This preclinical study demonstrates that renal nerve afferent and efferent activities are modulated by systemic blood pressure, venous distension, subcapsular pressure, and ischemia in cats.
Does not support clinical use; leaves open renal nerve contributions to human hypertension.
In anesthetized cats efferent as well as afferent activity has been recorded in the kidney nerves. Pulse synchronous bursts of efferent impulses could regularly be recorded which after vagotomy and baroreceptor denervation were augmented and changed into a continuous type of discharge. The efferent activity could be modified by electrical stimulation of peripheral sensory nerves. It was inhibited by elevation of systemic blood pressure by i.v. noradrenaline injection, and greatly increased by lowering of blood pressure by i.v. acethylcholine. In the same nerves afferent activity also occurred, in a few instances spontaneously, but more often after elevation of renal vein pressure, elevation of arterial perfusion pressure (by pump), mechanical pressure applied to the hilus area or local dilution of the blood by close intraarterial injection of Ringer solution. Local ischemia for one minute or less elicited intense afferent activity. The results indicate that venous distension and increased subcapsular pressure are adequate stimuli for these afferent responses and (hat more than one kind of fibers are engaged in the afferent response. The functional significance of the afferent activity remains to be determined.
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Åström et al. (1968) studied this question.
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