Effect of Somatostatin on Rabbit Isolated Coronary Arteries

Abstract

ABSTRACT-Somatostatin analogues are capable of inhibiting vascular smooth muscle and endothelial cell proliferation. However, little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries in vitro. The aim of this work was to determine whether or not somatostatin prevented the contractile response induced by 5-hydroxytryptamine and acetylcholine in endothelium-denuded rabbit coronary arteries. Somatostatin attenuated the contraction produced by 5-hydroxytryptamine in both proximal (PC) and distal coronary (DC) arteries (contraction induced by 10 -4 M 5-hydroxytryptamine was inhibited by 10 -6 M somatostatin by 90.8 ± 11.0% (P<0.001, n = 9) and by 46.2 ± 14.0% (P<0.05, n = 9) in DC and PC, respectively), but concentration-dependently decreased the contraction induced by U46619 (11a-epoxy-methanoprostaglandin F2=) only in PC arteries, suggesting that the response of PC and DC arteries to somatostatin were qualitatively different. Furthermore, we suggest that somatostatin may enhance acetylcholine-induced relaxation by combination of increasing endothelium-dependent relaxation (by a NO-dependent mechanism) and blocking contraction at the muscle level.Keywords: Somatostatin, Coronary artery, Acetylcholine, 5-Hydroxytryptamine, Nitric oxide Vascular diseases as well as surgical interventions such as coronary angioplasty induce endothelial denudation (1, 2) in coronary arteries. Loss of the endothelial layer alters vascular responses to certain agonists; thus 5-hydroxytryptamine and acetylcholine, which induce vasodilatation in normal coronary arteries, might be impaired or even turn into vasoconstriction in endothelium-denuded coronary arteries, leading to coronary spasm (1, 3, 4). In addition, thromboxane A2 released by platelets (5) is another candidate for the mediation of coronary vasospasm (6) since it is found in increasing concentration at the site of coronary arterial stenosis (7).Somatostatin (SRIF) is a neouroendocrine peptide (8) that exerts a wide range of physiological actions. However, the vascular effects of somatostatin are still unclear. A variety of studies have demonstrated species and regional differences in the blood flow responses to somatostatin. Thus, while in the rat superior mesenteric artery, octreotride (a somatostatin analogue) boosts vasoconstriction induced by a -agonists (9), in the vascular bed of cats, somatostatin showed opposite effects (10). On the other hand, we and others have shown that, although somatostatin has no effect on arteries kept under resting tension, it relaxes arteries precontracted with noradrenaline in vitro (11,12). Despite positive effects of somatostatin found in animal models of coronary restenosis, based on the antiproliferative effect of this peptide on both vascular smooth muscle (13) and endothelial cells (14, 15), little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries. The purpose of this work was to determine whether or not somatostatin, in an 'in ...

Somatostatin induces rapid contraction of neuroendocrine cells

“…Somatostatin‐induced relaxation of smooth muscle has been observed in the gastrointestinal system and in blood vessels [5–7]. However, it has also been reported that somatostatin can induce contraction of smooth muscle [5,8].…”