cAMP inhibits norepinephrine-induced vascular smooth muscle contraction by inhibiting alpha-adrenoceptor-mediated signal transduction, and inhibits high K+-induced contraction by decreasing Ca2+ sensitivity.
Findings remain preclinical; leaves open whether cAMP elevation modulates human vascular tone or hypertension therapy.
Dibutyryl cyclic AMP and forskolin inhibited the contraction induced by norepinephrine (NE) more strongly than the high K(+)-induced contraction in isolated rat aorta. These inhibitors inhibited the 45Ca2+ influx stimulated by NE but not that by high K+, and they inhibited NE-induced inositol monophosphate accumulation. These results suggest that cAMP inhibits NE-induced contraction, at least partly, by inhibiting the alpha-adrenoceptor-mediated signal transduction and high K(+)-induced contraction by decreasing Ca2+ sensitivity but not Ca2+ influx.
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Ahn et al. (1992) studied this question.
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