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Inhibitory mechanism of N(G)-nitro-L-arginine on acetylcholine-induced depressor responses in dogs.

Abstract：

:The significance of the blood pressure elevation caused by N(G)-nitro-L-arginine (L-NNA) to inhibitory mechanism of the drug on depressor responses to acetylcholine in anesthetized dogs was investigated. L-NNA (50 mg kg(-1), i.v.) elevated blood pressure to a plateau of 30-50 mm Hg above baseline level and shifted the dose-response curve for acetylcholine-induced responses to the right by about 70-fold. Prevention by hydralazine (1 mg kg(-1), i.v.) of the blood pressure elevation over baseline level caused by L-NNA attenuated the inhibitory effect of L-NNA on the responses to acetylcholine. Intravenous neostigmine (30 microg kg(-1) bolus followed by 15 microg kg(-1) min(-1)) attenuated the inhibitory effect of L-NNA. The magnitude of the rightward shift in the dose-response curve for carbachol-induced depressor responses was only 3-fold. These results suggest that the accelerated acetylcholine metabolism by blood pressure elevation contributes to a considerable degree to the inhibitory mechanism of L-NNA.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Nakahara T,Nejishima H,Nakayama K,Ishii K

doi

10.1016/s0014-2999(99)00288-5

keywords:

subject

Has Abstract

pub_date

1999-06-04 00:00:00

pages

201-5

issue

2-3

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(99)00288-5

journal_volume

373

pub_type

杂志文章

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