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Effects of des-Asp-angiotensin I on the electrically stimulated contraction of the rabbit pulmonary artery.

Abstract：

:In the presence of 3 x 10(-6) M captopril, 5 x 10(-7) M des-Asp-Angiotensin I was found to inhibit the electrically (1 and 2 Hz) induced contraction of the rabbit pulmonary artery but had no significant effect on the noradrenaline-stimulated contraction. 2.8 x 10(-6) M indomethacin and 10(-6) M losartan but not 10(-6) M (S) 1-([4-(dimethylamino)-3-methylphenyl]methyl)-5-(diphenylacetyl)-4, 5,6,7- tetrahydro-1H-imidazo(4,5-c]pyridine-6-carboxylic acid, ditrifluoroacetate, dihydrate (PD123319) attenuated the inhibition. The inhibition of the electrically stimulated contraction by 5 x 10(-7) M des-Asp-angiotensin I coincided with a significant drop in the accompanying evoked 3H overflow from re-uptaken [3H]noradrenaline. The results indicate that des-Asp-angiotensin I acts presynaptically on a subtype of angiotensin receptor that involves the release of prostaglandin(s). In addition, this receptor subtype is susceptible to blockade by angiotensin AT1- but not AT2-specific receptor antagonists. It was suggested that this receptor subtype is identifiable with the recently described angiotensin AT1B receptor subtype found in the brain, pituitary and adrenal glomerulosa. These findings demonstrated a direct action of sub-micromolar concentrations of des-Asp-angiotensin I on a blood vessel and indicate that the nonapeptide is an active angiotensin per se.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Sim MK,Soh KS

doi

10.1016/0014-2999(95)00461-s

subject

Has Abstract

pub_date

1995-09-15 00:00:00

pages

215-9

issue

1-2

eissn

0014-2999

issn

1879-0712

pii

0014-2999(95)00461-S

journal_volume

284

pub_type

杂志文章

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