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Mathilde Aalling

The Role of Endogenous H(2)S in Cardiovascular Physiology

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Recent research has shown that the endogenous gas hydrogen sulphide (H(2)S) is a signalling molecule of considerable biological potential and has been suggested to be involved in a vast number of physiological processes. In the vascular system, H(2)S is synthesized from cysteine by cystathionine-γ-lyase (CSE) in smooth muscle cells (SMC) and 3-mercaptopyruvate sulfuresterase (3MST) and CSE in the endothelial cells. In pulmonary and systemic arteries, H(2)S induces relaxation and/or contraction dependent on the concentration of H(2)S, type of vessel and species. H(2)S relaxes SMC through a direct effect on K(ATP)-channels or K(v)-channels causing hyperpolarization and closure of voltage-dependent Ca(2+)-channels followed by a reduction in intracellular calcium. H(2)S also relaxes SMC through the release of endothelium-derived hyperpolarizing factor (EDHF) and nitric oxide (NO) from the endothelium. H(2)S contracts SMC through a reduction in nitric oxide (NO) availability by reacting with NO forming a nitrosothiol compound and through an inhibitory effect on endothelial nitric oxide synthase (eNOS) as well as a reduction in SMC cyclic AMP concentration. Evidence supports a role for H(2)S in oxygen sensing. Furthermore, reduced endogenous H(2)S production may also play a role in ischemic heart diseases and hypertension, and treatment with H(2)S donors and cysteine analogues may be beneficial in treatment of cardiovascular disease.
Original languageEnglish
JournalCurrent Pharmaceutical Biotechnology
Pages (from-to)1385-1393
Number of pages8
Publication statusPublished - 2011

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