Carotid baroreceptor reflexes in humans during orthostatic stress

Orthostatic stress, including standing, head-up tilting and lower body suction, results in increases in peripheral vascular resistance but little or no change in mean arterial pressure. This study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was enhanced during conditions of decreased venous return. We studied eight healthy subjects and determined responses of pulse interval (ECG) and forearm vascular resistance (mean finger blood pressure divided by Doppler estimate of brachial artery blood velocity) to graded increases and decreases in carotid transmural pressure, effected by a neck suction/pressure device. Responses were determined with and without the application of lower body negative pressure (LBNP) at -40 mmHg. Stimulus-response curves were determined as the responses to graded neck pressure changes and the differential of this provided estimates of reflex sensitivity. Changes in carotid transmural pressure caused graded changes in R-R interval and vascular resistance. The cardiac responses were unaffected by LBNP. Vascular resistance responses, however, were significantly enhanced during LBNP and the peak gain of the reflex was increased from 1.2 +/- 0.3 (mean +/- S.E.M.) to 2.2 +/- 0.3 units (P < 0.05). The increased baroreflex gain may contribute to maintenance of blood pressure during orthostatic stress and limit the pressure decreases during prolonged periods of such stress.     

Characteristics of the carotid baroreflex in man during normal and flow-restricted exercise.

Eight subjects were studied in the supine position at rest, during normal dynamic leg exercise (control exercise) and with blood-flow restriction in the working legs (flow-restricted exercise). Graded muscle blood-flow restriction was accomplished by applying a supra-atmospheric pressure of 50 mmHg to the working legs. During incremental-load exercise, flow restriction reduced exercise performance and peak heart rate by 36% and 13%, respectively. The function of the cardiac branch of the carotid baroreflex was studied over its full operational range, at rest and during constant-load control and flow-restricted exercise, by measuring R-R intervals during application of pulse-synchronous graded pressures (40 to -65 mmHg) in a neck-chamber device. Heart rate and arterial pressure were higher during flow-restricted than control exercise, indicating that the flow restriction activated the muscle chemoreflex. Raising the carotid transmural pressure (systolic arterial pressure minus neck-chamber pressure) was accompanied by increasing R-R intervals in all conditions. The set point (point of baseline carotid transmural pressure and R-R interval) coincided with the midportion of the pressure-response curve at rest and with the threshold point of the curve during exercise. The maximal rate of change in relative R-R intervals and the corresponding carotid transmural pressure range were higher during control exercise than at rest and highest during flow-restricted exercise, indicating that exercise and especially flow-restricted exercise increased carotid baroflex sensitivity, and shifted the carotid baroreflex optimal buffering range to higher pressures. The results suggest that the carotid baroflex attenuates exercise heart rate increases mediated by the muscle chemoreflex and/or by central command.     

Baroreflex modulation of sympathetic activity and sympathetic neurotransmitters in humans

We raised and lowered arterial pressures with stepwise intravenous infusions of phenylephrine and nitroprusside in ten healthy young men and measured changes of R-R intervals, post-ganglionic peroneal nerve muscle sympathetic activity, and antecubital vein plasma noradrenaline and neuropeptide Y concentrations. Respiratory peak-valley R-R interval changes declined with arterial pressure reductions, but did not rise with pressure elevations. Sympathetic activity was modulated by respiration over the entire range of pressures and, at each pressure, was more prominent in expiration than inspiration. Levels of muscle sympathetic nerve activity were low during supine rest, were suppressed almost completely during small increases of pressure, and were increased proportionally during pressure reductions. Over a range of average diastolic pressures from 69 to 89 mmHg, antecubital vein plasma noradrenaline levels were related linearly (r = 0.86, P = 0.0001) to muscle sympathetic nerve activity. Neuropeptide Y levels increased proportionally with muscle sympathetic nerve activity during pressure reductions, but did not decline during pressure elevations. Our results suggest that in man, muscle sympathetic outflow is modulated finely by small changes of baroreceptor input, and that during pharmacologically induced changes of arterial pressure, changes of antecubital vein plasma noradrenaline concentrations provide excellent estimates of changes of sympathetic nerve traffic to skeletal muscle.     

Haemodynamic changes during neck pressure and suction in seated and supine positions

We sought to quantify the contribution of cardiac output ( Q ) and total vascular conductance (TVC) to carotid baroreflex-mediated changes in mean arterial pressure (MAP) in the upright seated and supine positions. Acute changes in carotid sinus transmural pressure were evoked using brief 5 s pulses of neck pressure and neck suction (NP/NS) via a simplified paired neck chamber that was developed to enable beat-to-beat measurements of stroke volume using pulse-doppler ultrasound. Percentage contributions of Q and TVC were achieved by calculating the predicted change in MAP during carotid baroreflex stimulation if only the individual changes in Q or TVC occurred and all other parameters remained at control values. All NP and NS stimuli from +40 to −80 Torr (+5.33 to −10.67 kPa) induced significant changes in Q and TVC in both the upright seated and supine positions (   P < 0.001  ). Cardiopulmonary baroreceptor loading with the supine position appeared to cause a greater reliance on carotid baroreflex-mediated changes in Q. Nevertheless, in both the seated and supine positions the changes in MAP were primarily mediated by alterations in TVC (percentage contribution of TVC at the time-of-peak MAP, seated 95 ± 13, supine 76 ± 17 %). These data indicate that alterations in vasomotor activity are the primary means by which the carotid baroreflex regulates blood pressure during acute changes in carotid sinus transmural pressure.     

The effects of lower body negative pressure on baroreceptor responses in humans

In healthy human subjects the immediate responses of pulse interval and the steady-state responses of arterial blood pressure and cardiac output to changes in carotid sinus transmural pressure were determined before and during the application of a subatmospheric pressure to the lower part of the body. Increases in carotid sinus transmural pressure, effected by applications of subatmospheric pressure to the neck (neck suction) resulted in prolongation of pulse interval and decrease in blood pressure; opposite responses were obtained to application of a positive pressure (neck pressure). Application of lower body negative pressure resulted in a decrease in pulse interval (heart rate increase) but little change in blood pressure. During lower body negative pressure, the responses of pulse interval to neck pressure were reduced but those to neck suction were unaffected; the responses of blood pressure to neck suction were enhanced but those to neck pressure were unaffected. From experiments in which cardiac output was also determined, it was seen that lower body negative pressure reduced cardiac output, increased calculated total body vascular resistance and augmented the resistance response to neck suction although not to neck pressure. These results are compatible with the view that application of lower body negative pressure does not change the sensitivity of the baroreceptor reflex and that the changes in the responses are due to non-linearities of the stimulus-response curves.     

Cardiovascular responses to carotid sinus baroreceptor stimulation during moderate to severe exercise in man

Our objective was to assess the importance of arterial baroreflexes in maintaining vasoconstriction in active muscle during moderate to severe exercise. Eight subjects exercised for 8-15 min on a cycle ergometer at three levels (averages 94, 194, 261 W) requiring 40-88% of VO2 max. Four times during each exercise level pulsatile negative pressure (-50 mmHg) was applied over the carotid sinuses for 30 s; suction was applied at each ECG R-wave for 250-400 ms. Before and during each neck suction, femoral venous blood flow (FVBF) was measured by constant infusion thermal dilution. At 94 W neck suction significantly reduced blood pressure (BP) (15 mmHg) and heart rate (HR) (7 beats min-1), and raised leg vascular conductance (LVC) (11.4%) without changing FVBF. At 194 W, neck suction reduced BP (9 mmHg), HR (4 beats min-1) and FVBF (5.1%, 240 ml min-1), and raised LVC (5.2%). At 261 W, LVC was unchanged by neck suction, but BP and FVBF both fell (9 mmHg and 650 ml min-1 or 7.4%). We conclude that competing local vasodilation and sympathetic vasoconstriction control muscle blood flow during moderate exercise, and vasoconstrictor tone can be withdrawn by baroreceptor stimulation. High levels of vasoconstrictor outflow to muscle in severe exercise may not originate from baroreflexes.     

Characteristics of the carotid baroreflex in man during normal and flow-restricted exercise

EIKEN, O., CONVERTINO, V. A., DOERR, D. F., DUDLEY, G. A., MORARIU, G. & Mekjavic; I. B. 1992. Characteristics of the carotid baroreflex in man during normal and flow-restricted exercise. Acta Physiol Scand 144 , 325–331. Received 27 May 1 991 , accepted 29 October 1991. ISSN 0001–6772. School of Kinesiology, Simon Fraser University, Burnaby, B.C., Canada. Eight subjects were studied in the supine position at rest, during normal dynamic leg exercise (control exercise) and with blood-flow restriction in the working legs (flow-restricted exercise). Graded muscle blood-flow restriction was accomplished by applying a supra-atmospheric pressure of 50 mmHg to the working legs. During incremental-load exercise, flow restriction reduced exercise performance and peak heart rate by 36% and 13%, respectively. The function of the cardiac branch of the carotid baroreflex was studied over its full operational range, at rest and during constant-load control and flow-restricted exercise, by measuring R-R intervals during application of pulse-synchronous graded pressures (40 to -65 mmHg) in a neck-chamber device. Heart rate and arterial pressure were higher during flow-restricted than control exercise, indicating that the flow restriction activated the muscle chemoreflex. Raising the carotid transmural pressure (systolic arterial pressure minus neck-chamber pressure) was accompanied by increasing R-R intervals in all conditions. The set point (point of baseline carotid transmural pressure and R-R interval) coincided with the midportion of the pressure-response curve at rest and with the threshold point of the curve during exercise. The maximal rate of change in relative R-R intervals and the corresponding carotid transmural pressure range were higher during control exercise than at rest and highest during flow-restricted exercise, indicating that exercise and especially flow-restricted exercise increased carotid baroflex sensitivity, and shifted the carotid baroreflex optimal buffering range to higher pressures. The results suggest that the carotid baroflex attenuates exercise heart rate increases mediated by the muscle chemoreflex and/or by central command.     

Responses of abdominal vascular capacitance in the anaesthetized dog to changes in carotid sinus pressure.

1. The abdominal circulation of anaesthetized dogs was vascularly isolated without opening the abdomen, by cutting or tying all structures immediately above the diaphragm and tying the proximal ends of the hind limbs. The region was perfused at constant flow through the aorta and drained at constant pressure from the inferior vena cava. 2. Vascular resistance responses were expressed as the changes in perfusion pressure and capacitance responses were determined by integrating changes in vena caval outflow. 3. Decreasing the pressure in the isolated carotid sinuses over the whole baroreceptor sensitivity range increased mean perfusion pressure from 91 to 149 mmHg (a 67% increase in resistance) and decreased mean capacitance by 111 ml. (5 ml. kg-1). 4. The range of carotid sinus pressures over which capacitance responses occurred was at a significantly higher level than the corresponding range for resistance responses. 5. Comparison of the reflex responses with the responses to direct stimulation of efferent sympathetic nerves shows that quantitatively similar responses of resistance and capacitance to those induced by a large step decrease in carotid pressure could be produced by stimulating maximally the efferent sympathetic nerves at 5 Hz. These results also suggest that at all levels of carotid sinus pressure there is no difference in the impulse traffic to resistance and capacitance vessels.     

Influence of carotid baroreceptors on different components of the vascular system

1. Reflex changes in wall tension of the lateral saphenous vein of one hind limb, the splenic veins and capsule, and the resistance vessels of the other hind limb caused by changes in baroreceptor activity were measured in vagotomized dogs under thiopentone-chloralose anaesthesia.2. Three different methods were used to alter pressure in one or both carotid sinuses. (1) Both carotid sinuses were vascularly isolated and filled with fully oxygenated Krebs-Ringer bicarbonate solution (pH 7.4) from a reservoir in which the pressure could be altered at will. (2) One sinus was denervated, and the contralateral sinus was perfused with arterial blood at different flow rates. (3) One sinus was denervated, and the innervated sinus was perfused with arterial blood at constant flow, the pressure being altered by changing the outflow resistance.3. The left saphenous vein was perfused at constant flow with autologous blood; changes in perfusion pressure were used as a measure of changes in veno-motor activity. The right common iliac artery was perfused at constant flow to measure changes in resistance vessel activity. Blood flow through the spleen was temporarily arrested, trapping a fixed volume of blood in the organ. Under these conditions, changes in splenic vein pressure were a measure of changes in smooth-muscle tension in the splenic capsule and veins.4. In order to assess the responses to baroreceptor stimulation in terms of alterations in sympathetic nerve traffic to different components of the peripheral vascular system, ;frequency-response curves' were constructed for spleen, saphenous vein, and limb resistance vessels by electrical stimulation of the splenic nerves and lumbar sympathetic chains.5. The saphenous vein showed no consistent response to changes in baroreceptor activity. Reduction in carotid sinus pressure from 180 to 100 mm Hg caused an increase in venous pressure in the isovolumetric spleen and in the iliac artery perfusion pressure. These results were confirmed by electrical stimulation of the carotid sinus nerve. Whereas the peak responses of the limb resistance vessels corresponded to an increase in lumbar sympathetic nerve traffic of 6-10 c/s, the maximal splenic responses were equivalent to an increase in splenic nerve traffic of 1-4 c/s. These results are consistent with selective autonomic nervous control of different components of the peripheral vascular system.     

PRES: The Controlled Noninvasiv Stimulation of the Carotid Baroreceptors in Humans

To study physiological and psychological effects of baroreceptor activity, the cervical neck cuff technique has been frequently used to stimulate the carotid baroreceptors mechanically. Using this technique, no satisfying control conditions to date have been available. Because the carotid stretch receptors are sensitive not only to the pressure level, but also to the rate of change, it is possible to manipulate the receptor firing through changes in carotid pulse amplitude. The device described here relies on the application of short changes in cuff pressure tied to different phases within the cardiac cycle (phase related external suction (PRES)). A brief external suction during systole has potent stimulatory effects on baroreceptors whereas the application of the very same pressure pulse during diastole inhibits the firing burst associated with the pulse wave. To allow an ongoing period of stimulation, a sequence of alternating negative/positive pressure pulses is applied. In the stimulation condition, the R-wave of the electrocardiogram triggers a negative pulse which is followed by a positive one during diastole. In the control condition this relationship is reversed. Two experiments are reported confirming different baroreceptor effects of the two conditions. PRES allows for blind or double-blind experiments to investigate effects of baroreceptor activity on physiology and behavior.     

Modulation of arterial baroreflex dynamic response during muscle metaboreflex activation in humans

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflexes (as reflected by alterations in the dynamic responses shown by muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) in humans. In nine healthy subjects (eight male, one female) who performed a sustained 1 min handgrip exercise at 50 % maximal voluntary contraction followed by forearm occlusion, a 5 s period of neck pressure (NP) (30 and 50 mmHg) or neck suction (NS)(-30 and -60 mmHg) was used to evaluate carotid baroreflex function at rest (CON) and during post-exercise muscle ischaemia (PEMI). In PEMI (as compared with CON): (a) the augmentations in MSNA and MAP elicited by 50 mmHg NP were both greater; (b) MSNA seemed to be suppressed by NS for a shorter period, (c) the decrease in MAP elicited by NS was smaller, and (d) MAP recovered to its initial level more quickly after NS. However, the HR responses to NS and NP were not different between PEMI and CON. These results suggest that during muscle metaboreflex activation, the dynamic arterial baroreflex response is modulated, as exemplified by the augmentation of the MSNA response to arterial baroreflex unloading (i.e. NP) and the reduction in the suppression of MSNA induced by baroreceptor stimulation (i.e. NS).     

Pressure-induced local venous constrictor responses in human fingers

Particularly in humans, systemic veins are often exposed to extensive changes in transmural pressure at altered body positions, when centrally conveyed constrictor reflexes provide compensation to maintain a proper venous return. The present aim was to explore whether also purely local mechanisms, of e.g. myogenic and/or axon reflex nature and operating at the venular-small vein levels, may contribute to offset venous pooling at local pressure increases. For such purposes the capacitance vascular responses were recorded plethysmographically in human fingertips, as most of the blood content is here contained in venules and small veins. Local increases in transmural pressure, induced by graded venous outflow obstructions, first induced a corresponding passive-venous distension which within a few seconds was followed by a venoconstrictor response that could return the local blood content to nearly control level within 25–35 s. On sudden release of venous obstruction this ‘active’ response was unmasked as a prompt volume ‘undershoot’ that subsided in another 15–30 s. These microvascular responses could be powerful enough almost to offset the venodistension caused by transmural pressures up to 90–100 mmHg, and at brisk pressure increases they could be quite rapid in onset. As general reflex influences seemed to be excluded, these results in humans suggest that also the capacitance microvessels, like the precapillary resistance ones, can display myogenic responses to offset pressure increases. As the venular-small vein compartment contains up to 40% of the total blood volume such local responses, if generalized, may importantly contribute to venous control in humans.     

Evidence that the arterial baroreceptors influence muscle blood flow and not subcutaneous flow in man

Studies in man indicate that skeletal muscle blood flow is modulated via high pressure baroreceptors located in the carotid body. However, whether subcutaneous blood flow is influenced in this way remains controversial. Therefore, the aim of the present study was to determine whether subcutaneous as well as skeletal muscle blood flow was influenced by direct carotid body stimulation; this was done by means of neck suction. Six young healthy males were investigated. Subcutaneous and skeletal muscle blood flow in the forearm was measured by the local 133Xe washout technique. Neck suction of -20 mmHg was applied through a tight helmet covering the head and neck. In the supine position heart rate increased about 10%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged, but skeletal muscle blood flow increased about 70%. Measurements were repeated during neck suction, -20 mmHg, and 45 degrees head-up tilt (which is known to decrease subcutaneous blood flow and skeletal muscle blood flow by increasing sympathetic vasoconstrictor activity). Heart rate increased by about 20%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged and skeletal muscle blood flow increased about 100%. These results indicate that skeletal muscle blood flow is modulated through carotid baroreceptors. Subcutaneous blood flow seems not to be influenced by high pressure baroreceptor modulation, although a vasoconstrictor response to head-up tilt was demonstrated in this as well as other recent studies.     

Does pulsatile and sustained neck pressure or neck suction produce differential cardiovascular and sympathetic responses in humans?

Although square-wave sustained and R wave-triggered pulsatile stimuli have been used to assess carotid baroreflex (CBR) function in humans, it remains unclear whether these different stimulus protocols elicit comparable responses and whether CBR responses adapt during prolonged stimulation. Thus, we measured muscle sympathetic nerve activity (MSNA), heart rate (HR) and mean arterial pressure (MAP) in response to +30 Torr neck pressure (NP) and -30 Torr neck suction (NS) delivered for 20 s either as a sustained or pulsatile stimulus. CBR-mediated changes in MSNA, HR and MAP were similar with sustained and pulsatile stimuli. The time course of MSNA and HR responses identified that significant changes occurred during the initial 5 s and were better maintained over 20 s with NP than with NS. Changes in MAP exhibited a slower onset with the peak increase during NP occurring at 10 s (sustained, 7 +/- 1 mmHg; pulsatile, 7 +/- 1 mmHg; P > 0.05) and the nadir during NS occurring at 20 s (sustained, -7 +/- 1 mmHg; pulsatile, -9 +/- 2 mmHg; P > 0.05). These data demonstrate that sustained and pulsatile NP and NS produce comparable CBR-mediated responses. Furthermore, despite MSNA and HR returning towards baseline during NS, CBR-mediated changes in MAP are well maintained over 20 s of NS and NP.     

Bursting into space: alterations of sympathetic control by space travel

AIM: Astronauts return to Earth with reduced red cell masses and hypovolaemia. Not surprisingly, when they stand, their heart rates may speed inordinately, their blood pressures may fall, and some may experience frank syncope. We studied autonomic function in six male astronauts (average +/- SEM age: 40 +/- 2 years) before, during, and after the 16-day Neurolab space shuttle mission. METHOD: We recorded electrocardiograms, finger photoplethysmographic arterial pressures, respiration, peroneal nerve muscle sympathetic activity, plasma noradrenaline and noradrenaline kinetics, and cardiac output, and we calculated stroke volume and total peripheral resistance. We perturbed autonomic function before and during spaceflight with graded Valsalva manoeuvres and lower body suction, and before and after the mission with passive upright tilt. RESULTS: In-flight baseline sympathetic nerve activity was increased above pre-flight levels (by 10-33%) in three subjects, in whom noradrenaline spillover and clearance also were increased. Valsalva straining provoked greater reductions of arterial pressure, and proportionally greater sympathetic responses in space than on Earth. Lower body suction elicited greater increases of sympathetic nerve activity, plasma noradrenaline, and noradrenaline spillover in space than on Earth. After the Neurolab mission, left ventricular stroke volume was lower and heart rate was higher during tilt, than before spaceflight. No astronaut experienced orthostatic hypotension or pre-syncope during 10 min of post-flight tilting. CONCLUSION: We conclude that baseline sympathetic outflow, however measured, is higher in space than on earth, and that augmented sympathetic nerve responses to Valsalva straining, lower body suction, and post-flight upright tilt represent normal adjustments to greater haemodynamic stresses associated with hypovolaemia.     

Effects of blood-volume distribution on the characteristics of the carotid baroreflex in humans at rest and during exercise

Seven supine subjects were studied at rest and during mild to moderate dynamic leg exercise with and without unloading of the cardiopulmonary baroreceptors accomplished by exposing the lower portion of the body to a subatmospheric pressure of 20 mmHg (Lower Body Negative Pressure, LBNP). The function of the cardiac branch of the carotid baroreflex was studied over its full operational range by measuring R-R intervals during application of pulse synchronous graded pressures (40 to – 65 mmHg) in a neck-chamber device. Raising the carotid transmural pressure (systolic arterial pressure minus neck-chamber pressure) induced increasing R-R intervals in all conditions. In conformity with previous results from our laboratories it was found that the maximal rate of change in relative R-R intervals and the corresponding transmural pressure were higher during exercise than at rest, indicating that exercise increased the carotid baroreflex sensitivity and shifted its optimal buffering range to higher arterial pressures. LBNP did not affect the characteristics of the reflex at rest nor during exercise. It is concluded that reduced central venous pressure with consequent selective cardiopulmonary receptor disengagement exerts no influence on the carotid baroreflex control of heart rate (HR), as tested over the entire arterial pressure-effector response relation, either at rest or during mild-moderate exercise.     

Effect of central venous pressure on arterial baroreflex control of heart rate.

There is considerable evidence that the level of afferent cardiopulmonary receptor activity modulates sinus node responses to arterial baroreflex stimulation in experimental animals. We tested the hypothesis that this reflex interaction occurs also in man by measuring sinus node responses to arterial baroreceptor stimulation with phenylephrine injection or neck suction, before and during changes of central venous pressure provoked by lower body negative pressure or leg and lower trunk elevation. Variations of central venous pressure between 1.1 and 9.0 mmHg did not influence arterial baroreflex mediated bradycardia. Baroreflex sinus node responses were augmented by intravenous propranolol, but the level of responses after propranolol was comparable during the control state, lower body negative pressure, and leg and trunk elevation. Sinus node responses to very brief baroreceptor stimuli applied during the transitions of central venous pressure also were comparable in the three states. We conclude that physiological variations of central venous pressure do not influence sinus node responses to arterial baroreceptor stimulation in man.     

Differential effects of behaviour on sympathetic outflow during sleep and exercise

The responses of renal and lumbar sympathetic outflow to changes in behavioural states were reviewed in this paper. During rapid eye movement (REM) sleep, renal sympathetic nerve activity was decreased while lumbar sympathetic nerve activity increased. These diverse changes in sympathetic nerve activity observed during REM sleep help explain the responses in regional blood flow to REM sleep; that is renal blood flow increased while muscle blood flow decreased. By contrast, exercise increased both renal and muscle sympathetic nerve activity. The degree of physical activity was correlated with the magnitude of the increases in renal and muscle sympathetic nerve activity. There was a significant (P<0.05) linear relationship between renal sympathetic nerve activity and systemic arterial pressure over the transition between non-rapid eye movement (NREM) sleep, quiet awake, moving and grooming states in the rats. This suggests that sympathetic outflows seem to be modulated quantitatively to meet cardiovascular demand caused by changes in the level of physical activity. It is therefore concluded that sympathetic outflow seems to be regulated in a state-specific manner during sleep and exercise.     

Types of nervous activity which may be recorded from the carotid sinus nerve in the sheep foetus

1. In the sinus nerve of mature foetal sheep (120-147 days gestational age) three types of nerve activity have been demonstrated: (a) baroreceptor afferent, in which the nerve activity was synchronous with the pulse pressure wave and which followed pressure changes in the carotid sinus including those caused by compressing the umbilical cord. The discharge of nine out of twelve baroreceptor afferents increased with sympathetic stimulation, (b) a subtype of (a) in which there was irregular activity from pressure receptors which most probably represented baroreceptors discharging at or about threshold, and (c) in the older foetuses (130-147 days), there was activity which was unaffected by changes in carotid sinus pressure, P(a, O2) or NaCN but which increased in discharge rate with compression of the umbilical cord or with stimulation of the cervical sympathetic; this activity then increased with injection of NaCN and was thus identified as chemoreceptor in origin. In addition, a pathway originating in the cervical sympathetic and which passed through the superior cervical ganglion was demonstrated by evoking a compound action potential on stimulation of the preganglionic cervical sympathetic nerve.2. Recordings from pre- or post-ganglionic cervical sympathetic nerves showed that spontaneous activity was present and increased when the umbilical cord was compressed.3. These results suggest that the carotid body chemoreceptors in the foetus are relatively insensitive to chemical changes and that, in their activation at birth, the sympathetic could be involved. Possible neural pathways and the mechanism of activation are discussed.     

Sympathetic nervous response to induced fall and rise of arterial blood pressure in anesthetized rabbits

Summary The baroreceptor reflex is thought to counteract both a rise and a fall in arterial blood pressure, but the evidence for this is incomplete. In 19 anesthetized rabbits, the relationship between blood pressure/aortic nerve activity and efferent sympathetic activity in renal and splanchnic nerves was therefore investigated during induced rise and fall of arterial pressure. Baroreceptor activity increased and sympathetic activity decreased with raised pressure. In contrast, reduction of baroreceptor activity during acute hemorrhagic hypotension had little or no effect on activity in the two sympathetic nerves. Following complete barodenervation, however, sympathetic activity rose on average to 238% of control values. We therefore conclude that the baroreceptor reflex mainly counteracts a rise in arterial blood pressure. Reduction of baroreceptor activity in the first few minutes of acute hemorrhagic hypotension does not lead to increased sympathetic activity. The small activity remaining in baroreceptor nerves at low pressures had a very potent sympathetic inhibitory effect.