Abstract
Hypertension develops from a complex interaction of environmental and genetic factors although more than 90% of cases do not have clear etiology. Vasoactive peptide systems are among the major contributing factors to abnormal sustained blood pressure levels together with increased sympathetic nervous system activity, long-term high sodium intake, and inadequate dietary intake of potassium and calcium. For instance, an altered renin secretion related to the elevated activity of the renin-angiotensin aldosterone system (RAAS) leads to the formation of the vasoconstrictor peptide angiotensin II. Both hyperactivity of the angiotensin-converting enzyme (ACE), resulting in overproduction of angiotensin II (Ang II), and deactivation of the vasodilator kallikrein-kinin system (KKS) also alter the vascular tone. Otherwise, reduction of nitric oxide (NO) bioavailability also induces abnormalities in vessel resistance due to vascular inflammation and increased activity of vascular growth factors and metalloproteinases. There is evidence that elevated vasopressin (AVP) and neuropeptide Y (NPY) levels contribute to hypertension in a subset of human subjects by alterations in the corporal water homeostasis and acting centrally as an inhibitor of sympathetic outflow, respectively. Disturbances in the natriuretic peptide system inhibit renin release and sodium reabsorption as well as enhance the central sympathetic outflow, adrenal catecholamine release, and actions of angiotensin II and aldosterone. Although not directly linked to peptidic systems, adipocytokines, oxidative stress, and cells of both the innate and adaptive immune systems will be addressed in this chapter as recent contributions to cardiovascular dysfunction and end-organ damage in hypertension. Thus, taken together, dysregulation in vasoactive peptide systems, adipocyte hormones, redox balance, and cellular immunogenicity compose a current keystone for maintained high blood pressure levels, cardiac remodeling, and vascular stiffness in hypertensive disease.
Abbreviations
- ACE:
-
Angiotensin-converting enzyme
- Ang I:
-
Angiotensin I
- Ang II:
-
Angiotensin II
- Ang III:
-
Angiotensin III
- Ang IV:
-
Angiotensin IV
- ANP:
-
Atrial natriuretic peptide
- AT1R:
-
Angiotensin II type 1 receptor
- AT2R:
-
Angiotensin II type 2 receptor
- AVP:
-
Vasopressin
- B1:
-
Bradykinin type 1 receptor
- B2:
-
Bradykinin type 2 receptor
- BNP:
-
Brain natriuretic peptide
- CD8:
-
Cluster of differentiation 8
- CD-80:
-
Cluster of differentiation 80
- CD-86:
-
Cluster of differentiation 86
- DNA:
-
Deoxyribonucleic acid
- ERK-1:
-
Extracellular signal-regulated kinases types 1
- ERK-2:
-
Extracellular signal-regulated kinases types 2
- Hsp27:
-
Heat shock protein 27
- IFN-γ:
-
Interferon gamma
- IL-1β:
-
Interleukin-1β
- IL-23:
-
Interleukin-23
- IL-6:
-
Interleukin-6
- LVH:
-
Left ventricular hypertrophy
- MAPK:
-
Mitogen-activated protein kinase
- MMP:
-
Metalloproteinase
- MMP-2:
-
Metalloproteinase-2
- MMP-9:
-
Metalloproteinase-9
- MMPs:
-
Metalloproteinases
- NO:
-
Nitric oxide
- NPY:
-
Neuropeptide Y
- NTS:
-
Nucleus of the tractus solitarius
- PGI2 :
-
Prostacyclin
- RAAS:
-
Renin-angiotensin-aldosterone system
- ROS:
-
Reactive oxygen species
- TGF β-1:
-
Transforming growth factor β-1
- TIMPs:
-
Tissue inhibitor of metalloproteinases
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Yugar-Toledo, J.C., Faria, A.P.C., Moreno, H. (2018). Vasoactive Peptides. In: Berbari, A., Mancia, G. (eds) Disorders of Blood Pressure Regulation. Updates in Hypertension and Cardiovascular Protection. Springer, Cham. https://doi.org/10.1007/978-3-319-59918-2_8
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