In the mammalian cardiovascular system, H2S joins carbon monoxide (CO) and endothelial derived relaxing factors, (EDRFs)-nitric oxide (NO), as the third gasotransmitter. In the vasculature, cystathionine-γ-lyase (CSE) is the main enzyme responsible for H2S biosynthesis starting from the substrate e.g. L-cysteine. There is a growing body of evidence that supports a role for H2S in regulating the vascular homeostasis. H2S (NaHS) is known to induce a concentration-dependent relaxation of large conduit arteries.
Interestingly, H2S also relaxes peripheral resistance vessels such as mesenteric arteries suggesting a role for H2S also in the regulation of vascular resistance and systemic blood pressure. This vasodilatory effect is dependent on the activation of KATP channels. However, a cross-talk exists between the L-Argine/NO and L-cysteine/H2S pathways.
Furthermore, it has been shown that H2S acts as an endogenous non-selective inhibitor of phosphodiesterase activity. Compelling evidence links H2S to regulation of erectile function while it remains unclear whether the L-cysteine/H2S pathway plays a pathogenetic role in erectile dysfunction. Despite the rapid growth of the field, it should be noted that several aspects of H2S physiology in the cardiovascular system remain unsolved and the lack of reliable inhibitors and donors remains a major limitation.
Keywords: Hydrogen sulphide, vasodilatation, cGMP, phosphodiesterase, cardioprotection, angiogenesis, gasotransmitter, KATP channels, H2S biosynthesis, cardiovascular system
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