AJP - Renal Physiology, Vol 271, Issue 2 246-F252, Copyright © 1996 by American Physiological Society

ARTICLES

Impaired effect of nitric oxide synthesis inhibition on tubuloglomerular feedback in hypertensive rats

C. Thorup and A. E. Persson
Department of Physiology and Biophysics, University of Lund, Sweden.

Experiments were conducted to compare the effects of intratubular inhibition [N omega-nitro-L-arginine (L-NNA)] of nitric oxide (NO) on the tubuloglomerular feedback (TGF) mechanism between anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and between the Milan hypertensive (MHS) and the Milan normotensive (MNS) strains of rats. Changes in proximal tubular stop-flow pressure (Psf) in response to various loop of Henle perfusion rates and measurements of early proximal flow rate (EPFR) were used to characterize TGF. Maximal drop in Psf (delta Psf) were used to indicate TGF reactivity and the flow rate eliciting half-maximal delta Psf (turning point; TP) to indicate TGF sensitivity. Under control conditions, TGF sensitivity was significantly higher in SHR than in WKY, but, after L-NNA infusion, TP was decreased in WKY and not in SHR. L-NNA infusion increased delta Psf by 95% in WKY but to a lesser extent (by 26%) in SHR. In the same way, L-NNA decreased TP in MNS but not in MHS. The increase in delta Psf was 99% in MNS but only 32% in MHS. The EPFR reduction after TGF activation was significantly increased in WKY and MNS but relatively unchanged in SHR and MHS. The results show that the effect of intratubular NO synthase inhibition on TGF is impaired in both strains of hypertensive rats.

This article has been cited by other articles:

				L. Yanes, D. Romero, R. Iliescu, V. E. Cucchiarelli, L. A. Fortepiani, F. Santacruz, W. Bell, H. Zhang, and J. F. Reckelhoff Systemic arterial pressure response to two weeks of Tempol therapy in SHR: involvement of NO, the RAS, and oxidative stress Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2005; 288(4): R903 - R908. [Abstract] [Full Text] [PDF]

				C. M. Sorensen, P. P. Leyssac, O. Skott, and N.-H. Holstein-Rathlou NO mediates downregulation of RBF after a prolonged reduction of renal perfusion pressure in SHR Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2003; 285(2): R329 - R338. [Abstract] [Full Text] [PDF]

				C. K. Roberts, N. D. Vaziri, R. K. Sindhu, and R. J. Barnard A high-fat, refined-carbohydrate diet affects renal NO synthase protein expression and salt sensitivity J Appl Physiol, March 1, 2003; 94(3): 941 - 946. [Abstract] [Full Text] [PDF]

				A. Ichihara, M. Hayashi, N. Hirota, and T. Saruta Superoxide Inhibits Neuronal Nitric Oxide Synthase Influences on Afferent Arterioles in Spontaneously Hypertensive Rats Hypertension, February 1, 2001; 37(2): 630 - 634. [Abstract] [Full Text] [PDF]

				E. TURKSTRA, B. BRAAM, and H. A. KOOMANS Impaired Renal Blood Flow Autoregulation in Two-Kidney, One-Clip Hypertensive Rats Is Caused by Enhanced Activity of Nitric Oxide J. Am. Soc. Nephrol., May 1, 2000; 11(5): 847 - 855. [Abstract] [Full Text]

				W. J. Welch, A. Tojo, and C. S. Wilcox Roles of NO and oxygen radicals in tubuloglomerular feedback in SHR Am J Physiol Renal Physiol, May 1, 2000; 278(5): F769 - F776. [Abstract] [Full Text] [PDF]

				E. Turkstra, P. Boer, B. Braam, and H. A. Koomans Increased Availability of Nitric Oxide Leads to Enhanced Nitric Oxide Dependency of Tubuloglomerular Feedback in the Contralateral Kidney of Rats With 2-Kidney, 1-Clip Goldblatt Hypertension Hypertension, October 1, 1999; 34(4): 679 - 684. [Abstract] [Full Text] [PDF]

				K. Brannstrom and W. J. Arendshorst Resetting of exaggerated tubuloglomerular feedback activity in acutely volume-expanded young SHR Am J Physiol Renal Physiol, March 1, 1999; 276(3): F409 - F416. [Abstract] [Full Text] [PDF]