Abstract
The inhibitory potencies of several amiloride congeners towards Na+-Ca2+ and Na+-H+ exchange were compared in rat aortic myocytes. N-(2,4-Dimethylbenzyl)amiloride (DMB) was 10 times more potent towards Na+-Ca2+ than Na+-H+ exchange. Amiloride and ethylisopropylamiloride were about 5,000 and 10,000 times more potent towards Na+-H+ than Na+-Ca2+ exchange respectively. N-(3,4-Dichlorobenzyl)amiloride was almost equipotent towards both exchangers. About 40 nM ethylisopropylamiloride inhibited Na+-H+ exchange by 50%. Ethylisopropylamiloride (10 μM) had no effect on basal or angiotensin-evoked 45Ca2+ efflux or net Ca2+ efflux. In contrast to ethylisopropylamiloride, 25–50 μM DMB, which strongly inhibits Na+-Ca2+ exchange, markedly decreased both 45Ca2+ efflux and net Ca2+ efflux produced by angiotensin. Replacing extracellular Na+ with N-methyl-D-glucamine inhibited angiotensin-evoked 45Ca2+ efflux similarly to DMB. Neither DMB nor Na+ placement had any effect on basal or angiotensin-evoked production of [3H]inositol phosphates. These findings suggest that Na+-H+ exchange has no major influence on short-term Ca2+ regulation and provide evidence that Na+-Ca2+ exchange is a major pathway of rapid Ca2+ efflux in stimulated arterial muscle cells.
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