A marked fall in blood pressure occurs during desynchronized sleep in cats, particularly when the buffering action of the chemoreceptors is removed. This fall appears to be due to inhibition of sympathetic activity present during wakefulness. Advantage was taken of these prior observations to assess the importance of the sympathetic nervous system in the maintenance of experimental renovascular hypertension. Profound falls of blood pressure were observed during desynchronized sleep in hypertensive animals particularly after sino-aortic deafferentation. That the sympathetic nervous system was involved in the maintenance of the hypertension was indicated by the fact that the hypotensive response during desynchronized sleep was almost completely abolished after surgical sympathectomy. However, sympathectomy did not prevent the development of a chronic renovascular hypertension. The latter result was interpreted to mean that in the absence of the sympathetic system other mechanisms will respond to the hypertensive stimulus provided by the renal arterial stenosis. An enhanced response to exogenously administered noradrenaline also was observed after renal artery stenosis in sympathectomized but not in nonsympathectomized cats. The enhanced response to catecholamines may have contributed to the hypertension seen in the sympathectomized animals.