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

0343342 - FGÚ 2011 RIV GB eng J - Článek v odborném periodiku
Pintérová, Mária - Karen, Petr - Kuneš, Jaroslav - Zicha, Josef
Role of nifedipine-sensitive sympathetic vasoconstriction in maintenance of high blood pressure in spontaneously hypertensive rats: effect of Gi-protein inactivation by pertussis toxin.
Journal of Hypertension. Roč. 28, č. 5 (2010), s. 969-978. ISSN 0263-6352. E-ISSN 1473-5598
Grant CEP: GA MŠMT(CZ) 1M0510; GA ČR(CZ) GA305/08/0139; GA AV ČR(CZ) IAA500110902
Výzkumný záměr: CEZ:AV0Z50110509
Klíčová slova: calcium channels * inhibitory G proteins * pertussis toxin
Kód oboru RIV: FA - Kardiovaskulární nemoci vč. kardiochirurgie
Impakt faktor: 3.980, rok: 2010

The overexpression of pertussis toxin (PTX)-sensitive inhibitory G-proteins (Gi) participating in the development and maintenance of high BP in SHRs suggested us to study Gi-protein involvement in the pathway through which noradrenergic vasoconstriction and calcium influx can be coupled. PTX pretreatment of SHRs significantly decreased BP and reduced sympathetic vasoconstriction, which was partially substituted by enhanced angiotensin II-dependent vasoconstriction. PTX pretreatment of SHRs also decreased BP component sensitive to acute blockade of calcium entry by nifedipine. Thus the enhanced contribution of SNS to hypertension maintenance in SHRs is mediated by Gi-protein-coupled pathway controlling calcium influx through L type of voltage-dependent calcium channels
Trvalý link: http://hdl.handle.net/11104/0185845