2007 JASN IMPACT FACTOR 7.111	HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP
advanced	CURRENT ISSUE	ARCHIVES	JASN Express	ONLINE SUBMISSION

This Article Full Text Full Text (PDF) 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 PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sigmon, D. H. Articles by Beierwaltes, W. H. Search for Related Content PubMed PubMed Citation Articles by Sigmon, D. H. Articles by Beierwaltes, W. H.

Role of Nitric Oxide in the Renal Hemodynamic Response to Unilateral Nephrectomy

David H. Sigmon^*, Edgard Gonzalez-Feldman, Maria A. Cavasin, D’Anna L. Potter and William H. Beierwaltes

*Science Division of Mercy College of Northwest Ohio, Toledo, Ohio; and Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan.

Correspondence to Dr. William H. Beierwaltes, Hypertension and Vascular Research Division, 7121 E & R Building, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202-2689. Phone: 313-916-7494; Fax: 313-916-0524; E-mail: wbeierw1{at}hfhs.org

ABSTRACT. Reduction of renal mass by unilateral nephrectomy results in an immediate increase in renal blood flow (RBF) to the remnant kidney, followed by compensatory renal hypertrophy. Whether the increase in RBF after unilateral nephrectomy is mediated by nitric oxide (NO) was tested. It was found that immediately after nephrectomy, blood flow to the remaining kidney increased by 8% (P < 0.01), and inhibition of NO synthesis with N-nitro-L-arginine methyl ester (L-NAME) blocked the increase in RBF. In addition, 2 d after nephrectomy, there was a 49% increase in RBF (corrected per gram of kidney weight), a 25% increase at 7 and 14 d, and a 16% increase after 28 d. Acute inhibition of NO synthesis with L-NAME in uninephrectomized rats caused a greater decrease in RBF on days 2 and 7 compared with controls, whereas by 14 and 28 d, the response to L-NAME was similar to controls. Urinary excretion of cyclic guanosine monophosphate, a marker for renal NO production, increased 2.5-fold by 2 d after uninephrectomy (P < 0.005) and remained at this level through 28 d. Pretreating rats chronically with a subpressor dose of L-NAME beginning 2 d before nephrectomy blocked the increase in RBF seen at 2 and 7 d and retarded the renal hypertrophy that should have developed by 7 d. It is concluded that after unilateral nephrectomy, immediate and sustained increases in RBF are mediated at least in part by NO. The hypertrophic response to unilateral nephrectomy may be partially initiated by the signal of hemodynamic changes.

This article has been cited by other articles:

				H.-Y. Kim, C. Baylis, J. W. Verlander, K.-H. Han, S. Reungjui, M. E. Handlogten, and I. D. Weiner Effect of reduced renal mass on renal ammonia transporter family, Rh C glycoprotein and Rh B glycoprotein, expression Am J Physiol Renal Physiol, October 1, 2007; 293(4): F1238 - F1247. [Abstract] [Full Text] [PDF]

				A. Erdely, G. Freshour, Y.-L. Tain, K. Engels, and C. Baylis DOCA/NaCl-induced chronic kidney disease: a comparison of renal nitric oxide production in resistant and susceptible rat strains Am J Physiol Renal Physiol, January 1, 2007; 292(1): F192 - F196. [Abstract] [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673