Effect of adenosine and its analogues on calcium influx in coronary artery
Ramagopal, M.V.; Mustafa, S.J.
American Journal of Physiology 255(6 Pt 2): H1492-H1498
1988
ISSN/ISBN: 0002-9513 PMID: 3202209 Document Number: 321354
In the present study, we have investigated the changes in calcium influx during the relaxing responses to adenosine and its analogues. Calcium-45 influx was measured in bovine coronary artery rings in the presence of prostaglandin F2.alpha. (10-5M) and KCl (50 and 100 mM). Prostaglandin F2.alpha. and KCl caused increases in calcium influx. Prostaglandin F2.alpha. produced a further contraction when added to rings maximally contracted with KCl (100 mM or higher), suggesting two different mechanisms for prostaglandin F2.alpha.- and KCl-induced contractions. Similarly, a greater calcium influx was observed when prostaglandin F2.alpha. was mixed with KCl (50 or 100 mM). At all the concentrations tested, adenosine and its analogues [5'-(N-ethyl-carboxamdoadenosine, NECA; N6-(L-2-phenylisopropyl adenosine, L-PIA] significantly inhibited prostaglandin F2.alpha.-induced increases in calcium influx. However, only higher concentrations of adenosine, NECA, and L-PIA inhibited 100 mM KCl-induced calcium influx. Previous treatment with 8-phenyltheophylline blocked the inhibitory actions of adenosine, NECA, and L-PIA on calcium influx. The inhibition of calcium influx by adenosine, NECA, and L-PIA correlated well with their relaxing ability in the presence of prostaglandin F2.alpha. The data suggest that prostaglandin F2.alpha.-induced calcium influx was more sensitive to the action of adenosine and its analogues than the calcium influx induced by high K+ depolarization.