Abstract
Vasoactive intestinal peptide (VIP) a non-adrenergic non-cholinergic (NANC) transmitter widely distributed in both the central and peripheral nervous system is an endothelium-dependent vasodilator. The contribution of endothelium derived relaxing factors to VIP-induced relaxation remains unclear. We hypothesized that nitric oxide (NO) produced by endothelial NO synthase (eNOS) at the caveolae plays a role in this relaxation. We assessed the effect of VIP on isolated rat aorta rings in vitro which was incubated with either N-nitro-L-Arginine, L-NNA, (a NOS inhibitor), indomethacin (a cycloxygenase inhibitor), or methyl-beta-cyclodextrin (a membrane sequester that disassembles caveolae). In intact and denuded aortic rings precontracted with phenylephrine (PE, 0.1 μmol/L), the addition of VIP (1nmol/L to 1 μmol/L) produced relaxation in a dose-dependent manner. The maximal relaxation induced by VIP in endothelium-intact aortic rings (53 ± 9%, n=8) was impaired after removal of the endothelium (11 ± 2%, n=3, P<0.05), or in the presence of L-NNA (20 ± 11%, n=5, P <0.05) and methyl-β-cyclodextrin (20 ± 8%, n=6, P<0.05). In contrast, VIP-induced relaxation was enhanced in the presence of indomethacin (83 ± 7%, n=5, P<0.05). These data suggest that NO produced by eNOS at the caveolae plays a stimulatory role in VIP-induced relaxation in rat aorta, whereas prostaglandins play an inhibitory role.
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