Effects of adenosine analogues on tension and cytosolic ca2+ in
porcine coronary artery.
Olanrewaju, Hammed A., and S. Jamal Mustafa.
Department of Pharmacology, School of Medicine, East Carolina
University, Greenville, NC 27858, USA
APStracts 2:0275H, 1995.
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-2AM. The
ratio of fluorescence due to excitation at 340 nm (F340) to that at
380 nm (F380) reflects [Ca2+]i. Increased tension of the porcine
coronary artery contracted with prostaglandin F2[alpha] (PGF2[alpha],
20 [mu]M) was accompanied by increased [Ca2+]i. The adenosine
analogues, N6-cyclopentyladenosine (CPA), 2-chloroadenosine (CAD) and
2-[m-(carboxyethly)phenylamino]-5'-N-ethycarboxamidoadenosine (CGS
-22988) produced a concentration-dependent (10-80-4M) reduction of
[Ca2+]i and tension with a maximum relaxation of about 96 % and a
[Ca2+]i decrease of 88 % at a concentration of 10-4M. The order of
potency for relaxation was: CAD > CGS-22988 = CPA. Adenosine
receptor antagonists (8-PT, 10-6M; CGS-15943, 10-5M) shifted the
agonist-mediated relaxation and [Ca2+]i curve to the right in a
parallel fashion. In Ca2+-free buffer, PGF2[alpha] (20 [mu]M)
induced-contraction was significantly reduced (75 %). PGF2[alpha]
also caused a transient increase in [Ca2+]i which later was reduced
below the resting level. The order of potency for adenosine analogues
in Ca2+-free buffer for relaxation 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 is at least partly independent of extracellular Ca2+.
Received 12 September 1994; accepted in final form 4 June 1995.
APS Manuscript Number H820-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.