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Abstract

Phasic and tonic components in 5-HT2 receptor-mediated rat aorta contraction: participation of Ca++ channels and phospholipase C.

T Nakaki, B L Roth, D M Chuang and E Costa
Journal of Pharmacology and Experimental Therapeutics August 1985, 234 (2) 442-446;
T Nakaki
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B L Roth
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D M Chuang
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E Costa
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Abstract

The mechanisms of 5-hydroxytryptamine (5-HT)-induced contraction of rat aorta were investigated in vitro. The 5-HT-induced contraction could be analyzed into two distinct components (phasic and tonic) by the use of appropriate inhibitors; nifedipine, an inhibitor of voltage-dependent Ca++ channels, inhibited only the phasic component of 5-HT-induced contraction while totally blocking the KCl-induced contraction. 2-Nitro-4-carboxyphenyl-N,N-diphenylcarbamate, an inhibitor of phospholipase C, inhibited the tonic components of 5-HT-induced contraction as well as the 5-HT-induced stimulation of phosphoinositide hydrolysis in rat aorta. This component of contraction was mimicked by a protein kinase C activator 12-O-tetradecanoylphorbol-13-acetate. These results suggest that 5-HT2 receptors differentially regulate a voltage-dependent Ca++ channel and phospholipase C activity; the voltage-dependent Ca++ channel is involved in the phasic component of contraction whereas the phosphoinositide hydrolysis that results in the activation of protein kinase C and calcium mobilization by inositol triphosphate plays a physiologically important role in the tonic component of the aortic contraction.

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Journal of Pharmacology and Experimental Therapeutics
Vol. 234, Issue 2
1 Aug 1985
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Abstract

Phasic and tonic components in 5-HT2 receptor-mediated rat aorta contraction: participation of Ca++ channels and phospholipase C.

T Nakaki, B L Roth, D M Chuang and E Costa
Journal of Pharmacology and Experimental Therapeutics August 1, 1985, 234 (2) 442-446;

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Abstract

Phasic and tonic components in 5-HT2 receptor-mediated rat aorta contraction: participation of Ca++ channels and phospholipase C.

T Nakaki, B L Roth, D M Chuang and E Costa
Journal of Pharmacology and Experimental Therapeutics August 1, 1985, 234 (2) 442-446;
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