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Phorbol 12,13-diacetate-induced Contraction of the Canine Basilar Artery: Role of Protein Kinase C

Phorbol 12,13-diacetate-induced Contraction of the Canine Basilar Artery: Role of Protein Kinase C

M Sugawa, T Koide, S Naitoh, M Takato, T Matsui, T Asano

J Cereb Blood Flow Metab. 1991 Jan;11(1):135-42.

PMID: 1845765

Abstract:

The pharmacological and biochemical mechanisms of contractile responses to the protein kinase C (PKC) activator phorbol-12,13-diacetate (PDA) were investigated in canine basilar arteries. In the normal medium, PDA elicited a strong, dose-related, and slow-developing sustained contraction. Among the constrictors examined, including serotonin, prostaglandin F2 alpha, and endothelin, only PDA yielded contractions in a Ca2(+)-free medium. In both media, the PDA-induced contractions were virtually inhibited by either staurosporine, H-7, or quinacrine, while neither neurotransmitter blockades nor R24571 (calmidazolium) exerted significant effects. In addition, it was shown that 8-bromocyclic GMP, but not 8-bromocyclic AMP, markedly curtailed the PDA-induced contractions. Biochemical analysis, furthermore, showed that PDA induced increased phosphorylations of 27- and 96-kDa and proteins other than the myosin light chain (MLC) 20-kDa protein. Thus, the present results open up a novel mechanism of sustained cerebral artery contractions, where PKC activation rather than Ca2+/calmodulin/MLC system plays a key role that is regulated both by phospholipase A2 and by cyclic GMP.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP24928152	Phorbol 12,13-diacetate		24928-15-2	Price

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