Existence of two components in the tonic contraction of rat aorta mediated by α1‐adrenoceptor activation

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Abstract
1 The mechanisms involved in the contraction of rat aorta induced by the activation of α1-adrenoceptors were studied. Phenylephrine induced a phasic contraction in the aorta incubated in Ca2+-free medium containing 0.5 mm EGTA. Subsequent addition of Ca2+ induced a tonic contraction, which exhibited a stepwise development, an initial phase lasting 3 to 6 min (tonic-I) followed by a superimposing second phase (tonic-II). 2 2-Nitro-4-carboxyphenyl-N,N-diphenylcarbamate, which has been reported to inhibit phosphatidylinositol turnover, and H-7, a protein kinase C inhibitor, inhibited the tonic-I phase more effectively than the tonic-II phase. On the other hand, the tonic-II phase was more sensitive to nifedipine and cromakalim. 3 The rate of 45Ca2+ influx during the tonic-I phase in phenylephrine-treated muscles was not different from that in untreated muscles, while that during the tonic-II phase was significantly greater. Nifedipine inhibited the increased 45Ca2+ influx during the tonic-II phase, whereas H-7 did not affect the uptake during either phase. 4 These results suggest that the tonic contraction of rat aorta following α1-adrenoceptor activation involves two different mechanisms: one is directly related to consequences of the polyphosphoinositide cascade, probably to protein kinase C, and the other dependent on Ca2+ influx through nifedipine-sensitive Ca2+ channels.