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The relationship between directly recorded renal sympathetic nerve activity (RSNA) and simultaneous renal norepinephrine (NE) spillover rate across the kidney at rest and in response to changes in mean arterial pressure (MAP) was examined in six conscious rabbits. Integrated RSNA and renal NE spillover rate at rest were 5.1 +/- 1.1 microV/s and 20.8 +/- 3.0 ng/min, respectively. Sodium nitroprusside infusions at 10 and 20 microgram.kg-1.min-1 significantly increased RSNA by 42 +/- 14 and 84 +/- 14% and renal NE spillover rate 39 +/- 22 and 107 +/- 22% in response to falls in MAP of 15 +/- 2 and 21 +/- 2 mmHg (19 and 27%), respectively. During phenylephrine infusion at 8 micrograms.kg-1.min-1, RSNA and renal NE spillover rate significantly decreased by 65 +/- 14 and 67 +/- 16%, respectively, in response to a 15 +/- 2 mmHg (19%) rise in MAP. There was a highly significant positive correlation between changes in directly recorded RSNA and changes in renal NE spillover rate (r = 0.81, P less than 0.01). The ratio of renal to total NE spillover rate at rest was 0.44 +/- 0.06. This ratio was decreased during both sympathetic stimulation (0.30 +/- 0.04) and inhibition (0.26 +/- 0.06). This study indicates that the measurement of renal NE spillover rate is a useful reliable method for detecting the changes in RSNA and its relative contribution to overall sympathetic nerve activity in response to physiological stimuli in conscious rabbits.

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The effects of the tricyclic antidepressant, desipramine, on the baroreflex regulation of renal sympathetic nerve activity (SNA) and heart rate (HR), the nasopharyngeal reflex, plasma epinephrine and blood pressure (BP) were studied in conscious rabbits. Renal SNA and HR were recorded during slow ramp changes in mean arterial pressure (MAP) and during inhalation of cigarette smoke. Intracisternal (i.c.) and intravenous (i.v.) drug administration were compared, using doses which produced similar total central nervous system (CNS) concentrations. After a brief sympathoexcitation, i.c. desipramine inhibited renal SNA and MAP and increased plasma adrenaline and HR. The renal sympathetic baroreflex was substantially attenuated, with reflex range and gain reduced by 46 and 31%, respectively, but the cardiac baroreflex and nasopharyngeal reflex were affected minimally. Sixty-four percent of the desipramine remaining in the brain was concentrated in the medulla oblongata and spinalis; levels in cortex, thalamus, midbrain, lower spinal cord, and peripheral tissues were minimal. Treatment with i.v. desipramine decreased renal SNA and increased HR without altering MAP or epinephrine release. There was a slight attenuation of the nasopharyngeal reflex, a slight baroreceptor-independent reduction in renal SNA at most MAP levels, and an augmentation of the cardiac baroreflex. The drug was uniformly distributed throughout the CNS; only 20% of the centrally accumulated dose was in the medulla. Thus, i.c. desipramine produces a differentiated pattern of sympathoadrenal effects, probably by increasing norepinephrine (NE) concentrations at several sites within the medulla. The effects of i.v. desipramine were different, owing to poorer access to the medulla and the consequences of peripheral neuronal uptake blockade, which may include a modest inhibition at the sympathetic ganglia and an excitation at cardiac and vasoconstrictor neuroeffector junctions.

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Peripheral- and central nervous system (CNS)-mediated effects of desipramine (Des) on sympathetic nerves and the contribution of alpha 2-adrenoceptors to these effects were studied in conscious rabbits. Blood pressure, renal sympathetic nerve activity (SNA), and norepinephrine (NE) reuptake and spillover into plasma were measured before and after intracisternal (ic) or intravenous (i.v.) administration of Des. In other animals, NE spillover responses to i.v. Des were examined before and after alpha 2-adrenoceptor blockade with i.v. idazoxan. Treatment with i.v. Des blocked neuronal reuptake and decreased renal SNA but did not alter blood pressure or NE spillover. Decreased NE release by sympathetic nerves after i.v. Des was reflected by a decrease in the combined rate of NE reuptake and spillover. Treatment with ic Des (at 1.7% of the i.v. dose) decreased blood pressure and renal SNA and produced equivalent falls in NE reuptake and spillover, indicating little peripheral effect of centrally administered Des on the efficiency of neuronal reuptake. Thus Des had two distinct actions: the drug blocked neuronal reuptake by direct actions on nerve endings and reduced SNA by actions within the CNS. After ic Des, decreased SNA produced parallel falls in NE reuptake, spillover, and blood pressure. After i.v. Des, blockade of neurotransmitter reuptake increased NE concentrations at sympathoeffector junctions offsetting the fall in SNA, so that there was little change in NE spillover or blood pressure. However, after alpha 2-adrenoceptor blockade with i.v. idazoxan, NE spillover increased in response to i.v. Des. Thus the Des-induced decrease in NE release was partly mediated by an action of raised intrasynaptic NE concentrations on inhibitory alpha 2-adrenoceptors.

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In isolated organs, or when given in low dose intra-arterially, tricyclic antidepressant drugs are known to block reuptake of norepinephrine into sympathetic nerve varicosities, with a resultant increased norepinephrine washout. On the other hand, systemic administration of such drugs in humans reduces norepinephrine spillover to plasma. To clarify these seemingly contradictory findings, we have measured concurrently muscle sympathetic activity in the peroneal nerve (microneurography) and rates of norepinephrine spillover to plasma for the body as a whole and for the heart, the kidneys, and the forearm (radiotracer technique), both before and after intravenous infusion of desipramine, 0.5 mg/kg. Desipramine lowered the overflow of norepinephrine to plasma for the body as a whole and from the forearm and the kidneys (by 30-50%) but increased cardiac norepinephrine spillover by 25%. Both the number of sympathetic bursts per min in the peroneal nerve and their mean voltage amplitudes were markedly reduced after desipramine; total activity (bursts/min x mean burst amplitude) fell by approximately 90%. The effects of desipramine on norepinephrine spillover are explicable in terms of inhibition of central sympathetic outflow, balanced against the local blockade of transmitter reuptake. In most sites, the predominant effect is a reduction of norepinephrine overflow. For the heart, where reuptake is so important in transmitter disposition, the net effect is increased overflow.

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The role of the brain renin-angiotensin system (RAS) in the baroreflex regulation of renal sympathetic nerve activity (RSNA) and heart rate (HR) was studied in conscious rabbits. RSNA and HR were recorded during slow ramp changes in mean arterial pressure (MAP) before and after intraventricular infusion of 1) angiotensin II (ANG II), 2) ANG II receptor antagonist, [Sar1,Ile8]ANG II, or 3) converting enzyme inhibitor (CEI, enalaprilat). Central ANG II increased resting MAP and RSNA by 10.6 +/- 0.9 mmHg and 21 +/- 7%, respectively, but did not alter HR. There was a marked increase of 107 +/- 15% in the maximum RSNA evoked by slowly lowering MAP. In contrast, maximum reflex tachycardia was only modestly elevated, and baroreflex inhibition of RSNA and HR during MAP rises was unaffected. Central [Sar1,Ile8]ANG II had no effect on RSNA or HR, either at rest or during baroreflex responses, while CEI slightly enhanced maximal reflex responses. Thus exogenous ANG II causes a powerful excitation of renal sympathetic motoneurons, the magnitude of which is revealed when tonic baroreceptor inhibition is removed during transient pressure falls. However, in quietly resting conscious rabbits, we found no evidence for a tonic influence of endogenous ANG II on these neurons, and the physiological stimuli required for their activation by the brain RAS remain to be found.

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1. The stability of the renal sympathetic baroreflex and nasopharyngeal reflex, and the role of cardiac sensory receptors, was studied in conscious rabbits over a 5 h experimental period. 2. Renal sympathetic nerve activity (SNA) was recorded during (i) slow ramp changes in mean arterial pressure (MAP) of 1-2 mmHg/s induced by inflating perivascular balloon cuffs, and (ii) the inhalation of cigarette smoke. Experiments were repeated in other rabbits after blocking cardiac afferents with 5% intrapericardial procaine. 3. Baroreflex responses to the first two caval cuff inflations of the day were significantly greater than subsequent responses. After this, triplicate sets of reflex curves were relatively stable during a 2 h period in the morning. When the experiment was repeated in the afternoon, there was a significant attenuation of baroreflex range and a small fall in resting renal SNA which were abolished by pericardial procaine. 4. Changes in baroreflex properties were minimal when the reflex was assessed only twice, at the beginning and end of a 5 h period. No change was seen in the nasopharyngeal reflex whether the rabbits had been subjected to few or to many cuff inflations. 5. We conclude that time dependent changes can occur in the renal sympathetic baroreflex of conscious rabbits which must be allowed for by appropriate protocol design. These include increasing inhibitory influences from cardiac sensory receptors in experimental situations requiring multiple reflex estimations.

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We have studied the effect of acute hypertensive episodes on the renal sympathetic baroreceptor reflex in conscious rabbits and the role played by cardiac afferents and endogenous opiate mechanisms. Renal sympathetic nerve activity was recorded during brief perivascular balloon-induced ramp changes in mean arterial pressure before and during 40-minute elevations in resting pressure. Methoxamine infusion was adjusted to increase pressure by +30 and +45 mm Hg in the presence of autonomic blockade of the heart with atenolol and methscopolamine. Experiments were repeated in other rabbits after blocking cardiac afferents with 5% intrapericardial procaine or during intravenous naloxone (4-6 mg/kg, then 0.12 mg/kg/min). We found a progressively severe attenuation of the renal sympathetic baroreceptor reflex during increasing elevations in resting pressure. The upper plateau and range of the reflex curve were both reduced by one third and two thirds during moderate and severe hypertension, respectively. The average gain fell by 64% and 87%, and the range-independent gain and hypotensive reversal response were also reduced. There was no resetting of the reflex to higher pressures as would be expected. One third of the reflex inhibition was prevented by blocking cardiac afferents; none of it was affected by intravenous naloxone, which had previously been shown to reverse the renal baroreceptor reflex depression elicited by hemorrhagic hypotension. Factors possibly responsible for the remaining two thirds of the hypertension-induced sympathoinhibition are suggested to be either central depression of sympathetic tone after elevation of arterial baroreceptor discharge during the hypertensive episode or additional inhibitory afferent input arising from the pulmonary circulation.

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Sigmoidal mean arterial pressure (MAP)-heart rate (HR) curves were obtained in two genetically related strains of rabbits (groups I and II). We examined vagal (V) and sympathetic (S) effects on HR using perivascular cuffs and vasoactive drugs to alter MAP, and we studied the effects of intravenous naloxone, which affected only I. With the cuff method, both V and S components of gain were much greater in I than in II, and naloxone greatly reduced the difference. With the drug method, gain was similar in I and II and unaffected by naloxone. With both methods, the V component of HR range between plateaus was greater in I than in II because of more pronounced bradycardia at the lower plateau; naloxone eliminated the latter difference when the reflex was drug induced but not when it was cuff induced. The S component of HR range was similar in I and II; with both methods, the tachycardia plateau was reduced by naloxone. The cuff method alters cardiac load more than the drug method, leading to engagement of different groups of afferents for a given change in MAP (delta MAP). We have derived an input-output model, which suggests that with the drug method, gain is almost entirely determined by the input from the arterial baroreceptors, accounting for the minimal difference between I and II. With the cuff method, gain is determined by a nonlinear interaction involving the arterial and nonarterial baroreceptors, which accentuates the response. The opiate mechanism is associated with the nonarterial baroreceptor input and has amplifying properties, which account for the difference in gain between I and II. The two methods and naloxone provide a novel way of differentiating the effector patterns of the reflex; naloxone serves as a marker of activity in a particular pathway.

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1. We investigated the effects of the opiate antagonist naloxone on changes in renal nerve activity and the renal sympathetic baroreflex during haemorrhage and whether they could be mimicked by blocking afferent input from cardiac receptors. 2. Renal nerve activity, arterial pressure and heart rate were recorded in conscious rabbits during blood loss of either 18 or 34-40% of the blood volume. The renal sympathetic baroreflex was elicited by perivascular balloon-induced changes in arterial pressure, before and at the end of haemorrhage. The experiment was repeated during intravenous naloxone infusion (4 mg kg-1, then 0.12 mg kg-1 min-1), and after blocking afferent input from cardiac receptors (5% intra-pericardial procaine). 3. Moderate haemorrhage elicited a rise in renal nerve activity and modest inhibition of the range of the renal sympathetic baroreflex. Severe haemorrhage triggered an abrupt fall in nerve activity and arterial pressure which was accompanied by strong inhibition of the baroreflex range and other curve parameters. There were minimal changes in the baroreceptor-heart rate reflex. 4. Intravenous naloxone and pericardial procaine prevented the falls in renal nerve activity and pressure triggered by severe blood loss but did not affect the increase in activity elicited by moderate haemorrhage. Both drugs produced similar enhancement of the normovolaemic renal sympathetic baroreflex. Naloxone prevented the baroreflex inhibition elicited by both levels of haemorrhage while pericardial procaine prevented most (but not all) of the baroreflex inhibition seen during severe haemorrhage without affecting that found during moderate haemorrhage. 5. We conclude that cardiac receptors (probably ventricular baroreceptors) but not arterial baroreceptors have an opiate synapse on their reflex pathways to the renal nerve. A major part of the action of naloxone during haemorrhage can be explained by blockade of this type of synapse on baroreflex pathways to renal and probably other sympathetic vasoconstrictors. The presence of procaine-resistant but naloxone-sensitive effects during haemorrhage suggests a role for extra-cardiac baroreceptors with opioid central nervous connections.

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Reflex responses of renal postganglionic neurones to stimulation of arterial baroreceptors, arterial and central chemoreceptors and cutaneous nociceptors, and the rhythmicity of their resting activity were studied in paralyzed, artificially ventilated rabbits, anaesthetized with either alfathesin or chloralose-urethane. A 'vasoconstrictor' response pattern was seen in all units. Perivascular balloon-induced falls in blood pressure increased firing while pressure rises silenced 90% of units and reduced firing in the rest. Resting activity was linked to pressure changes within the cardiac cycle and to the artificial respiratory cycle. The largest excitation occurred during hypoxia and injections of CO2 saturated solutions into the carotid artery while hypercapnia and stimulation of cutaneous nociceptors only slightly increased firing. Parameters characterizing rhythmicities and reflex responses were unimodally distributed with no apparent subgrouping of units on quantitative grounds. Unit response patterns were similar to those recorded in the whole renal nerve. With one exception, no silent units were found which responded to the afferent inputs studied. Nor was there a small-spike fibre group which was excited by angiotensin. However, reflex responses were significantly influenced by the anaesthetic regime selected for use. Under alfathesin, baroreceptor and chemoreceptor reflexes were double those found with chloralose-urethane. Under chloralose-urethane, hypoxia increased both rhythmicities, while under alfathesin, cardiac rhythmicity was decreased and respiratory rhythmicity was variably affected. We concluded that renal sympathetic neurones are a functionally uniform population which behave like vasoconstrictors.

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In both anaesthetized and conscious rabbits, perivascular balloon inflations slowly raised or lowered mean arterial pressure (M.A.P.), at 1-2 mmHg/s, from resting to various plateau pressures. Deflations then returned the M.A.P. to resting. 'Steady-state' curves relating M.A.P. to unitary aortic baroreceptor firing, integrated aortic nerve activity and heart rate were derived during the primary and return pressure changes and they formed typical hysteresis loops. In single units, return M.A.P.-frequency curves were shifted in the same direction as the primary pressure changes by an average 0.37 mmHg per mmHg change in M.A.P. Shifts were linearly related to the changes in M.A.P. between resting and plateau levels for all pressure rises and for falls less than 30 mmHg. They were established within 30 s and were quantitatively similar to the rapid resetting of baroreceptor function curves found 15 min-2 h after a change in resting M.A.P. (Dorward, Andresen, Burke, Oliver & Korner, 1982). Unit threshold pressures were shifted within 20 s to the same extent as the over-all curve shift to which they contributed. In the whole aortic nerve, return M.A.P.-integrated activity curves were shifted to same degree as unit function curves in both anaesthetized and conscious rabbits. Simultaneous shifts of return reflex M.A.P.-heart rate curves were also seen in conscious rabbits within 30 s. During M.A.P. falls, receptor and reflex hysteresis was similar, but during M.A.P. rises, reflex shifts were double baroreceptor shifts, suggesting the involvement of other pressure-sensitive receptors. We conclude that hysteresis shifts in baroreceptor function curves, which follow the reversal of slow ramp changes in blood pressure are a form of rapid resetting. They are accompanied by rapid resetting of reflex heart rate responses. We regard this as an important mechanism in blood pressure control which produces relatively high-gain reflex responses, during slow directional pressure changes, over a wider range of absolute pressure levels than would otherwise be possible.

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Curves relating renal sympathetic nerve activity and mean arterial pressure were derived in conscious rabbits during ramp changes in mean arterial pressure, elicited by perivascular balloon inflation. The renal sympathetic nerve activity-mean arterial pressure relationship consisted of a high-gain sigmoidal region about resting, where renal sympathetic nerve activity rose or fell in response to moderate falls and rises of mean arterial pressure. With larger pressure rises, renal sympathetic nerve activity first fell to a lower plateau and then reversed at even higher mean arterial pressure. When mean arterial pressure was lowered below resting, renal sympathetic nerve activity rose to an upper plateau and then reversed abruptly toward resting at low mean arterial pressure. Both arterial and cardiac baroreceptors exerted substantial inhibitory influences on renal sympathetic nerve activity at all pressure levels. These effects appeared additive over the central high gain region of the curve, but beyond this region there were non-additive interactions. The latter were affected considerably by alfathesin anesthesia. In other experiments, we studied the effects of sustained alterations in resting mean arterial pressure induced by infusing nitroprusside and phenylephrine, which produced rapid resetting of the renal baroreflex. The latter could be accounted for, in part, by resetting of the threshold of the arterial baroreceptors and in part by contributions from other afferents, probably the cardiac receptors. During resetting associated with nitroprusside-induced falls in resting blood pressure, high-gain reflex adjustments in renal sympathetic nerve activity to moderate changes in mean arterial pressure were preserved, but during resetting associated with phenylephrine-induced rises in resting mean mean arterial pressure, the resting renal sympathetic nerve activity lay on the lower curve plateau, resulting in reduction in the apparent gain of the reflex renal sympathetic nerve activity response to moderate changes in mean arterial pressure.

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Local anaesthetic drugs were instilled into the pericardial sac of conscious rabbits through a chronically implanted catheter. Twenty mg of procaine HCl always caused complete blockade of cardiac vagal and sympathetic efferent nerves, tested by eliciting the baroreceptor-heart rate reflex, and abolished the reflex depression of renal sympathetic nerve activity elicited by impeding left ventricular outflow. It also slowed heart rate by a direct effect on the sinoatrial pacemaker. When the same dose of procaine was given intravenously there were only transient changes in blood pressure, heart rate and the baroreceptor-heart rate reflex. Lignocaine HCl and bupivacaine HCl were relatively less effective in blocking cardiac sympathetic efferent nerves. Intrapericardial procaine can be used in conscious animals to elucidate the part played by the cardiac receptor reflexes in control of the circulation.

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In conscious rabbits with indwelling intracisternal (i.c.) catheters i.c. injection of noradrenaline (range 20 - 2000 ng) elicited dose-related cutaneous vasoconstriction of the ear skin vessels and reduction in renal sympathetic vasoconstrictor activity (integrated mass discharge). In addition there was shivering and a rise in the animals "core" temperature, so that the injections of noradrenaline mimicked the normal thermoregulatory pattern of cooling. In 5 other rabbits with implanted hypothalamic thermodes we studied the responses of the ear temperature, renal sympathetic nerve activity and respiration rate to hypothalamic heating and cooling. The animals were studied: (i) under control conditions; (ii) after i.c. administration of noradrenaline: (iii) 24 h after 6-hydroxydopamine (6-OHDA) when there is marked depletion of CNS noradrenergic transmitter stores. After the drugs the temperature-response curves were displaced from control in approximately parallel fashion with little change in gain. Noradrenaline elicited shifts that were directionally opposite to those produced by 6-OHDA, suggesting that the changes in thermoregulatory properties were specific effects of the transmitter. Previous studies also suggest that the site of modulation of the thermoregulatory response is at bulbospinal levels, at least as far as the renal sympathetic response was concerned.

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1. The effects of changing intravascular pressures on integrated ear sympathetic nerve activity (ESNA) were studied in anesthetized artificially ventilated rabbits by inflating aortic and inferior vena caval perivascular balloons under conditions of normal arterial Po2 and during arterial hypoxia. 2. At normal Po2 ESNA was unaffected by arterial and cardiopulmonary baroreflex influences. The small inhibition of ESNA observed during rises in arterial pressure after vagotomy was also present after section of the carotid sinus and aortic nerves, and after cutting both vagi as well. 3. During hypoxia there was marked inhibition of ESNA, which was minimally influenced by vagotomy but abolished by section of the carotid sinus and aortic nerves, suggesting that it was chemoreceptor-mediated. There was a pressure-related rise in ESNA which was abolished by vagotomy and considered to be due to a central nervous chemoreceptor-cardiopulmonary baroreflex interaction.

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Sigmoid renal baroreflex curves relating mean arterial pressure to integrated renal sympathetic nerve activity were obtained in anaesthetized rabbits with previously implanted balloons to raise and lower blood pressure. Propranolol was infused to reach plasma levels averaging 324 ng/ml. This reduced blood pressure by 9.6 +/- 1.1 mm Hg, but had no effect on resting sympathetic discharge. Propranolol lowered the threshold of the renal baroreflex. Median blood pressure was reduced by 15.4 +/- 1.9 mmHg but there was no change in gain or sympathetic activity range. Thus, at a given blood pressure there was diminution of sympathetic discharge compared with control. Similar changes occurred after giving clonidine. However, "non-specific" produced by bleeding or nitroprusside infusion produced no resetting of the baroreflex curves, though the resting sympathetic discharge increased. The effects of propranolol (plasma levels 137 and 348 ng/ml) on arterial baroreceptor discharge were studied by deriving mean arterial pressure-integrated aortic nerve activity curves. Propranolol produced a reduction of aortic nerve discharge of about 7% of control. Single unit analysis showed a small reduction in firing frequency/sec near threshold, which was sufficient to explain the changes in integrated aortic nerve discharge. Since the changes in input from the aortic baroreceptors do not account for the reduction in threshold of the renal baroreflex, we conclude that the latter is due to the central nervous action of propranolol.

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1. Responses of receptors with fibres in the interosseous nerve of the duck's leg have been studied by recording unit discharges in filaments dissected from the sciatic nerve.2. Seventy-two of the ninety-four units examined served highly phasic, vibration-sensitive mechanoreceptors in the interosseous region interpreted as being Herbst corpuscles. Receptor types for most of the other units could not be determined, but some were slowly adapting mechanoreceptors.3. Rheobase threshold values for the most sensitive vibration-receptors were similar to those of mammalian Pacinian corpuscles.4. Threshold-frequency relationships for the vibration receptors showed a wider range of low frequency cut-off values, and a greater capacity to signal high frequencies, than is the case with Pacinian corpuscles.5. Fibres of the vibration-receptors had calculated diameters ranging from 5 to 10 mum and account for the bulk of the larger fibres in the interosseous nerve.6. It is suggested that Herbst corpuscles in the legs of birds might act as a warning device by detecting vibratory disturbances of the ground or other supporting surface.

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1. Response patterns of 116 muscle stretch receptor units isolated from the sciatic nerve of the duck have been studied, and the units classified as muscle spindles and tendon organs.2. Units classified as spindles had low threshold tensions for maintained discharge. From conduction-velocity measurements, the calculated fibrediameter spectrum appears to be unimodal, ranging from 5 to 11-12 mum.3. Spindle units showed essentially ;in parallel' behaviour, though increase in initial tension often led to the appearance of ;in series' responses. Although apparent ;alpha-excitation' during maximal tetanic contractions was a common occurrence, no direct evidence of alpha-innervation of spindles was obtained.4. Evidence has been obtained for motor innervation of spindles by fibres distinct from those constituting the alpha supply to extrafusal muscle fibres. Afferent response attributable to this fusimotor innervation is influenced by initial tension and stimulus-frequency. Electrical thresholds for fusimotor responses ranged from 1.1 to 4.03 times alpha maximum.5. Tendon organ units consistently showed ;in series' response patterns during muscle contractions. They were not influenced by stimulation of the high-threshold efferent nerve supply to the muscles.6. Threshold tensions required for maintained discharge in tendon organ units from m. gastrocnemius pars lateralis were characteristically high; however, many units from m. flexor perforans et perforatus d. 3 had unexpectedly low mechanical thresholds. The calculated fibre-diameter spectrum for tendon organ units is unimodal, ranging from 4-7 to 10-11 mum. As in mammals, they contribute to the coarse-fibre component in the muscle nerve and include the fastest fibres present.

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