Flow-dependent arteriolar dilation in normotensive rats fed low- or
high-salt diets.
Boegehold, Matthew A.
Department of Physiology, West Virginia University School of
Medicine, Morgantown, West Virginia 26506-9229
APStracts 2:0188H, 1995.
Ingestion of a high-salt diet has previously been shown to suppress
the endogenous influence of nitric oxide (NO) on arteriolar tone in
hypertension-resistant Dahl SR/Jr rats. Because luminal blood flow
can be an important stimulus for endothelial NO release, this study
was undertaken to determine if high salt intake can also lead to a
deficit in the direct flow-dependent regulation of arteriolar
diameter. The spinotrapezius muscle microvasculature was studied by
in-vivo microscopy in SR/Jr rats fed low (0.45%) or high (7%) salt
diets for 2 weeks, and arcade arteriole responses to increased
luminal flow (via parallel vessel occlusion) were studied in both
dietary groups. There was no significant difference between groups in
arterial pressure, or in resting arteriolar diameters, volume flows
or wall shear rates. In low-salt SR/Jr, a 36% increase in luminal
flow produced an average arteriolar dilation of 38% that was
significantly reduced by the NO synthase inhibitor NG-monomethyl L
-arginine (L-NMMA). In high-salt SR/Jr, a similar flow increase
produced an average dilation of only 16% (p<0.05 vs low-salt
SR/Jr), and this response was unaffected by L-NMMA. Inhibition of
cyclooxygenase activity with meclofenamate had no effect on this
response in either group. These findings suggest that NO release
mediates a portion of flow-dependent arteriolar dilation in rat
spinotrapezius muscle, and that high salt intake, in the absence of
hypertension, can attenuate this response via a suppression of NO
activity.
Received 4 November 1994; accepted in final form 24 April 1995.
APS Manuscript Number H990-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 9 May 1995.