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Hydrogen Sulfide: Physiological and Pathophysiological Functions

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Hydrogen Sulfide and its Therapeutic Applications

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Abstract

Hydrogen sulfide (H2S) has been recognized as an endogenous gaseous mediator. The past decade has seen an exponential growth of scientific interest in the physiological and pathological significance of H2S especially with respect to its roles in the central nervous and the cardiovascular systems. In cardiovascular system, H2S regulates heart contractile function and may serve as a cardioprotectant for treating ischemic heart diseases and heart failure. Alterations of the endogenous H2S level have been found in animal models with various pathological conditions such as myocardial ischemia, spontaneous hypertension, and hypoxic pulmonary hypertension. In the central nervous system, H2S facilitates long-term potentiation and regulates intracellular calcium concentration in brain cells. Intriguingly, H2S produces antioxidant, anti-inflammatory, and anti-apoptotic effects that may be of relevance to neurodegenerative disorders. Abnormal generation and metabolism of H2S have been reported in the pathogenesis of ischemic stroke, Alzheimer’s disease, Parkinson’s disease, and recurrent febrile seizure. Exogenously applied H2S is demonstrated to be valuable in the treatment against febrile seizure and Parkinson’s disease. In addition, H2S also regulates the physiological and pathological functions of kidney, pancreas and bone. Exogenously applied H2S may protect against ischemic kidney injuries and osteoporosis. This article surveys the growing recognition of H2S as an endogenous signaling molecule in mammals and its functions in different biological systems. We will emphasize on its physiological and pathological functions in the cardiovascular, central nervous and renal systems.

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Abbreviations

[Ca2+]i :

Intracellular Ca2+

±LVdp/dtmax :

Maximal/minimal left ventricular pressure development

1-K:

Uninephrectomy

2K1C:

2-Kidneys-1-clip

3-MST:

Mercaptopyruvate sulfurtransferase

6-OHDA:

6-Hydroxydopamine

AC:

Adenylyl cyclase

ACE:

Angiotensin-converting enzyme

AD:

Alzheimer’s disease

Ang II:

Angiotensin II

AOAA:

Aminooxyacetic acid

APD:

Action potential duration

ApoE:

Apolipoprotein E

ATN:

Acute tubular necrosis

ATP:

Adenosine triphosphate

AVF:

Arteriovenous fistula

BACE-1:

Beta-site amyloid precursor protein cleaving enzyme 1

BKCa :

Large Conductance Ca2+−activated potassium channels

BP:

Blood pressure

cAMP:

Cyclic adenosine monophosphate

CAT:

Cysteine aminotransferase

CBS:

Cystathionine β-synthase

cGMP:

Cyclic guanosine monophosphate

CKD:

Chronic kidney disease

CNS:

Central nervous system

CO:

Carbon monoxide

COX-2:

Cyclooxygenase 2

CSE:

Cystathionine γ-lyase

DA:

Dopamine/dopaminergic

DEANO:

Diethylamine nitric oxide

ECs:

Endothelial cells

EDHF:

Endothelium derived hyperpolarizing factor

ER:

Endoplasmic reticulum

ERK (MAPK):

Extracellular signal-regulated kinase

FENa :

Fractional excretion of Na+

FEK :

Fractional excretion of K+

FF:

Filtration rate

FS:

Febrile seizures

GABA:

Gamma-aminobutyric acid

GFR:

Glomerular filtration rate

GLT1:

Glial glutamate transporter 1

GSH:

Glutathione

GSK-3β:

Glycogen synthase kinase-3

GSSG:

Oxidized glutationine

H2S:

Hydrogen sulfide

HF:

Heart failure

HIF:

Hypoxia-inducible factors

HMC1.1:

Human mast cell line 1.1

HNO:

Nitroxyl anion

Hsp:

Heat shock protein

HUVECs:

Human umbilical vein endothelial cells

I/R:

Ischemia/reperfusion

ICAM-1:

Intercellular adhesion molecule 1

IKCa :

Intermediate conductance Ca2+-activated potassium channels

IL:

Interleukin

iNOS:

Inducible NO synthase

IPreC:

Ischemic preconditioning

IRR:

Intrarenal resistance

ISO:

Isoproterenol

JNK:

c-Jun N-terminal kinases

KATP :

ATP-sensitive potassium channel

LCA:

Left coronary artery

LDL:

Low-density lipoprotein

LPO:

Lipid hydroperoxidation

LPS:

Lipppolysaccharide

LTCC ICa, L :

L-type Ca2+ channels

MAP:

Mean arteriole pressure

MCAO:

Middle cerebral artery occlusion

MDA:

Malondialdehyde

MEK:

ERK Kinase

MI:

Myocardial infarction

MMP:

Matrix metalloproteinase

MPP+ :

1-Methyl-4-phenylpyridine

mPTP:

Mitochondrial permeability transition pore

MR:

Mental retardation

Na2S:

Sodium sulfide

NADPH:

Nicotinamide adenine dinucleotide phosphate

NaHS:

Sodium hydrosulfide

NF-E2:

Nuclear factor-erythroid-derived 2

NF-κB:

Nuclear factor kappa-light-chain-enhancer of activated B cells

NHE:

Na+/H+ exchanger

NO:

Nitric oxide

NOS:

Nitric oxide synthase

NRF-1:

Nuclear respiratory factor 1

Nrf2:

NF-E2 related factor 2

NSAIDs:

Non-steroidal anti-inflammatory drugs

ONOO- :

Peroxynitrite

PAG:

DL-Propargylglycine

PARP:

Poly (ADP-ribose) polymerase

p-CREB:

Phosphorlyated cAMP response element-binding protein

PD:

Parkinson’s disease

pHi :

Intracellular pH

PI3K:

Phosphoinositide 3-kinase

PKA:

Protein kinase A

PKC:

Protein kinase C

PGE:

Prostaglandin E2

PKG:

Protein kinase G

p-NR1:

Phosphorylated N-methyl-D-aspartate receptor 1 subunit

p-NR2A:

Phosphorylated N-methyl-D-aspartate receptor 2A subunit

p-NR2B:

Phosphorylated N-methyl-D-aspartate receptor 2B subunit

RAS:

Renin-angiotensin system

RBF:

Renal blood flow

ROS:

Reactive oxygen species

SBP:

Systolic blood pressure

SHR:

Spontaneously hypertensive rats

SIN-1:

3-Morpholinosydnonimine

SKCa :

Small conductance Ca2+-activated potassium channels

SMCs:

Smooth muscle cells

SNAP:

S-Nitroso-N-acetylpenicillamine

SNP:

Sodium nitroprusside

SOD:

Superoxide dismutase

SPreC:

H2S preconditioning

STAT:

Signal transducer and activator of transcription

TH:

Tyrosine hydroxylase

TNF:

Tumor necrosis factor

TUNEL:

Terminal deoxynucleotidyl transferase dUTP Nick end labeling

U.V:

Urine flow rate

UCP2:

Uncoupling protein 2

UK.V:

Urinary K+ excretion

UNa.V:

Urinary Na+ excretion

VCAM-1:

Vascular cell adhesion molecule-1

VEGF:

Vascular endothelial growth factor

WT:

Wild type

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Acknowledgements

This work was supported by research grants from Singapore National Medical Research Council (NMRC 1183 ⁄ 2008, 1219/2009) and Singapore Kidney foundation (NKFRC/2009/01/10).

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  1. Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 18 Medical Drive, Singapore, 117597, Singapore

    Yi Tong Liu & Jin-Song Bian

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  1. National Institut of Neuroscience, Tokyo, Japan

    Hideo Kimura

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Liu, Y.T., Bian, JS. (2013). Hydrogen Sulfide: Physiological and Pathophysiological Functions. In: Kimura, H. (eds) Hydrogen Sulfide and its Therapeutic Applications. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1550-3_6

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