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: 292/4/R1479    most recent 00435.2006v1 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 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 Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Ramchandra, R. Articles by Malpas, S. C. Search for Related Content PubMed PubMed Citation Articles by Ramchandra, R. Articles by Malpas, S. C.

RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Role of renal sympathetic nerve activity in hypertension induced by chronic nitric oxide inhibition

Circulatory Control Laboratory, Department of Physiology and Bioengineering Institute, University of Auckland, Auckland, New Zealand

Submitted 23 June 2006 ; accepted in final form 21 December 2006

Nitric oxide levels are diminished in hypertensive patients, suggesting nitric oxide might have an important role to play in the development of hypertension. Chronic blockade of nitric oxide leads to hypertension that is sustained throughout the period of the blockade in baroreceptor-intact animals. It has been suggested that the sympathetic nervous system is involved in the chronic increase in blood pressure; however, the evidence is inconclusive. We measured renal sympathetic nerve activity and blood pressure via telemetry in rabbits over 7 days of nitric oxide blockade. Nitric oxide blockade via N-nitro-L-arginine methyl ester (L-NAME) in the drinking water (50 mg·kg^–1·day^–1) for 7 days caused a significant increase in arterial pressure (7 ± 1 mmHg above control levels; P < 0.05). While the increase in blood pressure was associated with a decrease in heart rate (from 233 ± 6 beats/min before the L-NAME to 202 ± 6 beats/min on day 7), there was no change in renal sympathetic nerve activity (94 ± 4 %baseline levels on day 2 and 96 ± 5 %baseline levels on day 7 of L-NAME; baseline nerve activity levels were normalized to the maximum 2 s of nerve activity evoked by nasopharyngeal stimulation). The lack of change in renal sympathetic nerve activity during the L-NAME-induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits.

sympathetic activity; blood pressure

This article has been cited by other articles:

				F. D. McBryde, S. C. Malpas, S.-J. Guild, and C. J. Barrett A high-salt diet does not influence renal sympathetic nerve activity: a direct telemetric investigation Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2009; 297(2): R396 - R402. [Abstract] [Full Text] [PDF]