Adenosine affects the calcium dynamics of rat portal vein

1. The present study was carried out to characterize the effect of adenosine on calcium dynamics in the rat portal vein. Isolated portal vein of male albino rats was used as the experimental model as it exhibits autorhythmicity. 2. Adenosine and its analogues 2-CAD, N6-CHA and NECA were used to characterize the type of adenosine receptor involved and 2-CAD was used along with adenosine throughout the other part of study to characterize the effect of adenosine on Ca2+ dynamics. Adenosine and its analogues were found to inhibit the spontaneous contractions of rat portal vein in a concentration-related manner. The order of potency was NECA > 2-CAD > N6-CHA > adenosine. Incubation of the tissue with CGS-15943A, an adenosine receptor antagonist, had a per se enhancing effect on autorhythmicity. Adenosine and 2-CAD failed to reverse the contractile response produced by hypertonic KCl (80 or 30 mM). Whereas adenosine and 2-CAD effectively relaxed the tissues contracted with phenylephrine (10(-5) m). 3. Preincubation of the tissue with 2-CAD (10(-4), 10(-5) or 10(-6) m) for 5 min raised the threshold concentration of CaCl2 to evoke contractile response and also significantly increased the mean EC50 values of CaCl2. Nifedipine was found to be more potent than 2-CAD on Ca2+ channels. 4. The results of the present study suggest that the endogenous adenosine plays a significant role in producing vascular relaxation through the participation of A2 receptor subtype. This effect may be due to its inhibitory effect on release of Ca2+ from the intracellular stores. Further to this effect, 2-CAD had a major inhibitory effect on voltage-operated Ca2+ channels compared with receptor-operated Ca2+ channels. 5. It can be concluded that adenosine through its A2 receptor produces vasorelaxant effect by interfering with the release of Ca2+ from the intracellular stores coupled with influx of Ca2+ from the extracellular sources.