Abstract
The relative importance of sodium retention versus the renin–angiotensin pressor response in hypertension caused by constriction of one renal artery and contralateral nephrectomy in the rat was assessed. Attempts were made to lower the blood pressure by changing sodium balance while plasma renin activity was measured. Acute sodium depletion (furosemide) had no measurable effect on the pressure seemingly because activation of the renin–angiotensin system prevented a fall in pressure. However, the pressure decreased rapidly and markedly in response to sodium depletion when the renin-angiotensin system was suppressed by (a) removing the sole remaining kidney after the sodium depletion or (b) pretreating the animals with deoxycorticosterone and salt. These results emphasize the dual nature of the control of blood pressure by the kidney in experimental renal hypertension.