Norepinephrine (NE), prostaglandin F2 alpha (PG), 12-deoxyphorbol 13-isobutyrate (DPB) and high K+ induced sustained increase in cytosolic Ca2+ [( Ca2+]i) and muscle tension in rat aorta. Verapamil, at the concentration which abolished the high K(+)-induced changes, also abolished the increase in [Ca2+]i due to NE, PG and DPB although contractions were only partially inhibited. Excess EGTA further decreased [Ca2+]i although a part of the contraction was not inhibited. These results indicate that the sustained contractions induced by NE, PG and DPB are due to increase in [Ca2+]i, increase in Ca2+ sensitivity of contractile elements, and a Ca2(+)-independent mechanism.
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Ozaki et al. (1990) studied this question.
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