Hypertension, Vol 20, 59-66, Copyright © 1992 by American Heart Association
CA Bruner
Wistar-Furth rats have been shown to be resistant to mineralocorticoid-
salt hypertension, but the mechanism for this resistance is unknown. In the
current experiments, adult male Wistar and Wistar-Furth rats were given a
subcutaneous aldosterone infusion (0.15 microgram/hr) for 4 weeks, and
changes in blood pressure and vascular reactivity were studied. Rats
received a 1% NaCl, 0.2% KCl solution to drink. After 4 weeks of
aldosterone infusion, systolic blood pressure measured using a tail-cuff
technique had increased by 60 mm Hg in Wistar rats but was unchanged in
Wistar-Furth rats. Hypokalemia occurred in both strains in response to the
aldosterone infusion. Isolated, helically cut strips of common carotid
artery and aorta were prepared for isometric force recording. Cumulative
concentration-response curves to norepinephrine, serotonin, KCl, calcium,
nitroprusside, and acetylcholine were performed in carotid artery strips,
and concentration-response curves to ouabain were performed in aortic
strips. Increased vascular contractile sensitivity to KCl, ouabain,
norepinephrine, and serotonin was observed in vessels from Wistar rats
treated with aldosterone and salt. The same treatment in Wistar-Furth rats
produced only increased vascular sensitivity to ouabain and serotonin, and
these changes were of smaller magnitude than those seen in Wistar rats.
Aldosterone-salt treatment produced decreased vascular sensitivity to
acetylcholine and nitroprusside in both Wistar and Wistar-Furth rats. These
results support the hypothesis that resistance of Wistar-Furth rats to
aldosterone-salt hypertension is due to resistance to the effects of
aldosterone-salt treatment that normally result in increased
vasoconstrictor sensitivity.
ARTICLES
Vascular responsiveness in rats resistant to aldosterone-salt hypertension
Department of Pharmacology and Toxicology, Albany Medical College, NY 12208.
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