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Am J Physiol Heart Circ Physiol 270: H134-H141, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 270, Issue 1 134-H141, Copyright © 1996 by American Physiological Society

ARTICLES

Effects of adenosine analogues on tension and cytosolic Ca2+ in porcine coronary artery

H. A. Olanrewaju and S. J. Mustafa
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

This study evaluates the relaxing effects of adenosine analogues in relation to intracellular free Ca2+ concentration ([Ca2+]i) in porcine coronary artery. Changes in muscle tension and [Ca2+]i were measured simultaneously using the fluorescent Ca2+ indicator, fura 2-acetoxymethyl ester. The ratio of fluorescence due to excitation at 340 nm to that at 380 nm reflects [Ca2+]i. Increased tension of the porcine coronary artery contracted with prostaglandin F2 alpha (PGF2 alpha, 20 microM) was accompanied by increased [Ca2+]i. The adenosine analogues, N6-cyclopentyladenosine (CPA), 2-chloroadenosine (CAD), and 2-[m-(carboxyethyl)-phenylamino]-5'-N-ethylcarboxamidoadenosine (CGS-22988) produced a concentration-dependent (10(-8)-10(-4) M) reduction of [Ca2+]i and tension with a maximum relaxation of approximately 96% and a [Ca2+]i decrease of 88% at a concentration of 10(-4) M. The order of potency for relaxation was CAD > CGS-22988 = CPA. Adenosine receptor antagonists (8-phenyltheophylline, 10(-6) M; CGS-15943, 10(-5) M) shifted the agonist-mediated relaxation and [Ca2+]i curve to the right in a parallel fashion. In Ca(2+)-free buffer, PGF2 alpha (20 microM)-induced contraction was significantly reduced (75%). PGF2 alpha also caused a transient increase in [Ca2+]i that later was reduced below the resting level. The order of potency for relaxation for adenosine analogues in Ca(2+)-free buffer was found to be CAD = CGS-22988 > CPA. All curves were shifted to the right in the presence of receptor antagonists. These results indicate that adenosine receptor-mediated changes in [Ca2+]i and relaxation in porcine coronary smooth muscle are at least partly independent of extracellular Ca2+.




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