Experimental aldosterone hypertension in the rat

Abstract

We previously showed that hypertension induced in rats by administration of desoxycorti-costerone acetate and replacement of the drinking water by 1% NaCl solution (DOCA-NaCl hypertension) was associated with an increased critical opening pressure (COP) of tail vessels and an increased arteriolar smooth muscle reactivity to intravenous infusion of angiotensin II or norepinephrine. In the present investigation hypertension was induced in rats by administration of aldosterone (5 μg/100 g per day) and replacement of drinking water with 1% NaCl solution (aldosterone–NaCl hypertension). The hypertension was associated with an increase in COP of tail vessels when measured both before and after ganglionic blockade, but the reactivity of the smooth muscle of these vessels to angiotensin II or to norepinephrine was not increased. Administration of aldosterone alone by intramuscular injection in sesame oil induced hypertension, whereas it was previously shown that similar treatment of rats with DOCA alone did not. The onset of hypertension and increased COP of tail vessels in the rats so treated with aldosterone was usually delayed by 4 or more days. To define more precisely the time course of the changes in blood pressure and COP induced by aldosterone hypertension was induced in rats by continuous subcutaneous infusion of aldosterone in an alcohol – 5% dextrose in water vehicle. Under these circumstances the rise in blood pressure and COP occurred after a delay of 2 days when measured after ganglionic blockade. On termination of the infusion the hypertension was rapidly reversed, the blood pressure declining smoothly to normal levels within 7 days.These results confirm that aldosterone alone can in fact induce hypertension in rats and suggest that the mechanism(s) by which aldosterone produces hypertension may differ in certain important respects from that involved in DOCA hypertension.