Hypertension, Vol 2, 274-280, Copyright © 1980 by American Heart Association
GD Fink, A Takeshita, AL Mark and MJ Brody
Hypertension-resistant (R) rats of the Dahl strain remain normotensive on
diets containing excessive sodium chloride, while hypertension- sensitive
(S) rats rapidly become hypertensive when eating the same diet. In the
present study, renal hemodynamics were investigated in Dahl rats eating
normal or high salt chow for 4 weeks. The R rats eating sodium-enriched
chow were found to have significantly lower renal vascular resistance (RVR)
than R rats on normal chow; RVR was identical in S rats on either diet. The
reason for the failure of S kidneys to exhibit vasodilation during high
salt ingestion was explored by examining renal vascular responses to
interruption of the renal sympathetic nerves, renal sympathetic nerve
stimulation (SNS), and to several vasoactive agents. Changes in RVR to
nerve section and to SNS were similar in both strains regardless of diet.
Renal vascular responses to intraarterial norepinephrine were suppressed
significantly by high salt intake only in the R rats. Changes in RVR to
intraarterial angiotensin II were uniformly greater in S than in R rats,
but were not altered by salt intake in either strain. Renal vasodilation in
response to intraarterial acetylcholine was reduced in R rats on high salt
intake, but was not affected by salt intake in S rats. It is concluded that
S rats exhibit inappropriately high renal vascular tone during ingestion of
excessive salt, and that this alteration is not the result of increased
neurogenic activity or increased vascular reactivity to angiotensin II or
norepinephrine.
ARTICLES
Determinants of renal vascular resistance in the Dahl strain of genetically hypertensive rat