Hypertension, Vol 22, 78-83, Copyright © 1993 by American Heart Association
D Henrion and I Laher
Subthreshold concentrations of endothelin-1 potentiated the
norepinephrine-induced contraction in isometrically mounted rings of the
rabbit aorta. Pretreatment with endothelin-1 (0.1 nM) for 10 minutes
increased the sensitivity of the aortic rings to norepinephrine without
affecting the maximal contraction. This amplification was unaffected by
removal of the endothelium but was prevented by the protein kinase C
inhibitors staurosporine (0.01 microM) and calphostin C (0.1 microM).
Pretreatment of the aortic rings for 24 hours with phorbol 12-myristate
13-acetate (0.1 microM) also abolished the potentiation.
Norepinephrine-induced contraction was potentiated by pretreating with
phorbol 12-myristate 13-acetate (10 nM) and by increasing the concentration
of K+ in the bath solution from 4.6 to 8.6 mM. The potentiation of the
norepinephrine-induced contraction by endothelin-1 (0.1 nM) or by phorbol
12-myristate 13-acetate (10 nM) was not associated with an increase in
norepinephrine-induced 45Ca2+ uptake or influx, whereas the potentiation
due to an increase in the concentration of K+ in the bath solution from 4.6
to 8.6 mM was associated with an increase in norepinephrine-induced 45Ca2+
uptake. We conclude that endothelin-1 potentiation of the
norepinephrine-induced contraction occurs in the absence of changes in
stimulated Ca2+ entry and is endothelium independent. It is probable that
endothelin-1 increases the sensitivity of the contractile apparatus to Ca2+
by activating protein kinase C-dependent mechanisms.
ARTICLES
Potentiation of norepinephrine-induced contractions by endothelin-1 in the rabbit aorta
Department of Pharmacology, University of Vermont, College of Medicine, Burlington 05405-0068.
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