This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Debinski, W. K. Articles by Kuchel, O. G. Search for Related Content PubMed PubMed Citation Articles by Debinski, W. K. Articles by Kuchel, O. G.

Hypertension, Vol 13, 712-715, Copyright © 1989 by American Heart Association

ARTICLES

Responsiveness of noradrenergic neurons in rat experimental hypertension

WK Debinski and OG Kuchel
Clinical Research Institute of Montreal, Quebec, Canada.

We investigated possible abnormalities of cholinergic-noradrenergic neurotransmission in superior cervical ganglia in vitro in spontaneously hypertensive, Dahl salt-sensitive and deoxycorticosterone- salt-hypertensive rats by measuring the de novo synthesis of catecholamines from their labeled precursor tritiated tyrosine in response to cholinergic stimulation. Labeled tyrosine was incorporated into dopamine and its main neuronal metabolite dihydroxyphenylacetic acid as well as into norepinephrine. Dihydroxyphenylacetic acid and norepinephrine, but not dopamine, generation was linear with time under basal and stimulated conditions. However, norepinephrine incorporation remained similar before and after cholinergic stimulation of ganglionic neurons. Only young, prehypertensive spontaneously hypertensive rats showed altered responses when compared with their controls. Although endogenous dihydroxyphenylacetic acid content and baseline tyrosine incorporation into dihydroxyphenylacetic acid were lower in 4-week-old spontaneously hypertensive rats than in age-matched Wistar-Kyoto rats, cholinergic stimulation increased labeled dopamine and dihydroxyphenylacetic acid generation significantly more in juvenile spontaneously hypertensive rats. Such a hyperresponsiveness was not observed in either young Dahl rats or in any of the other models when they became hypertensive. These results probably reflect a genuine hyperreactivity of postganglionic noradrenergic neurons to acetylcholine or their increased catecholamine-synthesizing ability after centrally evoked enhanced sympathetic outflow known to occur during the early development of hypertension in spontaneously hypertensive rats.