Is the peripheral sympatho-adrenal nervous system necessary for renal hypertension?

Two-kidney renal hypertension in the rat (left renal artery narrowing) was shown to be dependent on the vasoconstrictor action of renin-angiotensin throughout its time course as evidenced by the simultaneous: 1) rise in blood pressure; 2) elevation in plasma renin activity; and 3) vasodepressor sensitivity to the converting enzyme inhibitor SQ-20881. One-kidney renal hypertension (left renal artery narrowing plus contralateral nephrectomy), in contrast, was shown to be independent of the vasoconstrictor action of renin-angiotensin. The role played by the sympathetic nervous system in one-kidney renal hypertension was studied in animals in which the peripheral sympathetic nervous system was completely ablated by chronic guanethidine treatment and adrenal demedullation. The completeness of the sympathectomy was pharmacologically confirmed by 1) marked reduction of tyramine vasoconstriction; 2) lack of sensitivity to ganglionic blockade (pentolinium); and 3) complete reversal of blood pressure responsiveness to phentolamine. When such animals were subjected to unilateral nephrectomy and left renal artery constriction, they still developed a significant hypertension compared to their unclipped controls and the hypertension remained renin independent. One-kidney renal artery-clipped animals that were only neonatally guanethidine-treated or were only adrenal-demedullated, also developed low-renin renal hypertension. It can be concluded that one-kidney renal hypertension is not only low-renin hypertension but that it can develop in the complete absence of adrenal medullary and peripheral adrenergic function.