Influence of pertussis toxin pretreatment on the development of L-NAME-induced hypertension

Title:

Influence of pertussis toxin pretreatment on the development of L-NAME-induced hypertension

Creator:

Josef Zicha, Jaroslav Kuneš, Vranková, S., Lýdia Jendeková, Zdena Dobešová, Mária Pintérová, and Oľga Pecháňová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:59823aea-2ada-406d-8f4a-f2e7c893b6ba
uuid:59823aea-2ada-406d-8f4a-f2e7c893b6ba

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, sympatický nervový systém, oxid dusnatý, krevní tlak, physiology, sympathetic nervous system, nitric oxide, blood pressure, inhibitory G proteins, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

High blood pressure (BP) of L-NAME hypertensive rats is maintained not only by the absence of nitric oxide (NO)-dependent vasodilatation but also by the enhancement of both sympathetic and angiotensin II-dependent vasoconstriction. The aim of the present study was to evaluate the role of inhibitory G (Gi) proteins, which are involv ed in tonic sympathetic vasoconstriction, in the pathogenesis of NO-deficient hypertension. We therefore studied BP response to chronic L-NAME administration (60 mg/kg/day for 4 weeks) in rats in which the in vivo inactivation of Gi proteins was induced by injection of pertussis toxin (PTX, 10 μg/kg i.v.). The impairment of sympathetic vasoconstriction due to PTX-induced Gi protein inactivation prevents the full development of NO-deficient hypertension because BP of PTX-treated rats subjected to chronic L-NAME administration did not reach hypertensive values. Nevertheless, chronic NO synthase inhibition per se is capable to increase moderately BP even in PTX-treated rats. Our data suggest that the sympathetic vasoconstriction is essential for the development of established NO-deficient hypertension., J. Zicha ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

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

Source:

Physiological research | 2009 Volume:58 | Number:5

Harvested from:

CDK

Metadata only:

false