Renovascular hypertension in sodium-depleted dogs: role of renin and carotid sinus reflex

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Abstract
To determine if renovascular hypertension can be induced without salt retention renal artery stenosis was produced in 7 trained, unilateral nephrectomized dogs maintained on a low Na+ diet. Bilateral carotid artery loops were prepared to assess the role of the carotid sinus reflex. Mean aortic pressure (MAP), the pressor response to carotid occlusion, Na and fluid balance, plasma renin activity (PRA), plasma aldosterone concentration (PAC), hematocrit (Hct), weight (wt) and plasma volume (PV) were monitored before renal artery constriction and for 6-14 days of sustained renal arterial hypotension produced by reducing renal arterial pressure to 60-70 mmHg. MAP rose 37 .+-. 4 mmHg within 1 h of constriction and remained at this level throughout the experiment. Na and fluid retention did not occur. No change in Hct, wt or PV occurred. PRA and PAC increased 11.2 .+-. 1.7 ng .cntdot. ml-1 .cntdot. h-1 and 361 .+-. 91 pg .cntdot. ml-1, respectively, within 1 h and remained at these levels. The pressor response to carotid occlusion increased from 18.3 .+-. 3.2 in the control experiments to 30 .+-. 4 mmHg 1 h after renal artery constriction. During the next 48-72 h the response to carotid occlusion decreased to a new plateau of 20 .+-. 3 mmHg by day 3, remaining significantly greater than the preconstriction response. Apparently renovascular hypertension can be produced in dogs kept on a low-Na+ diet which prevents salt and water retention; the hypertension is maintained primarily by the renin-angiotensin system and the resetting of the arterial baroreceptors is incomplete after 14 days.

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