SUMMARY1. The effect of electrical stimulation of the distal cut ends of the renal nerves of unilaterally nephrectomized, anaesthetized cats was studied. Using stimulation parameters of 15 pulses per second (pps), 15 V and 0-2 msec duration, there was an immediate sharp drop in renal blood flow, as determined by an electromagnetic flowmeter, which was maintained for about 2 min. Flow gradually returned to control values over approximately the next 10 min in spite of continued stimulation for up to 30 min.2. Plasma renin activity (PRA) increased markedly after 10 min of stimulation but 20 min later fell towards pre-stimulation values whether stimulation was maintained or not.3. Phentolamine, an az-adrenergic-receptor antagonist, abolished both the blood flow and PRA responses to a 10 min period of renal nerve stimulation.4. When the renal artery was constricted in order to produce blood flow changes similar to those found with renal nerve stimulation, the rise in PRA was similar to that observed with renal stimulation.5. In phentolamine-blocked animals, renal artery constriction, as described, produced the same effect on PRA as was observed with renal nerve stimulation.6. Propranolol, a fl-adrenergic-receptor antagonist, did not block the blood flow response to renal nerve stimulation, but did block the rise in PRA normally associated with renal nerve stimulation.7. It is suggested that the effect of renal nerve stimulation on PRA is mediated, primarily, by changes in renal blood flow and that one of the steps leading to renin release following stimulation is sensitive to propranolol. This step must be distal to the effect on vascular smooth muscle.

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SUMMARY1. Spontaneous and reflex activity was recorded from renal and splanchnic nerves and thoracic white rami during discrete electrical stimulation within the medulla oblongata of anaesthetized cats.2. Inhibition or excitation of spontaneous sympathetic nerve activity was obtained from several medullary regions.3. The long-circuited reflex elicited in renal nerves and the spinally mediated reflex discharge produced in white rami by single shock stimulation of intercostal nerves were inhibited by stimulation within the sympatho-inhibitory areas of the medulla.4. Activation of spontaneous sympathetic nerve activity or inhibition of spontaneous and reflex sympathetic nerve activity was obtained during electrical stimulation within the lateral funiculi of the cervical spinal cord in unanaesthetized decerebrate cats, spinalized at C1.5. There was a correlation between the position of some sympathoinhibitory regions of the medulla and spinal cord and the position of the cell bodies and axons of descending monoamine-containing neurones.6. Intravenous administration of the precursor of noradrenaline, L-DOPA, to unanaesthetized decerebrate cats, spinalized at C1, was followed by a depression of spontaneous activity in renal nerves and reflex responses elicited in renal nerves and white rami.7. Similarly the precursor of 5-hydroxytryptamine, 5-HTP, caused a depression of reflex activity elicited in renal nerves and white rami, but had no effect on spontaneous renal nerve activity.8. It is suggested that there exist both noradrenergic and tryptaminergic pathways which descend to the spinal cord from the medulla and which are inhibitory to sympathetic outflow.

SUMMARY1. The onset and time course of baroreceptor inhibition of pre-and post-ganglionic sympathetic reflex activity has been examined in the anaesthetized cat.2. The shortest time to the onset of inhibition of an intercostal evoked reflex response in cardiac and renal nerve was less than 90 msec following a rise in pressure in a carotid sinus blind sac, and around 55 msec following stimulation of the ipsilateral sinus nerve. The cardiac nerve response was completely inhibited before the renal nerve response.3. Because of the long delays in the somato-sympathetic reflex pathway it is argued that these minimum times will be much less than the real central delay of baroreceptor inhibition. These were estimated by adding on the central times for the somato-sympathetic reflexes to give latencies of 94-143 msec for the inhibition. 4. A spinal sympathetic reflex was inhibited by 30-75 % following a rise in pressure in a carotid sinus blind sac or sinus nerve stimulation. The minimum time for this inhibition was around 100 msec.5. The baroreceptor inhibition of the spinal sympathetic reflex was abolished following section of a restricted region in the dorsolateral part of the lateral funiculus of the cervical spinal cord.6. Both pre-and post-ganglionic reflexes could be inhibited when stimulating within three regions of the medulla oblongata. The latency to inhibition elicited from the ventromedial reticular formation was short, some 5-30 msec, whereas that elicited from a ventrolateral region or the mid line raphe nucleus was long, some 90-160 msec.7. The possibility is discussed that the baroreceptor inhibition of both the pre-and post-ganglionic reflexes examined in this study is occurring at the spinal level via a pathway from either the raphe nuclei or ventrolateral medulla.

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