Sympathetic outflow influences the renal release of renin through modifications of the tonic activity of the renal nerves and the plasma concentration of catecholamines. These influences may initiate changes in the rate of renin secretion or modulate the response initiated by another of the mechanisms that control renin release. Beta-adrenoceptor mediated stimulation of renin release has been demonstrated in vivo, in the isolated perfused kidney and in preparation in vitro. Likewise an array of evidence has accumulated pointing to the existence of alpha-adrenoceptor mediated inhibition of renin release. However, the cellular location, the physiological significance, and even the existence of these alpha-adrenoceptors is still disputed. Receptors sensitive to alterations in the vascular volume have been identified in areas of low and high pressure of the circulation. There is evidence that input from both types of receptors may cancel each other, and that to demonstrate experimentally the effects on renin release of the low pressure cardiopulmonary receptors it is necessary to avoid changes in the input from the high pressure arterial receptors, and vice versa. Again there are dissenting voices that disclaim a tonic inhibitory effect of cardiopulmonary receptor initiated impulses on renin release. The majority of the pharmacological evidence identifies the beta-adrenoceptors in JG cells as of the beta 1-subtype. However, some species may make exception to this generalization. As in other tissues, beta-adrenoceptor mediated influences appear to relate to activation of adenylcyclase in the cell membrane. Considerable interest in the role of calcium in the process of activation of renin release has met with some unexpected, though consistent, experimental findings.