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Pharmacological nature of nicotine-induced contraction in the rat basilar artery: involvement of arachidonic acid metabolites.

Abstract：

:The pharmacological nature of nicotine-induced contraction in the rat basilar artery is poorly understood. The purpose of this study was to investigate the endothelium dependency and involvement of arachidonic acid metabolites in nicotine-induced contraction in the rat basilar artery. The rat basilar artery was removed from the brain and cut into a spiral preparation. Nicotine (3x10(-5) to 10(-2) M) induced the concentration-dependent contraction in the rat basilar artery, and the maximal contraction was obtained at 3x10(-3) M. The contraction induced by nicotine (3x10(-3) M) was significantly attenuated by the presence of saponin (0.05 mg/ml, 15 min). Phospholipase C (PLC) inhibitors (NCDC and U-73122), calcium-independent phospholipase A(2) (iPLA(2)) inhibitor (BEL), cyclooxygenase-2 (COX-2) inhibitors (nimesulide, L-745,337 and celecoxib), and a 5-lipoxygenase (5-LOX) inhibitor (ZM-230487) concentration-dependently attenuated the nicotine-induced contraction. A cytosolic phospholipase A(2) (cPLA(2)) inhibitor (AACOCF3), secretory phospholipase A(2) (sPLA(2)) inhibitor (indoxam), and cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen and ketoprofen) did not affect the nicotine-induced contraction. From these results, it was suggested that nicotine-induced contraction in the rat basilar artery is endothelium-dependent and is due to arachidonic acid metabolites.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Ji X,Nishihashi T,Trandafir CC,Wang A,Shimizu Y,Kurahashi K

doi

10.1016/j.ejphar.2007.08.011

subject

Has Abstract

pub_date

2007-12-22 00:00:00

pages

109-14

issue

1-3

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(07)00901-6

journal_volume

577

pub_type

杂志文章

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