[The role of extracellular calcium in the vasoconstriction evoked by endothelin-1]

Some mechanisms responsible for extracellular Ca++ entry into rat aortic smooth muscle cells were studied in response to endothelin-1 (ET-1). Isometric tension of de-endothelialized aortic strips was recorded. It was shown that the calcium-free medium or nifedipine blockade of calcium entry diminished responses to ET-1 to 20-30% of the control levels. Depolarization of the specimens with hyperpotassium solution also reduced constriction almost by 50%. When sodium ions were replaced by NMDG in the medium, a response to ET-1 showed a 50% reduction. The findings suggest that the potential-dependent calcium channels of the L-type are involved in cellular calcium entry, the opening of the channels depending upon the entry of Na+.