Chronic renovascular hypertension in sheep induced by renal artery constriction was not necessarily associated with abnormal peripheral renin or aldosterone concentrations.
The study demonstrates that chronic renovascular hypertension is not necessarily driven by abnormal peripheral renin or aldosterone levels, and emphasizes the critical role of total body sodium balance.
Sheep were made chronically hypertensive by constriction of one renal artery. Blood levels of renin, aldosterone and cortisol were measured. Sodium balance was estimated from measured food intake and renal and fecal sodium loss. Animals with a clipped single kidney and animals with mild hypertension after unilateral clipping showed only a temporary increase of renin, aldosterone and cortisol in peripheral blood. Animals with severe hypertension after unilateral clipping became sodium depleted, due to increased renal excretion of sodium. Renin and aldosterone blood levels did not return to normal levels but increased progressively with the sodium deficit. The findings demonstrate that chronic renovascular hypertension is not necessarily associated with abnormal concentration of renin or aldosterone in peripheral blood, and suggest that the renin-angiotensin system is not the cause of the continuing hypertension. Severe hypertension may cause sodium depletion in animals with both kidneys in situ. The effect of this on blood levels of renin and aldosterone indicates that knowledge of the total body sodium balance is essential when assessing the significance of the renin-angiotensin system in the hypertension. (Endocrinology83: 1199, 1968)
Blair‐West et al. (1968) studied Experimental Renal Hypertension. Constriction of one renal artery was evaluated on Blood levels of renin, aldosterone and cortisol, and sodium balance. Chronic renovascular hypertension in sheep induced by renal artery constriction was not necessarily associated with abnormal peripheral renin or aldosterone concentrations.
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