DOCA-salt hypertension does not develop in rats with hereditary lack of vasopressin (DI rats) nor in rats with lesion of the anteroventral region of the third ventride (AV3V), an area controlling vasopressin (VP) release. We examined, therefore, the effect of VP treatment on the development of DOCA salt hypertension in AV3V-lesioned (AV3V-L) normal Sprague-Dawley rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). We also examined changes in vascular reactivity in isolated, perfused kidneys in the experimental groups. Whereas sham-lesiooed (SL) rats showed hypertension at 5 weeks, AV3V-L rats showed no change in arterial pressure (AP) after DOCA. AV3V-L rats given VP exhibited only an intermediate rise in AP in spite of the fact that plasma VP levels were comparable in DOCA-treated SL rats and AV3V-L rats. SL and AV3V-L rats given VP showed enhanced renal vascular activity whereas no vascular changes occurred in AV3V-L rats. At 5 weeks post DOCA, intact DI rats given VP were hypertensive and exhibited enhanced renal vascular reactivity. AV3V lesion in DI rats completely prevented VP-induced DOCA/salt hypertension and enhanced vascular responsiveness. These data suggest that VP plays a primary role in DOCA-salt hypertension through an induction of enhanced vascular reactivity and through central mechanisms requiring the integrity of the AV3V region.
- Central nervous system brattleboro rats
- Diabetes insipidus
- Doca hypertension