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NEUROGENIC VASODILATATION IN ISOLATED PERFUSED SEGMENTS OF RABBIT JEJUNAL ARTERY
Author(s) -
La M.,
Rand M. J.
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb01704.x
Subject(s) - vasodilation , calcitonin gene related peptide , medicine , endocrinology , stimulation , nitric oxide , propranolol , atropine , tetrodotoxin , acetylcholine , nitric oxide synthase , chemistry , neuropeptide , receptor
SUMMARY 1. Vasodilator responses were elicited by field stimulation in isolated perfused segments of rabbit jejunal arteries when noradrenergic and purinergic vasoconstrictor responses had been abolished and the smooth muscle partly contracted by endothelin. 2. The stimulation‐induced vasodilator responses were abolished by tetrodotoxin, but were not affected by atropine, propranolol or a nitric oxide synthase inhibitor. 3. After recovery from the vasodilator action of capsaicin, the stimulation‐induced vasodilator responses were greatly reduced or abolished. 4. A competitive antagonist of calcitonin gene‐related peptide (CGRP) blocked vasodilator responses elicited by field stimulation and exogenously administered CGRP. 5. The findings indicated that the mediator of the stimulation‐induced vasodilator responses is neurogenic in origin, and it is not acetylcholine, noradrenaline acting on P‐adrenoceptors, nitric oxide or an endothelium‐dependent vasodilator. It appears to be CGRP, presumably released from sensory nerves in the periarterial plexus.