Control mechanisms for total renal blood flow (RBF) or regional blood flow were reviewed. Physiological and experimental conditions will usually cause simultaneous activation of several control mechanisms. The many interactions and secondary effects through release of intrarenal hormones, i.e., the renin-angiotensin system, prostaglandins and the kallikrein-kinin system, complicate the picture even more; but they also make it easy, and tempting, to construct various feedback control systems for renal hemodynamics. 1. There is no functional evidence for renal vasodilator nerves, while both pre- and postglomerular resistance vessels are supplied by adrenergic constrictor nerves. Nervous vasoconstrictor tone is absent or low under basal conditions, but may be activated by a number of afferent stimuli. 2. Intrarenal distributions of adrenergic alpha- and beta-receptor are homogeneous and beta-receptor may be selectively located in the afferent arterioles. On the other hand, the distribution of dopamine and acetylcholine receptor is not uniform, and they are distributed more in the inner cortex than in the outer cortex. 3. The renal arterioles are highly sensitive to the vasoconstrictor action of angiotensin II and to the vasodilator action of prostaglandin E2 and bradykinin. Under basal conditions, there seems to be no resting "angiotensin vasoconstrictor tone" and "bradykinin vasodilator tone", whereas salt depletion and certain types of renal hypertension may be associated with sustained renal vasoconstriction caused by angiotensin II. 4. Autoregulation tends to keep RBF and GFR constant at varying arterial pressure. There is no direct evidence for a metabolic autoregulation of RBF and for a contribution of intrarenal humoral factors for autoregulation. Thus, in spite of only indirect evidence, a Bayliss mechanism is still an attractive hypothesis, and would in fact seems to satisfy more experimental observations than any other mechanism.