Inhibitory effects of forskolin on vascular smooth muscle of rabbit aorta.

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Effects of forskolin on the contractions in rabbit aorta were examined. The sustained contraction induced by 10-6 M norepinephrine was inhibited by 10-8-10-5 M forskolin in a concentration-dependent manner. In the high K+-depolarized and verapamil-treated aorta, the norepinephrine-induced sustained contraction was similarly inhibited by forskolin. However, forskolin showed only a slight inhibitory effect on the sustained contraction induced by 65.4 mM KCl. Forskolin inhibited the increase in Ca2+ influx due to norepinephriiie, but not that due to high K+. In a Ca2+-free solution, 10-6 M norepinephrine induced a transient contraction which is due to Ca2+ release from the store site. This contraction was inhibited by 3×10-7-10-5 M forskolin. However, caffeine-induced transient contraction was not inhibited by 10-5 M forskolin. 45Ca2+ in a cellular site was released by 10-6 M norepinephrine or 10 mM caffeine. Forskolin inhibited the Ca2+ release induced by norepinephrine, but not that by caffeine. Forskolin increased the tissue cAMP content in resting, 10-6 M norepinephrine-treated or 65.4 mM K+-treated aorta. It is concluded that forskolin inhibits the norepinephrine-induced sustained contraction by relatively selectively inhibiting the receptor-linked Ca2+ channel, and it inhibits the norepinephrine-induced transient contraction by inhibiting Ca2+ release from the cellular store.
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