1. The anaesthetized cat, unilaterally nephrectomized and with renal nerves sectioned, has been used in a study of the specificity of the inhibitory effect of propranolol on renin release.
2. The effect of (+)-propranolol on the rise in plasma renin activity (PRA) induced by renal nerve stimulation has been examined. When administered at approximately the same dose as the racemic mixture which blocks renin release in response to this stimulus, (+)-propranolol did not significantly reduce the magnitude of the response. Therefore the action of racemic propranolol in blocking the response to neural stimulation can be attributed to the (−)-isomer.
3. Renal artery constriction, producing blood flow changes similar to those resulting from renal nerve stimulation, also induces a rise in PRA. (±)-Propranolol, in amounts which block the rise in PRA observed with renal nerve stimulation, did not prevent the increase seen with renal artery constriction.
4. Reduction of renal perfusion pressure within the autoregulatory range for 20 min resulted in a rise in PRA in all experiments. (±)-Propranolol did not significantly affect the response.
5. It is concluded that the release of renin in response to renal nerve stimulation cannot be attributed to associated changes in renal blood flow. The evidence is compatible with a direct action of the neurotransmitter on renin-containing cells via a β-adrenergic receptor. When renin release is induced by non-adrenergic mechanisms propranolol blockade has no significant effect on the response.