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Hypertension, Vol 19, 131-137, Copyright © 1992 by American Heart Association
Y Dohi, AW Hahn, CM Boulanger, FR Buhler and TF Luscher
In cultured endothelial cells, endothelin is produced after stimulation
with angiotensin II. The effects of angiotensin II and endothelin-1 on
vascular sensitivity to norepinephrine were studied in perfused rat
mesenteric resistance arteries. Expression of endothelin messenger RNA
(mRNA) was determined in endothelial cells obtained from the mesenteric
circulation. Perfusion (5 hours) of the arteries with angiotensin II
(10(-7) M) potentiated contractions in arteries with endothelium induced by
norepinephrine in spontaneously hypertensive rats but not Wistar-Kyoto
rats. The potentiation was inhibited by phosphoramidon and an endothelin
antibody. Short-term stimulation (1 hour) with angiotensin II did not cause
the potentiation. Stimulation with angiotensin I (10(-7) M; 5 hours) caused
a potentiation prevented by captopril. In endothelial cells collected from
the mesenteric arterial bed of spontaneously hypertensive rats,
endothelin-specific mRNA was constitutively expressed, and the level of
endothelin transcripts was increased by angiotensin II (10(-7) M).
Threshold concentrations of exogenous endothelin-1 potentiated contractions
induced by norepinephrine in arteries with and without endothelium of
spontaneously hypertensive rats but not Wistar-Kyoto rats. Thus,
angiotensin II stimulates the endothelial production of endothelin in situ
and therapy potentiates contractions to norepinephrine in mesenteric
resistance arteries of spontaneously hypertensive rats. This suggests that
vascular endothelin production acts as an amplifier of the pressor effects
of the renin-angiotensin system that may play an important role in
hypertension.
ARTICLES
Endothelin stimulated by angiotensin II augments contractility of spontaneously hypertensive rat resistance arteries
Department of Research, University Hospital, Basel, Switzerland.
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