Affiliation:
1. Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858–4354, USA
Abstract
Abstract
We have investigated the mechanism of adenosine-induced relaxation in relation to its effects on intracellular organelles in Triton X-100- and saponin-skinned bovine coronary arteries. In intact coronary arteries, high K+ and prostaglandin F2α caused sustained contractions, whereas caffeine produced transient contractions. Triton X-100 treatment abolished these contractions. However, Triton X-100-skinned coronary arteries were responsive to added free calcium. There was no significant difference between calcium concentration-response curves obtained in the absence and presence of adenosine (50 μm). Unlike Triton X-100, in saponin-skinned arteries, caffeine produced transient contractions but high K+ and prostaglandin F2α did not. Adenosine had no effect on caffeine-induced contractions in saponin-skinned coronary arteries. These data suggest that adenosine had no direct inhibitory effect on either the contractile apparatus or calcium release from sarcoplasmic reticulum in coronary arteries.
Publisher
Oxford University Press (OUP)
Subject
Pharmaceutical Science,Pharmacology
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