Affordable Access

Alpha-adrenoceptor- and prostaglandin-mediated modulation of vascular adrenergic neurotransmission in spontaneously hypertensive rats.

Authors
Type
Published Article
Journal
Japanese journal of pharmacology
Publication Date
Volume
34
Issue
4
Pages
457–463
Identifiers
PMID: 6144809
Source
Medline
License
Unknown

Abstract

The modulation of vascular adrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) mediated by alpha-adrenoceptor and prostaglandin E2 (PGE2) were evaluated. The pressor responses of the perfused mesenteric vascular bed to perivascular adrenergic nerve stimulation (NS) and infusion of norepinephrine (NE) and the NS-induced 3H-efflux in preparations pretreated with 3H-norepinephrine were determined. In both SHR and WKY, a selective alpha 2 agonist, B-HT 920 (30-300 nM), inhibited neurogenic vasoconstriction, and B-HT 920 (100-300 nM) potentiated the pressor response to NE in a dose-dependent manner. The effects of B-HT 920 did not significantly differ in SHR and WKY. Another alpha 2 agonist, clonidine (100 nM), decreased the 3H-efflux approximately by 30% both in SHR and WKY. A selective alpha 2 blocking agent, yohimbine (3-300 nM), potentiated the neurogenic vasoconstriction and inhibited the pressor response to NE equally in SHR and WKY. No difference in enhancement of 3H-efflux by yohimbine (30-300 nM) was seen between SHR and WKY either in the absence or presence of cocaine (10 microM) and metanephrine (20 microM). PGE2 (0.1-1 microM) potentiated pressor responses to NS and NE in SHR and WKY, but this compound (1 microM) did not affect the NS-induced 3H-efflux in either group of rats. It appears that adrenergic neurotransmission is inhibited presynaptically via an alpha 2 receptor mechanism and facilitated postsynaptically by PGE2 in the rat mesenteric vascular bed. The hypertensive state in SHR can not be accounted for by alteration of these modulator mechanisms.

Statistics

Seen <100 times