45Ca2+ movements induced by Ca2+ chloride in isolated rat aorta under K(+)-free conditions

Abstract

Increasing the extracellular Ca2+ concentration induced a dihydropyridine-insensitive contraction in the isolated rat aorta bathed in K(+)-free solution. To obtain further insight into the mechanism of this contraction 45Ca2+ uptake measurements were carried out with isolated rat aorta. Increasing the extracellular Ca2+ concentration from 0.63 to 5.0 mM enhanced the 45Ca2+ uptake from 186 +/- 3 to 359 +/- 12 dpm/mg ww (n = 8). Under K(+)-free conditions increasing the extracellular Ca2+ concentration from 0.63 to 5.0 mM enhanced the 45Ca2+ uptake from 184 +/- 4 to 541 +/- 6 dpm/mg ww (n = 12) and elicited an increase in tension of 10.0 +/- 0.4 mN (n = 9). The Ca2(+)-induced 45Ca2+ uptake was not affected by the Ca2% channel antagonists, nifedipine (L-type), flunarizine (L- and T-type) and omega-conotoxin (N-type). Amiloride, a blocker of the Na+/Ca2+ exchange, indomethacin, a blocker of prostaglandin synthesis, the local anaesthetic, lidocaine, and the Ca2+ overload blocker. R 56865, had no effect on Ca2(+)-induced 45Ca2+ uptake. Additionally, R 56865 did not affect the Ca2(+)-induced contractile response. The inorganic Ca2+ entry blocker, lanthanum, reduced both the non-stimulated and stimulated 45Ca2+ uptake and inhibited the Ca2(+)-induced contractile response. We would like to suggest that the 45Ca2+ uptake induced by Ca2+ under K(+)-free conditions enters the cell via the leakage Ca2+ channel, because lanthanum was an effective antagonist and a significant contribution of any other Ca2+ pathway could not be demonstrated.