Increased renal vascular reactivity to angiotensin II but not to nerve stimulation or exogenous norepinephrine in renal hypertensive rats.

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Abstract
We isolated and perfused both the "clipped" and "contralateral" kidneys from Goldblatt renal hypertensive and sham-operated control rats, 1--104 days postoperatively. Responses to renal nerve stimulation were depressed in clipped kidneys from hypertensive rats (1 day postoperative), and these kidneys were supersensitive to exogenous norepinephrine (1--31 day) when compared with the contralateral organ of the same animal. Similar alterations were found between clipped and contralateral kidneys from sham-operated control rats. There was no difference in responses to renal nerve stimulation of norepinephrine between clipped kidneys from hypertensive and control rats, but clipped kidneys from hypertensive rats were supersensitive to angiotensin II (17 and 31 days). Comparison of contralateral kidneys from hypertensive and control rats revealed no change in norepinephrine sensitivity or in responses to renal nerve stimulation, but there was a reduction in the slope of the dose-response curve to norepinephrine and of the maximal effect of the catecholamine (104 days) and a pronounced supersensitivity to angiotensin II (17--104 days) in the hypertensive rats. These results indicate that (1) renal nerve function and norepinephrine sensitivity of the isolated renal vasculature are unchanged in renal hypertension, but clipping partially denervates the kidney causing depressed nerve function and unilateral norepinephrine supersensitivity, unrelated to hypertension; (2) the prolonged high pressure load on the contralateral kidney may impair the function of the vascular smooth muscle; and (3) bilateral supersensitivity to angiotensin II is associated with hypertension but is not solely a consequence of the high pressure.