Responses of neurons in paraventricular nucleus to activation of cardiac afferents and acute myocardial ischaemia in rats

Stimulation of cardiac sympathetic afferents increases sympathetic outflow and blood pressure. Chemicals released during myocardial ischaemia activate cardiac afferents. This study was to determine the responses of neurons in paraventricular nucleus (PVN) to the cardiac afferent activation caused by exogenous chemicals or myocardial ischaemia using an extracellular single-unit recording method. Rats were anaesthetized and underwent bilateral cervical vagal denervation (VD) and carotid and aortic baroreceptor denervation (BD). In 196 spontaneously active neurons in parvicellular PVN, 60 (30.6%), 36 (18.4%) and 91 (46.4%) neurons were respectively sensitive, mildly sensitive and insensitive to capsaicin, while nine (4.6%) neurons showed inhibitory responses to capsaicin. Epicardial application of capsaicin activated capsaicin-sensitive neurons in the PVN and increased mean arterial pressure. These neurons were also sensitive to exogenous bradykinin, adenosine and H(2)O(2). The neuron response is not secondary to a capsaicin-induced increase in mean arterial pressure because a similar degree of pressor response induced by aortic coarctation did not increase the neuron activity. Compared with intact rats, VD or BD or combined VD and BD increased the response of capsaicin-sensitive neurons to epicardial application of capsaicin, while stimulation of vagal afferents inhibited the response. Myocardial ischaemia caused increases in the activity of capsaicin-sensitive neurons and renal sympathetic nerve activity. The results indicate that chemical stimulation of cardiac sympathetic afferents activates capsaicin-sensitive neurons in parvicellular PVN, which is inhibited by the afferent activities of vagi and arterial baroreceptors. Acute myocardial ischaemia activates capsaicin-sensitive neurons in PVN and enhances sympathetic outflow.     

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat

The present study was designed to determine effect of the preganglionic splanchnic nerve activity (SNA) on the brief hypotension accompanied with the occlusion of left circumflex coronary artery (CxCAO) in chloralose anesthetized cats. Following CxCAO in animals with neuraxis intact, no significant alterations of SNA occurred despite the significant fall in mean blood pressure (MBP). A significant fall in MBP also occurred in vagotomized animals with arterial baroreceptors intact, but SNA was significantly augmented from 12.9 +/- 2.7 impulses/sec before CxCAO to 24.4 +/- 4.3 impulses/sec 60 sec after the occlusion. In vagotomized animals, in which their carotid sinuses were isolated and perfused with the constant pressure at a level equal to systemic blood pressure (112 +/- 6 mmHg) and with higher pressure (167 +/- 7 mmHg), SNA was not altered significantly during the hypotension due to CxCAO. When the carotid sinuses were perfused with lower pressure (53 +/- 8 mmHg), a significant increase in SNA occurred simultaneously with the decrease in MBP after CxCAO. The peak decreases in blood pressure during the coronary occlusion were significantly greater in the vagotomized group (-46 +/- 5 mmHg) and in the Low-CSP group (-50 +/- 5 mmHg) than in other groups. Onset of this excitatory efferent sympathetic response to the hypotension due to the coronary occlusion in the vagotomized and Low-CSP groups was delayed significantly despite a significant fall in arterial blood pressure. These results show that vagal afferents from the heart may play a role of inhibiting the sympathetic augmentation mediated by arterial baroreceptors during cardiogenic hypotension. An excessive activation of cardiac receptors with sympathetic afferents may be induced by the profound fall in blood pressure, resulting in further impairment of cardiac function due to progressive myocardial ischemia under the condition of high sympathetic tone activated by baroreceptor reflex.     

Spinal sympathetic reflexes initiated by coronary receptors

1. The main left coronary artery of vagotomized spinal cats was perfused at different flows and pressures. The changes in pressure were limited to the coronary bed.2. Increased coronary flow which increased coronary arterial pressure provoked a reflex increase in sympathetic discharge in the white ramus of the third thoracic spinal nerve and the inferior cardiac nerve. Reflex reductions in activity were not observed.3. Occlusion of the coronary sinus and myocardial ischaemia, due to cessation of pump inflow, evoked similar reflex increases of sympathetic activity. The effect of myocardial ischaemia was apparent before systemic arterial blood pressure fell or left ventricular end-diastolic pressure rose.4. Increased coronary arterial pressure, myocardial ischaemia and coronary sinus occlusion could activate the same preganglionic neurone.5. The afferent limb of the excitatory coronary-sympathetic reflex was in the cardiac sympathetic nerves, mainly on the left. Afferent nerve fibres running in these nerves and in the third left thoracic sympathetic ramus communicans were excited by increased coronary arterial pressure, myocardial ischaemia, and occlusion of the coronary sinus. Inhibition was not observed. Many of the receptors were further localized by direct probing over the coronary vessels and adjacent myocardium.6. Some receptors were excited by increased coronary arterial pressure alone, others by coronary sinus occlusion, and still others by myocardial ischaemia. In addition, some receptors were excited by all three stimuli.     

Role of cardiac sympathetics in the tonic circulatory restraint by vagal afferents.

In anesthetized cats with aortic nerves sectioned and carotid arteries occluded, we determined the role of cardiac sympathetic nerves on the tonic inhibitory restraint by cardiac vagal afferents on the cardiovascular system. The effect of afferent vagal blockade on mean arterial pressure and cardiac contractility was determined when sympathetic tone to the heart was altered. Bilateral cardiac sympathectomy produced a significant decrease in left ventricular dP/dt and attenuated the arterial pressure response to afferent vagal cold block to less than 40% of the control. The increase in dP/dt normally observed with vagal blockade was also reduced significantly. Increasing dP/dt by efferent stimulation of cardiac sympathetic nerves restored the arterial pressure response to vagal blockade to near control levels. While the vagal inhibitory activity appeared to be dependent on the resting dP/dt, left ventricular peak pressure did not seem to be contributing to the reflex. Thus, the inhibitory effects of vagally mediated reflexes from the heart which contribute to arterial pressure regulation appear to be influenced by changes in cardiac contractility induced by cardiac sympathetic nerve stimulation.     

Cardiopulmonary sympathetic afferent influences on renal nerve activity.

Cardiopulmonary sympathetic afferent nerves may affect renal control of intravascular volume by influencing renal sympathetic nerve activity. This influence was evaluated in alpha-chloralose anesthetized, vagotomized, sino-aortic denervated cats. When the afferent nerves were activated with a single electrical stimulus, the renal nerve responded with an excitatory burst of activity followed by a long period of inhibition. This response had characteristics of a supraspinal reflex. Repetitive stimulation of the sympathetic afferent nerve either inhibited or excited renal nerves and increased or decreased systemic blood pressure. The direction of these changes depended on stimulus parameters. No obligatory correlation in the direction of change of nerve activity and blood pressure was observed. Activation of cardiopulmonary sympathetic afferent nerves by intravascular volume expansion inhibited renal nerve discharge. Inhibition was elminated by sectioning the sympathetic afferent nerves. Volume expansion had no effect on lumbar sympathetic discharge monitored simultaneously with renal nerve activity. This observation suggests specificity of reflex influences of these afferent nerves on the kidney. In conclusion, cardiopulmonary sympathetic afferent nerves can reflexly alter renal nerve activity, and therefore may affect renal control of intravascular volume.     

Interaction between the hypothalamic defence reaction and cardiac ventricular receptor reflexes.

The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.     

Effects of sex and ovarian hormones on the initial renal sympathetic nerve activity response to myocardial infarction

The physiological mechanisms contributing to sex differences following myocardial infarction (MI) are poorly understood. Given the strong relationship between sympathetic nerve activity (SNA) and outcome, we hypothesized there may be a sex difference in SNA responses to MI. In anaesthetized, open-chest male, female and ovariectomized (OVX) female Wistar rats, mean arterial pressure, heart rate and renal SNA were recorded in response to ligation of the left coronary artery. In males, renal SNA increased by 30 ± 6% in the first minute of coronary occlusion (P < 0.05) and remained elevated at 18 ± 7% above baseline (P < 0.05) at 2 h following MI. In response to MI, ovary-intact females displayed no change in renal SNA, whereas OVX females displayed a significant increase, similar to that seen in the males (increases of 43 ± 11% at 1 min and 21 ± 7% at 2 h post-MI, P < 0.05 versus intact females). Arterial baroreflex control of renal SNA had a smaller range in females (ovary intact and OVX) than males; no changes in arterial baroreflex responses were observed 1 h post-MI in males or females. Denervating the arterial baroreceptors abolished the renal SNA response to MI in the males, whereas in ovary-intact females and OVX females the response was unaltered. These findings suggest that ovarian hormones are able to blunt the initial sympathetic activation post-MI in females and that the importance of the arterial baroreflex in mediating initial sympathetic activation post-MI is different between the sexes.     

Action potentials in parasympathetic and sympathetic efferent fibres to the trachea and lungs of dogs and cats

1. Action potentials were recorded from seventy-four single and twenty-nine small multifibre nerve strands efferent to the trachea and lungs of cats and dogs. From the pathway (vagal or sympathetic), spontaneous activity, conduction velocity and responses to various interventions the efferent fibres were classified in the following way.2. Group I, vagal. These had a mean conduction velocity of 9.7 m/sec, and had a respiratory but seldom a cardiac rhythm. Their discharge was inhibited during hypertension caused by injections of adrenaline and during inflation of the lungs, but was increased during tracheal occlusion, stimulation of peripheral chemoreceptors and irritation of the larynx. The fibres are thought to be constrictor to the airways.3. Group II, sympathetic. These had a mean conduction velocity of 0.85 m/sec and usually had inspiratory and cardiac rhythms. Their discharge usually responded qualitatively as that of group I fibres to the various interventions, but with clear quantitative differences. They are divided into three subgroups on the basis of their responses to injections of adrenaline and to asphyxial stimuli.4. Group III, vagal and sympathetic. These had a mean conduction velocity of 9.0 m/sec, very slow discharge rates and often an expiratory and cardiac modulation. They were activated during hypertension due to adrenaline and often by tracheal occlusion, chemoreceptor stimulation, laryngeal irritation and lung inflation. Their motor action is unknown.5. Group IV, vagal and sympathetic. These had conspicuous cardiac rhythms resembling those of vascular baroreceptors, but their discharge could not be correlated with arterial blood pressure. Their mean conduction velocity was 6.6 m/sec. Some were active after combined vagotomy and sympathectomy. Together with some unclassified fibres, those of group IV are thought to be aberrant afferent nerves or collateral afferent branches, and possibly to subserve local reflexes.6. The results are discussed in relation to nervous control of effector tissues in the airways and autonomic nervous control generally.     

The effect of baroreceptors on the latency of evoked responses in sympathetic nerves during the cardiac cycle

1. A rapid increase in pressure in a vascularly isolated perfused carotid sinus has been shown to inhibit a reflex response in efferent sympathetic nerves of the dog evoked by electrical stimulation of the radial nerve.2. In intact preparations with the carotid baroreceptors innervated, the mean latency and the variance of the latency of reflex sympathetic nerve responses was reduced when the stimuli evoking the responses were applied at one point of both cardiac and respiratory cycles. When the baroreceptors were denervated there were no significant differences in the responses to random and synchronized stimuli.3. In intact preparations the latency of evoked responses in sympathetic nerves was found to vary progressively during a cardiac cycle; the maximum increase in latency was observed with the responses that occurred at that phase of the cardiac cycle when the baroreceptors exert maximal inhibition on spontaneous sympathetic activity. After denervation of the carotid sinuses a much smaller change during the cardiac cycle was still present, possibly due to effects produced by baroreceptors of the aortic arch and elsewhere.4. It was concluded that changes in baroreceptor activity, due to beat to beat fluctuations of the systemic arterial pressure are a major factor causing variations in the latency of responses in sympathetic nerves evoked by stimuli applied to a cutaneous nerve.     

Bulbospinal tryptaminergic neurones

1. The possible role of bulbospinal tryptaminergic neurones in the control of sympathetic activity has been investigated in anaesthetised cats. 2. Depletion of spinal cord stores of 5-hydroxytryptamine was achieved by systemic administration of p-chlorophenylalanine or by intraspinal microinjections of 5,6-dihydroxytryptamine. 3. Blood pressure was little changed by these treatments, neither was the pattern of ongoing activity in sympathetic nerves (arterial pulse rhythmicity and respiratory modulation), the influence of pulmonary afferent nerves on this activity (determined by an airway occlusion technique), the sympatho-inhibitory influence of the carotid sinus baroreceptors, nor the sympatho-inhibitory or -excitatory influences of somatic afferent nerves. 4. Since both p-chlorophenylalanine and 5,6-dihydroxytryptamine treatment caused extensive disruption of the bulbospinal tryptaminergic neurones, it was concluded that these play no significant role in the mediation of the responses tested in anaesthetised cats in the present study.     

Inferior cardiac nerve activity in the cat during occlusion of the mesenteric artery.

A number of studies in this and other laboratories using hemodynamic and pharmacologic evidence have suggested that occlusion of the mesenteric artery evokes a pressor reflex initiated by mesenteric baroreceptors. To provide additional evidence in support of this hypothesis, neurophysiological recordings were made of inferior cardiac nerve activity during mesenteric artery occlusion (MAO). The results indicate that MAO enhances inferior cardiac nerve activity in the cat, providing that the carotid sinus nerves have been cut. Cutting of the mesenteric nerves further facilitates cardiac nerve activity and abolishes the response to mesenteric artery occlusion. The evidence suggests that MAO evokes a reflex sympathetic discharge which is subject to override by the carotid sinus depressor reflex. The afferent limb of the reflex is characterized by a tonic depressor outflow from the mesenteric pressure receptors.     

Baroreflex “resetting” by arterial hypoxia in the renal and cardiac sympathetic nerves of the rabbit

1. Renal and cardiac sympathetic baroreflex functions were studied in sodium pentobarbitone anaesthetized rabbits given succinylcholine, during constant artificial ventilation with air and with hypoxic gas mixtures. Mean arterial pressure (MAP) was raised and lowered between values of 40 and 140 mm Hg by means of aortic and vena caval periovascular balloons and integrated sympathetic nerve activity (SNA) was recordered. 2. The relationship between MAP and SNA was sigmoid, with upper and lower plateau levels. The curves were defined by calculating median blood pressure, SNA Range and reflex gain. In both renal and cardiac sympathetics section of the carotid sinus and aortic nerves completely abolished the MAP-related changes in SNA. 3. The renal baroreflex curves were reset from control levels during hypoxia. Median blood pressure increased, as did SNA Range and gain. These effects were due to central interactions between arterial baroreceptor, arterial chemoreceptor and vagal afferent activity. 4. The cardiac sympathetic baroreflex curves were shifted in the opposite direction from control with reduction in median blood pressure, SNA Range and reflex gain. These changes were due to chemoreceptor-arterial baroreceptor interactions. 5. Arterial hypoxia thus evokes a differentiated pattern of baroreflex resetting in the renal and cardiac sympathetic montoneuron pools with differing changes in neural response range and sensitivity to arterial pressure changes.     

Intravascular mechanoreceptor modulation of renal sympathetic nerve activity in the cat

Experiments were performed in chloralose-anesthetized cats to characterize intravascular mechanoreceptro input to renal nerve activity in the intact and vagotomized sinoaortic-denervated states. High-pressure intravascular mechanoreceptors were stimulated by rises in arterial pressure caused by norepinephrine. Low-pressure intravascular mechanoreceptors were stimulated by progressive blood volume expansion (14-23%) at a rate of 4.4 or 17.6 ml/min. In addition, veratrine was used to stimulate directly both high- and low-pressure receptors. In the intact animal the administration of norepinephrine or blood volume expansion was associated with substantial decreases in renal nerve activity. Veratrine also caused a large dose-related decrease in renal nerve activity. However, in the vagotomized sinoaortic-denervated animal there was no change in renal nerve activity with norepinephrine, volume expansion, or veratrine administration. These experiments demonstrate that the major afferent pathways for renal sympathetic circulatory reflexes are confined to the carotid sinus and aortic and vagus nerves. No evidence was found for a significant contribution from sympathetic afferent nerves.     

Tachypnea after stimulation of afferent cardiac sympathetic nerve fibers.

The role of afferent cardiac sympathetic nerve fibers in the regulation of respiration has been examined. Application of potassium chloride or lactic acid solutions to the left ventricular surface of anesthetized vagotomized dogs resulted in a decrease in the manimum firing rate and shortening in period duration of firing of phrenic nerves. Also, application of the agents caused a decrease in amplitude and an increase in rate of respiratory thoracic movements. The same changes in phrenic nerve activity and respiratory movements were produced by coronary artery occlusion and centrifugal electrical stimulation of the left inferior cardiac nerves. The results indicate tachypnea that can be produced by excitation of afferent cardiac sympathetic nerve fibers.     

Differential pattern of sympathetic outflow during upper airway stimulation with smoke

This study investigates directly the possibility that sympathetic discharge to the heart is decreased while it is increased to other organs during upper respiratory perfusion with cigarette smoke. Blood pressure (BP), heart rate, ECG, and respiratory movements were monitored in urethane-anesthetized rabbits. Insertion of two cannulas allowed respiration of room air while passing smoke across the upper respiratory irritant receptors and out through the nares. Through a retroplural incision, the left stellate ganglion was exposed and a cardiac branch isolated. Similarly, a left renal nerve was isolated. Multiunit nerve recordings were obtained from both nerves. In four control animals, cigarette smoke (50 ml) caused apnea, bradycardia (-116 beats/min) and increased BP (33 mmHg). Activity in the renal nerve increased (248% of control [C]) and activity in the cardiac nerve was reduced (62% C). In these animals after Flaxedil and artificial respiration, nerve activity responses were still pronounced (renal, 178% C; cardiac, 66% C). In four other barodenervated animals neural responses to smoke were similar to those observed with baroreceptors intact (renal, 211% C; cardiac, 51% C). In these animals after artificial ventilation and Flaxedil, responses were not significantly changed. These results indicate that smoke stimulation causes a differential pattern of sympathetic discharge. The responses observed cannot be accounted for by secondary adjustments through arterial baroreceptors, chemoreceptors, or pulmonary stretch receptors.     

Enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with heart failure induced by adriamycin

Our previous studies have shown that the cardiac sympathetic afferent reflex is enhanced in rats with chronic heart failure(CHF) induced by coronary artery ligation and contributes to the over-excitation of sympathetic activity.We sought to determine whether sympathetic activity and cardiac sympathetic afferent reflex were enhanced in adriamycin-induced CHF and whether angiotensin II(Ang II) in the paraventricular nucleus(PVN) was involved in enhancing sympathetic activity and cardiac sympathetic afferent reflex.Heart failure was induced by intraperitoneal injection of adriamycin for six times during 2 weeks(15 mg/kg).Six weeks after the first injection,the rats underwent anesthesia with urethane and α-chloralose.After vagotomy and baroreceptor denervation,cardiac sympathetic afferent reflex was evaluated by renal sympathetic nerve activity and mean arterial pressure(MAP) response to epicardial application of capsaicin(1.0 nmol).The response of MAP to ganglionic blockade with hexamethonium in conscious rats was performed to evaluate sympathetic activity.The renal sympathetic nerve activity and cardiac sympathetic afferent reflex were enhanced in adriamycin rats and the maximum depressor response of MAP induced by hexamethonium was significantly greater in adriamycin rats than that in control rats.Bilateral PVN microinjection of angiotensin II(Ang II) caused larger responses of the cardiac sympathetic afferent reflex,baseline renal sympathetic nerve activity and MAP in adriamycin rats than control rats.These results indicated that both sympathetic activity and cardiac sympathetic afferent reflex were enhanced and Ang II in the PVN was involved in the enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with adriamycin-induced heart failure.     

Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.     

Excitation of afferent cardiac sympathetic nerve fibres during myocardial ischaemia

1. Occlusion of the main left coronary artery of lightly anaesthetized cats provoked a pseudaffective reaction. The afferent pathway was in the cardiac sympathetic nerves.2. The compound action potential evoked in the inferior or middle cardiac nerves by stimulation of the thoracic sympathetic trunk contained two elevations, a small Adelta wave and a much larger sC wave. Occasionally a B wave was present.3. During coronary occlusion, the Adelta elevation was reduced by 35-55%, indicating afferent activity in these fibres. Multifibre preparations also showed increased afferent discharge during occlusion.4. It seems probable that the afferent activity in these fibres was mainly responsible for signalling the pseudaffective response elicited by coronary occlusion.5. Myocardial ischaemia produced by coronary occlusion was probably the stimulus for the increased activity.     

Interaction of somatic and cardiopulmonary receptors in control of renal circulation.

The purpose of this study was to determine if there is an important interaction between somatic and cardipulmonary receptors in the control of vasomotor outflow to the kidney. This interaction was examined by determining the renal vasoconstrictor responses to afferent electrical stimulation (30 V, 1 ms, 20--40 Hz) of the sectioned sciatic nerve in 8 chloralose-anesthetized dogs with sinoaortic deafferentation. During isovolemia, sciatic stimulation resulted in significant increases in arterial pressure and heart rate, and in renal vasoconstriction. Volume expansion significantly attenuated and vagotomy significantly augmented the renal vasoconstrictor responses to sciatic stimulation. These interventions did not significantly influence the arterial pressure or heart rate responses to sciatic stimulation. In 4 dogs with aortic nerves sectioned and carotid sinuses isolated and perfused at constant pressure (135 mmHg), the renal vasoconstrictor responses to stimulation were attenuated by volume expansion and augmented by vagotomy. These data show that in the absence of the arterial baroreceptors or with intermediate levels of carotid baroreceptor activation, volume expansion and, thus, augementation of discharge of cardiopulmonary receptors (vagal afferents) markedly attenuated the renal vasoconstrictor responses to somatic afferent stimulation.     

The effect of efferent discharges in renal nerves on the activity of arterial mechanoreceptors in the kidney in rabbit

1. The effect of sympathetic efferent flow in renal nerves on afferent discharges from renal arterial mechanoreceptors was observed in dissected filaments of renal nerves in the rabbit.2. An increase in afferent discharge rate was observed after renal nerve stimulation.3. Perfusate accumulated during renal nerve stimulation in an isolated kidney preparation showed a vasoconstrictor effect on blood vessels in rabbit ear.4. Infusion of a small amount of (+/-)-noradrenaline increased afferent discharge rate.5. Modification of blood pressure levels by chemical means modified renal afferent discharge rate.6. It is suggested that there is an efferent control mechanism on the activity of renal arterial mechanoreceptors by a vasomotor reflex.