Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery

Abstract

The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh- and VIP-induced effects. Acetylcholine caused endothelium-dependent and VIP endothelium-independent relaxations of facial artery. The effect of ACh was partly inhibited by NG-monomethyl-l-arginine (l-NMMA, a non-selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of l-NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 mm KCl. The VIP-induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by l-NMMA or S-methyl-l-thiocitrulline (l-SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected by indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium-derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3',5'-monophosphate (cAMP) in vascular smooth muscles and by VIP-induced release of NO from perivascular nerve fibers.

Location and Function of VPAC1, VPAC2 and NPR-C Receptors in VIP-Induced Vasodilation of Porcine Basilar Arteries

“…This would explain why there are multiple receptor types present (an in-built redundancy of some receptors due to the importance of VIP-induced vasodilation). This is in agreement with previous studies which have shown endothelium-independent VIP-induced vasodilation of cerebral arteries (Duckles and Said, 1982;Lee et al, 1984;Gaw et al, 1991;Stojic et al, 2003). Additional evidence that VIP acts through each of these receptors in porcine basilar arteries is provided by the significant attenuation of VIPinduced vasodilation by VPAC 1 , VPAC 2 or NPR-C antagonists.…”

“…Both VPAC 1 and VPAC 2 receptors have been shown to be expressed in equal amounts in human cerebral arteries regardless of endothelium; however, their location remains undetermined (Knutsson and Edvinsson, 2002). This finding concurs with previous experiments which have shown that VIP-induced vasodilation of cerebral arteries is independent of endothelium (Duckles and Said, 1982;Lee et al, 1984;Edvinsson and McCulloch, 1985;Nozaki et al, 1990;Gaw et al, 1991;Stojic et al, 2003). A third receptor has been identified to mediate VIP-induced relaxation of gastric smooth muscle: this is the natriuretic peptide clearance receptor (NPR-C) receptor (Akiho et al, 1995;Murthy et al, 2000).…”

Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit

“…The vasomotor function of parotid arteries from diabetic and control rabbits was examined in vitro by measurement of isometric tension, as described previously (17). In brief, parotid arteries were carefully removed and placed in oxygenated Krebs solution.…”

The Relaxant Effect of Vasoactive Intestinal Polypeptide in the Isolated Canine Uterine Artery: The Role of Endothelium

“…There are few studies reporting endothelium‐independent action of VIP in the different blood vessels, e.g. in human, bovine, rat and rabbit pulmonary artery, in porcine and canine coronary artery and rabbit facial artery (Beny et al., 1986; Greenberg et al., 1987; Nakashima et al., 1997; Stojic et al., 2003). On the contrary, in the rat and mouse aorta, rat mesenteric artery, porcine opthalmic artery endothelium‐dependent relaxation induced by VIP has been observed (Davies and Williams, 1983; Hattori et al., 1992; Bakken et al., 1995; Pomerleau et al., 1997).…”