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Existence of two components in the tonic contraction of rat aorta mediated by α 1 ‐adrenoceptor activation
Author(s) -
Nishimura Kanami,
Ota Mikio,
Ito Katsuaki
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb12156.x
Subject(s) - tonic (physiology) , nifedipine , contraction (grammar) , chemistry , medicine , muscle contraction , endocrinology , phenylephrine , egta , calcium , biology , blood pressure
1 The mechanisms involved in the contraction of rat aorta induced by the activation of α 1 ‐adrenoceptors were studied. Phenylephrine induced a phasic contraction in the aorta incubated in Ca 2+ ‐free medium containing 0.5 m m EGTA. Subsequent addition of Ca 2+ 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 45 Ca 2+ 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 45 Ca 2+ 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 α 1 ‐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 Ca 2+ influx through nifedipine‐sensitive Ca 2+ channels.