Role of nifedipine-sensitive sympathetic vasoconstriction in maintenance of high blood pressure in spontaneously hypertensive rats: effect of Gi-protein inactivation by pertussis toxin

2010 ◽  
Vol 28 (5) ◽  
pp. 969-978 ◽  
Author(s):  
Mária Pintérová ◽  
Petr Karen ◽  
Jaroslav Kuneš ◽  
Josef Zicha
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Pertussis Toxin ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Protein Inactivation ◽  
Sympathetic Vasoconstriction ◽  
Gi Protein

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

2009 ◽  
pp. 751-755
Author(s):  
J Zicha ◽  
J Kuneš ◽  
S Vranková ◽  
L Jendeková ◽  
Z Dobešová ◽  
...  
Keyword(s):  
Pertussis Toxin ◽  
Hypertensive Rats ◽  
Protein Inactivation ◽  
Full Development ◽  
Sympathetic Vasoconstriction ◽  
Induced Hypertension ◽  
Gi Protein ◽  
Gi Proteins

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 involved 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.

Role of endothelin in mediating postmenopausal hypertension in a rat model

2005 ◽  
Vol 288 (1) ◽  
pp. R229-R233 ◽  
Author(s):  
Licy L. Yanes ◽  
Damian G. Romero ◽  
Valeria E. Cucchiarelli ◽  
Lourdes A. Fortepiani ◽  
Celso E. Gomez-Sanchez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Spontaneously Hypertensive Rats ◽  
Renal Cortex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Peptide Expression ◽  
Premenopausal Female

Cardiovascular disease is the leading cause of death in women after menopause. Hypertension, a major cardiovascular risk factor, becomes more prevalent after menopause. The mechanisms responsible for the increase in blood pressure (BP) in postmenopausal women are unknown. We have recently characterized the aged, postestrous-cycling (PMR) spontaneously hypertensive rats (SHR) as a model of postmenopausal hypertension. The purpose of the present study was to determine whether endothelin plays a role in the increased BP in PMR. Premenopausal female SHR, aged 4–5 mo (YF), and PMR, aged 16 mo, were studied. Expression of preproendothelin-1 mRNA was not different in either renal cortex or medulla between PMR and YF ( n = 7–8/group). In contrast, ET-1 peptide expression was significantly higher in renal cortex of PMR than in renal cortex of YF, but there was no difference in medullary ET-1. Expression of endothelin ETA receptor (ETAR) mRNA was lower in renal cortex and medulla of PMR than of YF. Additional groups of rats ( n = 6–7/group) were treated for 3 wk with the ETAR antagonist ABT-627 (5 mg·kg−1·day−1). BP was significantly higher in PMR than in YF. ETAR antagonist reduced BP in PMR by 20% to the level found in control YF. ETAR antagonist had no effect on BP in YF. These data support the hypothesis that the increase in BP in PMR is mediated in part by endothelin and the ETAR.

Sign in / Sign up

Export Citation Format

Share Document