Actions and interactions of nitric oxide, carbon monoxide and hydrogen sulphide in the cardiovascular system and in inflammation — a tale of three gases!

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

“…H 2 S acts as a regulator of cardiovascular function [33,34] . The opening of smooth K ATP channels by H 2 S has been suggested to be one of the mechanisms responsible for H 2 S-induced vasorelaxation in vascular smooth muscle both in vitro and in vivo [24] . H 2 S can open K ATP channels in the cell membrane of aortic vascular smooth muscle, causing cytomembrane hyperpolarization.…”

“…So we tested the protein and mRNA expression of SUR2B and Kir6.1 in aortic and pulmonary arteries to investigate the possible mechanisms responsible for the regulation of vasorelaxation by H 2 S. H 2 S deficiency has been observed in animal models of systemic and pulmonary hypertension [16][17][18] . It also plays important roles in the pathogenesis of cardiovascular diseases [16][17][18][19][20][21][22][23][24] . The main mechanism for the cardiovascular actions of H 2 S was considered to be the activation of K ATP channels, because H 2 S increased whole-cell K ATP channel currents in rat aortic vascular smooth muscle cells [15] .…”

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

“…• NO) and carbon monoxide (CO; reviewed in explicit detail elsewhere [6][7][8][9][10]) have been proposed to induce, inhibit and regulate the inflammatory process.…”

“…However, a generalized overview to familarize the reader with the topic is pertinent. H 2 S has been proposed as a third physiological gaseous mediator along with CO and • NO, for which there appears to be considerable interplay (reviewed elsewhere [6,12]). Its formation in vivo is catalyzed predominantly by the pyridoxal phosphatedependent enzymes cystathionine-g-lyase (CSE) and cystathionine b-synthase (CBS), utilizing the amino acids l-cysteine, l-homocysteine and l-cystathionine (reviewed in [12]).…”

“…Its formation in vivo is catalyzed predominantly by the pyridoxal phosphatedependent enzymes cystathionine-g-lyase (CSE) and cystathionine b-synthase (CBS), utilizing the amino acids l-cysteine, l-homocysteine and l-cystathionine (reviewed in [12]). In the last decade, H 2 S has been shown to regulate a steadily growing list of physiological functions, such as blood pressure [13], insulin secretion [14,15], nociception [16], learning and memory [17] and inflammation [6], in part via the modulation of K ATP channel activity. As such, modulation of endogenous H 2 S through either inhibitors of its enzymatic synthesis or H 2 S-donor molecules represent viable and potentially therapeutic targets for a variety of human diseases where perturbed H 2 S synthesis is involved, such as hypertension [13,18,19], diabetes and obesity [18], hemorrhagic [20], endotoxic shock [21] and chronic inflammation (e.g., arthritis [22] and inflammatory bowel disease [23].…”