The effect of high sodium intake and angiotensin antagonist in rabbits with severe and moderate hypertension induced by constriction of one renal artery.

The role of renin was assessed in moderate and severe one-clip, two-kidney hypertension in rabbits during normal and high Na intake. Severe hypertension occurred with high levels of plasma renin and creatinine and with extracellular volume depletion. In this group, hypertension was significantly reduced by the 1-hour intravenous infusion of 1,000 ng/kg of an angiotensin II antagonist or by correcting the volume depletion with a high Na intake, which also decreased renin activity and creatinine. The infusion of the antagonist after a high salt diet failed to decrease blood pressure further. Moderate hypertension occurred with plasma levels of renin that were slightly below normal and with no significant abnormalities in extracellular volume depletion or creatinine. In this group, the administration of an angiotensin II antagonist or a high salt diet did not affect any of the three parameters. In normotensive controls, the blood pressure level was not affected by either the angiotensin II antagonist or the high salt diet, despite a reduction in plasma renin activity. Thus, high levels of renin are important in maintaining severe hypertension, and these increased levels probably are accompanied by a concomitant depletion of extracellular volume. Correction of the extracellular volume depletion by a high salt diet is followed by a decrease in renin activity and in blood pressure. In contrast, renin activity does not seem to be important in maintaining moderate hypertension, the pathogenetic mechanism of which remains to be elucidated.