Coronary artery hypoxic vasorelaxation is augmented by perivascular adipose tissue through a mechanism involving hydrogen sulphide and cystathionine‐β‐synthase

Abstract

PVAT augments hypoxic relaxation of coronary arteries through a mechanism involving H S and CBS, pointing to an important role in regulation of coronary blood flow during hypoxia.

Perivascular adipose tissue: A new possible tissue augmenting coronary vasodilatation in response to acute hypoxia

“…H 2 S is an active regulator of the vascular tone as it also causes relaxation in large porcine coronary arteries. 1 Blockers of the H 2 S synthesizing enzymes in the vascular wall inhibit coronary artery relaxation induced by hypoxia, 1,3,4 hence suggesting H 2 S is involved in the response to acute hypoxia. H 2 S is produced endogenously in mammals from L-cysteine by cystathionine-γ-lyase (CSE) or cystathionine-ß-synthase (CBS), and from 3-mercaptopyruvate by 3-mercaptopyruvate sulfurtransferase (MPST).…”

“…H 2 S is produced endogenously in mammals from L-cysteine by cystathionine-γ-lyase (CSE) or cystathionine-ß-synthase (CBS), and from 3-mercaptopyruvate by 3-mercaptopyruvate sulfurtransferase (MPST). 1 The limitations of the methods is relatively low sensitivity and that the measurements are based on measurements in homogenates, which makes it difficult to establish a relationship to effect of acute hypoxia in intact tissue or vascular tone. 1 Blockers of the H 2 S synthesizing enzymes in the vascular wall inhibit coronary artery relaxation induced by hypoxia, 1,3,4 hence suggesting H 2 S is involved in the response to acute hypoxia.…”

“…9 Only few studies have investigated the effect of acute hypoxia on the anticontractile effect of perivascular tissue, and these studies repeatedly show an augmentation of the anticontractile effects of the perivascular tissue in the presence of hypoxia. 1 The present discovery is important, as epicardial , and endothelial release of nitric oxide (NO) through activation of soluble guanylate cyclase (sGC) increases cyclic inositol monophosphate (cIMP) and activates rho kinase (ROCK) leading to vasocontraction in response to acute hypoxia. In the large porcine coronary arteries, acute hypoxia induces contraction followed by relaxation, and while the presence of myocardium or PVAT inhibited contraction, only the presence of PVAT augmented the relaxations induced by acute hypoxia.…”

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Ralevic, V. 2018. Coronary artery hypoxic vasorelaxation is augmented by perivascular adipose tissue through a mechanism involving hydrogen sulphide and cystathionine -β synthase.

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Intermittent hypoxia: Friend and foe

“…Perivascular adipose tissue has gained growing attention because of its capacity to modulate vascular reactivity in response to hypoxia . Large porcine coronary arteries respond to acute hypoxia with an initial contraction followed by sustained vasodilation . Coronary perivascular adipose tissue has been reported to weaken endothelium‐dependent vasodilation by modulating K + channel activity and potentiate coronary artery contraction .…”