Hypertension, Vol 17, 63-71, Copyright © 1991 by American Heart Association
WB Jeffries, S McArdle, C Bockman, PW Abel and WA Pettinger
In previous studies we found that vasopressin stimulation of both cyclic
AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium
reabsorption in isolated perfused kidneys was markedly exaggerated in rats
with mineralocorticoid hypertension. In the present study, we tested the
response (cAMP accumulation) of cortical and outer medullary collecting
tubules (OMCT) to vasopressin in two rat models that are resistant to
deoxycorticosterone acetate (DOCA)-induced hypertension, the Wistar-Furth
strain and NaCl-deficient rats. The blood pressure of normal outbred Wistar
rats rose to hypertensive levels (systolic pressure more than 165 mm Hg)
during a 5-week treatment with DOCA (10 mg/week) and 1% saline to drink.
Significant hypertrophy of the heart and kidneys was also observed.
Vasopressin (10(-8) M)-induced cAMP formation was enhanced 3.4-fold in the
CCT (OMCT unchanged) of hypertensive rats compared with normotensive
controls. Significant hypertrophy (as indexed by tubule diameter) of the
CCT but not the OMCT was also observed in DOCA-salt hypertensive rats.
Restriction of dietary NaCl (0.13% in chow, tap water to drink) completely
prevented DOCA-induced hypertension, organ and CCT hypertrophy, and
enhancement of vasopressin-stimulated cAMP formation in the CCT. In
Wistar-Furth rats, DOCA-salt treatment did not alter blood pressure or
cause significant organ hypertrophy. However, DOCA- salt treatment enhanced
vasopressin-stimulated cAMP formation by 4.1- fold in CCT of Wistar-Furth
rats, with significant tubular hypertrophy in the CCT but not the OMCT. We
conclude that DOCA-induced hypertension and changes in CCT function are
dependent on excess dietary NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension
Department of Medicine, Creighton University School of Medicine, Omaha, Neb.
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