Hypotensive Effect of Agmatine, Arginine Metabolite, is Affected by NO Synthase

Title:

Hypotensive Effect of Agmatine, Arginine Metabolite, is Affected by NO Synthase

Creator:

Gerová, M. and Török, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:1d2aeae7-ce90-40e2-9cdd-f20d62d0575c
uuid:1d2aeae7-ce90-40e2-9cdd-f20d62d0575c

Subject:

Agmatine, Hypotension, NO synthase, NO-deficient hypertension, and Aorta relaxation

Type:

article, model:article, and TEXT

Description:

The metabolites of arginine were recently shown to be involved in cardiovascular control. The study addresses the general cardiovascular response of anaesthetized rats to agmatine, a decarboxylated arginine. The relation between two arginine metabolic pathways governed by arginine decarboxylase and nitric oxide synthase was investigated. Intravenous administration of agmatine 30 and 60 μM/0.1 ml saline elicited remarkable hypotension of 42.6±4.6 and 70.9±6.5 mm Hg, respectively. The hypotension was characterized by long duration with half-time of return 171.6±2.9 and 229.2±3.8 s, respectively. The time of total blood pressure (BP) recovery was about 10 min. Dose-dependent relaxation to agmatine was also found in aorta rings in vitro. Both doses of agmatine administered 60-180 min after NO synthase inhibition (L-NAME 40 mg/kg i.v.) caused greater hypotension 59.0±7.6 and 95.8±8.8 mm Hg (P<0.01 both) compared to animals with intact NO synthase, but this was accompanied by a significant shortening of the half-time of BP return. If agmatine was administered to hypertensive NO-deficient rats (treated with 40 mg/kg/day L-NAME for 4 weeks), similar significant enhancement of hypotension was observed at both agmatine doses, again with a significant shortening of half-time of BP return. It can be summarized that the long-lasting hypotension elicited by agmatine was amplified after acute or chronic NO synthase inhibition, indicating a feedback relation between the two metabolic pathways of arginine.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2004 Volume:53 | Number:4

Harvested from:

CDK

Metadata only:

false