Chronic l-name hypertension in rats and autoregulation of
juxtamedullary preglomerular vessels.
Bouriquet, Nathalie, and Daniel Casellas.
Groupe Rein et Hypertension, Hopital St. Charles, Montpellier,
France
APStracts 2:0036F, 1995.
The impact of chronic L-NAME-induced hypertension (20 mg.Kg-1.day-1, p
o, for 25 days) on pressure-responsiveness was assessed in vessels
ranging from arcuate arteries (ArcA) to juxtaglomerular afferent
arterioles (JAA), using videomicroscopy and blood-perfused
juxtamedullary nephron preparations. Respective tail-cuff pressures
of Control and L-NAME rats were 127+/-2 mmHg (n=8) and 173+/-4 mmHg
(n=5). Corresponding vessels of both groups had similar calibers at
60mmHg. Increasing blood perfusion pressure to 200 mmHg constricted
Control ArcA and JAA by 26+/-4 % (n=20) and 43+/-5 % (n=15),
respectively. Instead, a respective 3+/-4 % (n=15) and 21+/-9 % (n=6)
pressure-induced dilation occurred in L-NAME vessels, and 86+/-2 % of
glomeruli expressed [alpha]-smooth muscle actin. Responses to
acetylcholine (1 [mu]M) but not to nitroprusside (1 mM) were impaired
by L-NAME. Maximal relaxation induced by Mn2+ (10 mM) revealed equal
basal tone and similar passive visco-elastic properties in Control
and L-NAME vessels. No vascular hypertrophy was found in L-NAME
vessels. Chronic L-NAME hypertension is therefore associated with a
selective loss of vascular autoregulation in juxtamedullary nephrons,
which may contribute to glomerular injury.
Received 30 November 1994; accepted in final form 8 March 1995.
APS Manuscript Number F424-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 March 1995.