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Tempol Lowers Blood Pressure and Sympathetic Nerve Activity But Not Vascular O2−in DOCA-Salt Rats

 

作者: Hui Xu,   Gregory Fink,   James Galligan,  

 

期刊: Hypertension: Journal of The American Heart Association  (OVID Available online 2004)
卷期: Volume 43, issue 2, Part 2  

页码: 329-334

 

ISSN:0194-911X

 

年代: 2004

 

出版商: OVID

 

关键词: super oxide;antioxidants;blood pressure

 

数据来源: OVID

 

摘要:

Abstract—This study tested the hypothesis that depressor responses caused by tempol are not associated with reductions in vascular O2−levels in urethane-anesthetized deoxycorticosterone acetate (DOCA)-salt hypertensive rats. We compared the effects of intravenous (IV) administration of tempol, apocynin, superoxide dismutase-polyethylene glycol (PEG-SOD), and SOD on mean arterial blood pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA). In DOCA-salt rats, tempol (30 to 300 &mgr;mol/kg) dose-dependently decreased RSNA, MAP, and HR. Tempol (300 &mgr;mol/kg) decreased MAP from 140±5 to 83±4 mm Hg (P<0.05). HR decreased from 435±15 to 390±12 bpm (P<0.05). RSNA was reduced by 54%±6% from baseline. However, in the same rats, tempol did not reduce dihydroethidium-induced fluorescent signals in the aorta and vena cava. Apocynin (200 &mgr;mol/kg) did not lower MAP (142±5 mm Hg versus 140±6 mm Hg) or HR (428±15 bpm versus 420±13 bpm) and apocynin did not potentiate depressor responses caused by tempol. PEG-SOD (10 000 U/kg, bolus or 5000 U/kg bolus followed by a 30-minutes infusion of 500 U/kg/min) or SOD (25 000 U/kg, bolus or 10 000 U/kg bolus followed by a 30-minutes infusion of 1000 U/kg per minute) did not alter MAP or HR. It is concluded that depressor responses and decreases in HR and RSNA caused by acute tempol treatment are caused by direct sympathetic nerve activity inhibition that is not accompanied by SOD-mimetic action in the aorta or vena cava.

 

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