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1 Department of Pharmacology and Toxicology, Biocenter Oulu, 90014 University of Oulu, Finland; 2 First Department of Medicine, Semmelweis University of Medicine, 1089 Budapest, Hungary; and 3 Department of Medicine, Christchurch Hospital, 8001 Christchurch, New Zealand
We characterize herein the impact
of myocardial nitric oxide (NO) synthesis on the inotropic response to
two cardioactive peptides, endothelin-1 (ET-1) and adrenomedullin (AM).
In the isolated perfused rat heart preparation, intracoronary infusion of AM (0.03 and 1 nmol/l) and ET-1 (0.08 and 1 nmol/l) for 30 min
induced a dose-dependent, gradual increase in developed tension, the
maximal responses being equal. Inhibition of myocardial NO synthase
(NOS) by N
-nitro-L-arginine
methyl ester (L-NAME; 300 µmol/l) enhanced the inotropic
response to ET-1 at a concentration of 1 nmol/l; meanwhile, the effect
of AM was not augmented significantly. The inotropic response to
simultaneous administration of low, equipotent doses of AM (0.03 nmol/l) and ET-1 (0.08 nmol/l) was significantly smaller than that of
either peptide alone. This depressed response was more than overcome by
concomitant administration of L-NAME. In conclusion, this
study reveals that the maximal inotropic response to ET-1 can be
augmented by inhibition of myocardial NOS, whereas it has only a minor
impact on the effect of AM. The inotropic response to combined
administration of low doses of AM and ET-1 is substantially suppressed
by endogenous NO, whereas the individual effects of the peptides at
these doses are not the subject of secondary modulation by NO.
myocardial contractility; N-nitro-L-arginine methyl ester; perfused rat heart
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