Open AccessPossible Involvement of KATP Channel Activation in Depressor Responses to Vasoactive Neuropeptides in Rats
Author(s) -
Keiji Saito,
Kazushige Sakai
Publication year - 1998
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.76.227
Subject(s) - vasoactive intestinal peptide , calcitonin gene related peptide , cromakalim , endocrinology , medicine , neuropeptide , acetylcholine , chemistry , calcitonin , substance p , heart rate , glibenclamide , blood pressure , receptor , diabetes mellitus
I.v. bolus injections of vasoactive intestinal polypeptide (VIP) (0.3 or 1 microg/kg), calcitonin gene-related peptide (CGRP) (0.3 microg/kg) or substance P (0.1 microg/kg) to anesthetized rats reduced blood pressure, accompanied by slight increases in heart rate. Cromakalim (0.3 microg/kg/min) infused i.v. significantly potentiated the depressor responses to VIP and CGRP, but not those to substance P and acetylcholine (ACh) (0.1 microg/kg). Glibenclamide (20 mg/kg, i.v.) significantly inhibited not only the depressor responses to VIP and CGRP, but also the augmentation of the effects of the two agents by cromakalim. These results suggest that the depressor responses to VIP and CGRP are mediated in part through K(ATP) channel activation.