Open AccessInfluence of pertussis toxin pretreatment on the development of L-NAME-induced hypertension
Author(s) -
Josef Zicha,
Jaroslav Kuneš,
Stanislava Vranková,
Lýdia Jendeková,
Z Dobešová,
M Pintérová,
Oľga Pecháňová
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931898
Subject(s) - vasoconstriction , pertussis toxin , vasodilation , angiotensin ii , nitric oxide , medicine , endocrinology , blood pressure , nitric oxide synthase , pathogenesis , pharmacology , g protein , receptor
High blood pressure (BP) of L-NAME hypertensive rats ismaintained not only by the absence of nitric oxide (NO)-dependent vasodilatation but also by the enhancement of bothsympathetic and angiotensin II-dependent vasoconstriction. Theaim of the present study was to evaluate the role of inhibitory G(Gi) proteins, which are involved in tonic sympatheticvasoconstriction, in the pathogenesis of NO-deficienthypertension. We therefore studied BP response to chronicL-NAME administration (60 mg/kg/day for 4 weeks) in rats inwhich the in vivo inactivation of Gi proteins was induced byinjection of pertussis toxin (PTX, 10 μg/kg i.v.). The impairmentof sympathetic vasoconstriction due to PTX-induced Gi proteininactivation prevents the full development of NO-deficienthypertension because BP of PTX-treated rats subjected to chronicL-NAME administration did not reach hypertensive values.Nevertheless, chronic NO synthase inhibition per se is capable toincrease moderately BP even in PTX-treated rats. Our datasuggest that the sympathetic vasoconstriction is essential for thedevelopment of established NO-deficient hypertension.