Mechanism of renin release during renal nerve stimulation in dogs

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Abstract
During renal nerve stimulation, a predominant vasoconstrictory effect on small arteries would lower blood pressure in the afferent arterioles and induce arteriolar dilation and renin release by the auto regulation mechanism. This hypothesis was examined in anaesthetized dogs by stimulating renal nerves at 4 Hz which permitted continuous reduction of renal blood flow (RBF) by 3040%; renin release increased almost equally at control and low blood pressure, and in the non-filtering kidney during ureteral occlusion. Examinations of the relationship between RBF and arterial perfusion pressure during mechanical constriction of the renal artery showed that the lowest auto regulating pressure was 25—35 mmHg higher during nerve stimulation than in control experiments, consistent with the hypothesis of arteriolar dilation. Phenoxybenzamine, an inhibitor of a adrenoceptors, abolished vasoconstriction and the effect of nerve stimulation on renin release at control blood pressure; renin release rose from 0.9 ± 0.4 to 17 ± 5 μg/ min before, and from 1.7 ± 0.5 to 4.6 ±1.4 μg/min after phenoxybenzamine infusion. At pressures below the range of auto regulation, phenoxybenzamine did not alter the renin release response to nerve stimulation. Propranolol, a β-adrenergic inhibitor, attenuated the effect of nerve stimulation on renin release both at control and low blood pressure. We conclude that during renal nerve stimulation (1) renin release is caused by β-adrenergic stimulation provided the afferent arterioles are dilated and (2) that α-adrenergic stimulation dilates the afferent arterioles as a consequence of a predominant vasoconstrictory effect on small arteries. Hence, by inhibiting the β-adrenergic effect by propranolol, renin release does not increase during renal nerve stimulation. Phenoxybenzamine prevents renin release at control blood pressure because afferent arterioles are not dilated during nerve stimulation. In contrast, phenoxybenzamine does not reduce renin release during nerve stimulation at low blood pressure because afferent arterioles are dilated by the auto regulating mechanism.