HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/4/R903    most recent 00530.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Yanes, L. Articles by Reckelhoff, J. F. Search for Related Content PubMed PubMed Citation Articles by Yanes, L. Articles by Reckelhoff, J. F.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Systemic arterial pressure response to two weeks of Tempol therapy in SHR: involvement of NO, the RAS, and oxidative stress

Departments of ¹Physiology and Biophysics and ²Medicine, University of Mississippi Medical Center, Jackson, Mississippi; and ³Department of Physiopathology, University of Medicine, Asuncion, Paraguay

Submitted 5 August 2004 ; accepted in final form 15 December 2004

The roles of nitric oxide (NO) and plasma renin activity (PRA) in the depressor response to chronic administration of Tempol in spontaneously hypertensive rats (SHR) are not clear. The present study was done to determine the effect of 2 wk of Tempol treatment on blood pressure [mean arterial pressure (MAP)], oxidative stress, and PRA in the presence or absence of chronic NO synthase inhibition. SHR were divided into four groups: control, Tempol (1 mmol/l) alone, nitro-L-arginine methyl ester (L-NAME, 4.5 mg·kg^–1·day^–1) alone, and Tempol + L-NAME for 2 wk. With Tempol, MAP decreased by 22%: 191 ± 3 and 162 ± 21 mmHg for control and Tempol, respectively (P < 0.05). L-NAME increased MAP by 16% (222 ± 2 mmHg, P < 0.01), and L-NAME + Tempol abolished the depressor response to Tempol (215 ± 3 mmHg, P < 0.01). PRA was not affected by Tempol but was increased slightly with L-NAME alone and 4.4-fold with L-NAME + Tempol. Urinary nitrate/nitrite increased with Tempol and decreased with L-NAME and L-NAME + Tempol. Tempol significantly reduced oxidative stress in the presence and absence of L-NAME. In conclusion, in SHR, Tempol administration for 2 wk reduces oxidative stress in the presence or absence of NO, but in the absence of NO, Tempol is unable to reduce MAP. Therefore, NO, but not changes in PRA, plays a major role in the blood pressure-lowering effects of Tempol. These data suggest that, in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress but not blood pressure.

nitric oxide; superoxide; antioxidant; renin-angiotensin system

This article has been cited by other articles:

				S. J. Miller, L. E. Norton, M. P. Murphy, M. C. Dalsing, and J. L. Unthank The role of the renin-angiotensin system and oxidative stress in spontaneously hypertensive rat mesenteric collateral growth impairment Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2523 - H2531. [Abstract] [Full Text] [PDF]

				T. Vera, S. Kelsen, L. L. Yanes, J. F. Reckelhoff, and D. E. Stec HO-1 induction lowers blood pressure and superoxide production in the renal medulla of angiotensin II hypertensive mice Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1472 - R1478. [Abstract] [Full Text] [PDF]

				T. Schluter, R. Grimm, A. Steinbach, G. Lorenz, R. Rettig, and O. Grisk Neonatal sympathectomy reduces NADPH oxidase activity and vascular resistance in spontaneously hypertensive rat kidneys Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2006; 291(2): R391 - R399. [Abstract] [Full Text] [PDF]

				L. T. de Richelieu, C. M. Sorensen, N.-H. Holstein-Rathlou, and M. Salomonsson NO-independent mechanism mediates tempol-induced renal vasodilation in SHR Am J Physiol Renal Physiol, December 1, 2005; 289(6): F1227 - F1234. [Abstract] [Full Text] [PDF]