Mechanism of CGRP-induced vasodilation in the rat isolated perfused kidney


Ay I., Tuncer M.

PHARMACOLOGY, vol.71, no.4, pp.209-215, 2004 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 71 Issue: 4
  • Publication Date: 2004
  • Doi Number: 10.1159/000078087
  • Title of Journal : PHARMACOLOGY
  • Page Numbers: pp.209-215

Abstract

We investigated the intracellular mechanisms involved in calcitonin gene-related peptide (CGRP)-induced vasodilation in rat isolated perfused kidney. CGRP-1 receptor antagonist, CGRP-8-37, abolished the responses. Endothelial denudation by Triton X-100 or nitric oxide ( NO) synthase inhibition by N-G-nitro-L-arginine attenuated the maximum dilation by about 63 and 55%, respectively. Protein kinase A inhibitor, KT-5720, caused an about 72% inhibition in CGRP-induced maximum dilation. Soluble guanylate cyclase inhibitor, ODQ, and ATP-sensitive potassium channel blocker, glibenclamide, inhibited the CGRP-induced maximum responses by 75 and 55%, respectively. Cyclooxygenase inhibitor, indomethacin, had no effect. Our data suggest that CGRP-1 receptors, endothelium, NO synthase, protein kinase A, soluble guanylate cyclase, and ATP-sensitive potassium channels, but not the cyclooxygenase pathway, may play a role in CGRP-induced vasodilation in rat isolated perfused kidney. Copyright (C) 2004 S. Karger AG, Basel.