receptor OR51e2 may be activated by several androgens.
- 86.
Short-chain fatty acids are terminal products of fermentation by the gut microbiota that enter the blood circulation.
- 87.
Receptor OR51e2 is unresponsive to other SCFAs. Renin release by juxtaglomerular apparatus cells depends on calcium-inhibitable adenylate cyclase AC5 and/or AC6 isoforms. On the other hand, AC3 produced in macula densa cells participates in renin secretion by juxtaglomerular apparatus cells as a paracrine factor.
- 88.
Stretch-activated currents have been described in various mammalian cell types, such as vascular smooth myocytes, renal epithelicytes, somatosensory dorsal root ganglion neurons, and inner ear hair cells.
- 89.
Polycystic kidney disease-2.
- 90.
Previously called polycystin-1.
- 91.
Carbon monoxide is a messenger and regulator of TREK1 as well as epithelial Na + (ENaC) channels, in addition to calcium-activated K + (BK), KV2.1, CaV1, and ligand-gated ionotropic P2X (e.g., P2X2 and P2X4).
- 92.
Matricryptic sites are active sites, such as Arg–Gly–Asp (RGD) and Leu–Asp–Val (LDV), are hidden in the mature secreted form of matrix molecules. They become exposed upon conformational changes caused by oligomerization, adsorption, and mechanical stress. Matricryptic sites contribute in particular to acute changes in vascular permeability and fibrin–fibronectin polymerization in wound repair. Matricryptins are active fragments of matrix molecules with exposed active matricryptic sites. They can bind to specific integrins and regulate arteriolar tone using calcium and potassium channels.
- 93.
Hormone-like substances that act locally and briefly.
- 94.
The membrane is maintained in a relatively depolarized state, partially because of inhibition of K + channels.
- 95.
Skin circulation is mostly regulated via the rostral ventromedial medulla and medullary raphe [221].
- 96.
When it is not caused by vascular or renal disorders, hypertension can be due to a strong sympathetic tone.
- 97.
The parabrachial nucleus is separated by the brachium conjunctivum into 2 main regions: the lateral and medial parabrachial nuclei. The lateral parabrachial nucleus is connected to the rostral ventral lateral medulla and nucleus of the solitary tract. The lateral parabrachial nucleus can be further subdivided to the dorsal (dPBN), ventral (vPBN), central (cPBN), and external lateral (elPBN) parabrachial nuclei.
- 98.
In anesthetized cats, mean arterial pressure and renal sympathetic nerve activity rely on NO, especially that synthesized by NOS2 in the rostral ventrolateral medulla [224].
- 99.
Two groups of parasympathetic vasodilatory fibers originate from the chorda tympani nerve, a branch of the facial nerve, and from the trigeminal portion of the distal lingual nerve (probably via the glossopharyngeal nerve) [225].
- 100.
Formerly known as metastin, as it was originally identified as a human metastasis suppressor. Its alias is formed by 2 groups of letters “Ki” refering to the location of its discovery, Hershey, Pennsylvania, home of Hershey Chocolate Kiss and “SS” for suppressor sequence. Kisspeptin is encoded by the KISS1 gene. The gene product is a 145-amino acid precursor that is cleaved to 54-amino acid peptide, which can be further truncated to 14-, 13-, or 10-amino acid C-terminal fragments, the kisspeptins. Kisspeptin145 represents the precursor, kisspeptin54 (or kisspeptin \(_{(68--121)}\)) the peptide, and kisspeptin14 (or kisspeptin \(_{(108--121)}\)), kisspeptin13 (or kisspeptin \(_{(109--121)}\)), and kisspeptin10 (or kisspeptin \(_{(112--121)}\)) the C-terminal fragments. Kisspeptin signaling in the brain mediates the negative feedback action of sex steroids on gonadotropin secretion, generating the preovulatory GnRH–LH surge, triggering and guiding the tempo of sexual maturation at puberty, controlling seasonal reproduction, and restraining reproductive activity during lactation [226]. The KISS1 gene expression is regulated by estradiol (E2) in the hypothalamus. Kisspeptin-1 is also synthesized in the neocortex of fetal adrenal glands. It stimulates secretion of aldosterone [226]. It is also produced in pancreatic β cells, where it can stimulate insulin release (auto- and paracrine action). Kisspeptin54, -13, and -10 are potent vasoconstrictors. Kisspeptin-1 is a G-protein-coupled receptor ligand for GPR54 (or Kiss1R). The kisspeptin-Kiss1R complex initiates secretion of gonadotropin-releasing hormone (GnRH) at puberty. Synthesized in the brain, kisspeptin unleashes hormones that stimulate the production of estrogen or testosterone in ovaries and testes, starting the physical transformations of puberty. Menopause is characterized by ovarian follicle depletion, reduction of ovarian steroids, compensatory gonadotrophin hypersecretion, and hypertrophy of neurons expressing neurokinin-B (NKB), kisspeptin-1, and estrogen receptor-α within the hypothalamic infundibular (arcuate) nucleus.
- 101.
Neurokinin-B is encoded by the TAC3 (tachykinin-3) gene. On the other hand, the other human tachykinin gene, the TAC1 gene, encodes neurokinin-A (or substance-K), neuropeptide-K (or neurokinin-K), neuropeptide-γ, and substance-P.
- 102.
Dynorphin, an opioid peptide derived from the prodynorphin gene product, inhibits the reproductive axis. The dynorphin gene expression decreases in postmenopausal women. The secretion of luteinizing hormone can then rise [227].
- 103.
Secretion of GnRH into portal capillaries stimulates luteinizing hormone (LH) secretion from the anterior hypophysis, which stimulates the secretion of 17β-estradiol from the ovary. The negative feedback primed by 17β-estradiol via NR3a1 reduces the plasma LH level and decreases neurokinin-B and kisspeptin synthesis in KND+ neurons.
- 104.
Renal vasoconstriction reduces the blood supply, causing excessive renin secretion and inappropriate salt and water retention.
- 105.
In 1898, R. Tigerstedt and P. Bergman discovered that a cortical extract of rabbit kidney causes vasoconstriction when injected intravenously [236]. They isolated the substance that was named renin.
- 106.
The Na +–K + ATPase is a heteromeric enzyme that comprises a catalytic α and a glycosylated β subunit. The central isoform-specific region is targeted for protein kinase-C activation. This pump catalyzes the export of 3 Na + ions and import of 2 K + ions at the expense of 1 ATP molecule. α4-Isoform lodges exclusively in the sperm tail. In the heart, the cytosolic Ca 2+ concentration increases during contraction and decreases during relaxation via sarco(endo)plasmic reticulum Ca 2+ ATPase and plasmalemmal Ca 2+ ATPase and Na +–Ca 2+ exchanger. Tha latter uses the Na + gradient established by Na +–K + ATPase. Inhibition of Na +–K + ATPase raises cytosolic Na + concentration. Therefore, Na +–Ca 2+ exchanger augments cytosolic Ca 2+ concentration, thereby causing a positive inotropic effect. α2-Isozyme is a main regulator of calcium in the myocardium, its inhibition increasing calcium influx and contractibility [237]. α1-Isoform depresses cardiac contractility via excess extracellular K + level without apparent changes in intracellular calcium handling.
- 107.
Somali waabaayo: arrow poison. Ouabain is also called G-strophanthin. It is found in ripe seeds of African plants Strophanthus gratus and the bark of Acokanthera ouabaio. It is a poisonous cardiac glycoside at high (micromolar to millimolar) concentrations. It is structurally related to digoxin, another lipophilic cardiac glycoside. It binds to and inhibits plasmalemmal Na +–K + ATPase (sodium pump). At low (nanomolar and subnanomolar) concentrations, at least in guinea pig ventriculomyocytes, this endogenous substance stimulates the Na +–K + ATPase (α1–α3-isoforms) [239].
- 108.
Receptor AT1 is expressed by epithelialocytes throughout the nephron, in the glomerulus, and renal blood vessels. Once it is activated, it promotes sodium reabsorption by stimulating both sodium–proton antiporter and sodium–potassium ATPase on the apical (luminal) and basolateral plasma membrane, respectively, in the proximal tubule of the nephron. It stimulates epithelial sodium channels in the collecting ducts. Furthermore, activated vascular AT1 induces vasoconstriction, which subsequently reduces renal blood flow and sodium excretory capacity.
- 109.
Respiratory sinus arrhythmia is the variation in heart rate occurring simultaneously with respiration. On ECG traces, it induces fluctuations of the R–R interval series.
- 110.
Nerve fibers in adventitia act by electrochemical stimulation at neuromuscular junctions and biochemical processes (release of neurotransmitters) preferentially at external layers of the media.
- 111.
Flowing vasoactive hormones act after transmural migration up to internal layers of the media.
- 112.
Latin limbus: border, edge, fringe, hem, selvage.
- 113.
The hypothalamic paraventricular nucleus receives direct noradrenergic, adrenergic, and peptidergic innervation from the nucleus of the solitary tract [250].
- 114.
Postural hypotension is defined as at least a 2.66-kPa decrease in systolic blood pressure or 1.33-kPa decrease in diastolic blood pressure upon standing.
- 115.
Nitrogenous wastes are excreted as ammonia, urea, or uric acid.
- 116.
Protein Ser/Thr kinases of the WNK (with no lysine [Lys or K]) set are characterized by the absence of lysine usually found in the catalytic domain of all other protein serine/threonine kinases. Kinases WNK1 and WNK4 are expressed in the distal convoluted tubule, connecting tubule, and collecting duct of the nephron (Vol. 4 – Chap. 5. Cytoplasmic Protein Ser/Thr Kinases).
- 117.
Angiotensin-2 also directly stimulates renal sodium reabsorption, independently of aldosterone.
- 118.
Uncoupling protein-1 in mitochondria of brown adipose tissue produces heat by nonshivering thermogenesis, a primary process of heat generation in human infants.
- 119.
Receptors V1 and V3 are also called V1Ra and V1Rb receptors, respectively.
- 120.
Reflex control of the cardiovascular system mainly involves baroreceptors, afferents to the central nervous system, cardiovascular centers, and sympathetic and parasympathetic efferents to the heart and vasculature. The potentialization of baroreflexes is done via central action, activating V1-receptors in the area postrema, and sensitization of the arterial baroreceptors, as well as cardiac afferents.
- 121.
Lack in vasopressin or in V2 receptor in the collecting ducts is responsible for central and nephrogenic diabetes insipidus, respectively.
- 122.
A.k.a. NPRa and GCa.
- 123.
A.k.a. NPRb and GCb.
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Thiriet, M. (2014). Cardiovascular Physiology. In: Anatomy and Physiology of the Circulatory and Ventilatory Systems. Biomathematical and Biomechanical Modeling of the Circulatory and Ventilatory Systems, vol 6. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9469-0_3
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