Impaired effect of nitric oxide synthesis inhibition on
tubuloglomerular feedback in hypertensive rats.
Thorup, Christian, and A. Erik G. Persson.
Department of Physiology and Biophysics, University of Lund,
Sweden
APStracts 3:0032F, 1996.
Thorup, Christian and A. Erik G. Persson. Impaired effect of nitric
oxide synthesis inhibition on tubuloglomerular feedback in
hypertensive rats. Am.J.Physiol. 000:000-000, 0000.-Experiments were
conducted to compare the effects of intratubular inhibition (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 (_Psf) was used to
indicate TGF reactivity, and the flow rate eliciting half maximal
_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 _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 _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.
Received 22 October 1995; accepted in final form 5 February 1996.
APS Manuscript Number F364-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 24 February 96