Pulse Transit Time as an Indicator of Arterial Blood Pressure

The relationship between pulse-arrival times and diastolic blood pressure was measured in 10 anesthetized dogs. The pulse-arrival time was measured using the R-wave of the electrocardiogram (ECG) as a time reference. Pulse-transit time was also measured between the carotid and femoral pulses. Blood pressure was raised with epinephrine injected intravenously and lowered with vagal stimulation. In all cases, pulse arrival and transit times decreased with an increase in diastolic pressure for diastolic pressures ranging from 15 to 250 mmHg. The correlation between pulse-arrival time and pressure was poorest when the ECG was used as a timing reference. The best correlation was found with true pulse-transit time and diastolic pressure. When pulse-transit time was used to compute pulse-wave velocity, it was found to increase nearly linearly with blood pressure. From 90–100 mmHg, the pulse-wave velocity increased typically by slightly less than six percent.     

The carotid sinus baroreceptor reflex in the pregnant rabbit

1. The reflex responses to baroreceptor stimulation have been compared in eight pregnant and eight non-pregnant anaesthetized female rabbits.2. The vascularly isolated, innervated carotid sinus was exposed for 30 sec to a series of non-pulsatile pressures ranging from 30 to 230 mmHg. The contralateral sinus nerve and both aortic nerves were cut. Systemic arterial pressure and heart rate were measured at each sinus pressure.3. The range of arterial pressure change which could be evoked from the isolated innervated sinus was less in the pregnant than in the non-pregnant rabbits. Mean changes were 98 and 61 mmHg respectively. On the other hand changes in heart rate were similar in the two groups (45 and 43 beats/min respectively).4. The smaller blood pressure response in the pregnant animals resulted from a lesser rise in systemic arterial pressure at low levels of sinus pressure. At high sinus pressures the blood pressure fell to a similar level in both groups of animals.5. Pressure on the great vessels by the gravid uterus was not a factor since there was no consistent difference between the responses obtained with the rabbit lying on its back or on its side.6. Mechanisms which might be responsible for the difference found are discussed.     

The effect of time of electrical stimulation of the carotid sinus on the amount of reduction in arterial pressure

Summary On narcotised dogs, the carotid sinus nerve was stimulated by means on electrical R-wave-triggered pulse trains when depressor nerves were either intact or cut.The stimulation was begun in the range from 0–210 msec after the R-wave. The effectiveness of pulse trains was determined by the level of reduction in mean arterial pressure.In the time range studied, the level of reduction in pressure versus time of stimulation shows two maxima of reduction at 30 and 90 msec and a plateau from 110–150 msec. Stimuli applied later than 150 msec after the R-wave, display a contnuous reduction in effectiveness.The occurrence of the maxima is considered to be due to a coincidence of the pressor afferences from heart, aortic arch and carotid sinus, arriving at the circulatory centres spaced in time with the electrical stimuli.The times at which the maxima of reduction are found to occur could be significant in programming baropacers.     

Interplay among carotid sinus, cardiopulmonary, and carotid body reflexes in dogs.

Interactions among vascular reflexes evoked from carotid sinuses, carotid bodies, and cardiopulmonary region were examined in anesthetized, atropinized, and respired dogs with aortic nerves cut. The carotid sinuses were perfused at 220, 150, and 40-50 mmHg; the chemoreceptors were stimulated by perfusion with hypoxic hypercapnic blood. Cardiopulmonary vasomotor inhibition was interrupted by vagal cold block. Measurements were made of arterial blood pressure and of kidney and hindlimb vascular resistance. At sinus pressures less than 170-160 mmHg, cardiopulmonary vasomotor inhibition increased with increase in blood volume. At high sinus pressure, interruption of this augmented cardiopulmonary inhibition was as ineffective in changing vascular resistance as interruption of the lesser inhibition present during normovolemia. Chemoreceptor stimulation increased the response to vagal block at intermediate but not at high or low sinus pressure. The studies demonstrate the dominant role of the carotid sinus reflex when the three systems interact and the ineffectiveness of chemoreceptor stimulation when carotid or cardiopulmonary inhibition is maximal.     

Comparison of aortic and carotid baroreflexes in the dog

1. Experiments with vascularly isolated, blood-perfused aortic arch and carotid sinus preparations in sixteen dogs have provided evidence which suggests that, in the reflex regulation of normal arterial blood pressure, the aortic and carotid baroreflexes are not equivalent.2. Two different techniques were used. In one, a steel cannula was inserted into the ascending aorta and arch and fixed in position by ligatures about the aorta. The blood-filled space (aortic jacket) thus created could be distended with known pressures; the cardiac output passed through the cannula into the descending aorta. In the other, an extracorporeal circulation utilizing an isolated heart-lung preparation was used to separately perfuse the carotid sinuses, aortic arch, and systemic circulation of a test dog.3. Independent open-loop analysis of the aortic and carotid baroreflexes in each dog indicated that they were essentially similar in their over-all modus operandi but that there were quantitative differences between them which would suggest a predominant role for the carotid sinus reflex in the control of normal blood pressure.4. The carotid sinus Blutdruck-charakteristik curve was symmetrical about the range of normal blood pressure for the dog while the aortic arch curve was displaced to the right.5. The carotid sinus system had the greater gain (with reference to limb vascular resistance) and exhibited a greater maximal capacity to alter vascular resistance reflexly.6. When the carotid and aortic systems were activated simultaneously by distension, the reflex depressor responses were summed, essentially by a process of simple addition. A carotid-induced pressor response obscured a simultaneous aortic-induced depressor response of equal magnitude.7. In five dogs studied, the functional reflexogenic area of the aortic arch did not extend distally beyond the origin of the left subclavian artery.     

The effects of electrical stimulation of the distal end of the cut sinus and aortic nerves on peripheral arterial chemoreceptor activity in the cat

1. In anaesthetized cats, stimulation of efferent components of the carotid sinus or aortic nerves depressed chemoreceptor discharge from the relevant chemoreceptor afferents. The local application of 2% procaine hydrochloride to the sinus nerve trunk, peripheral to the site of the stimulating electrodes and proximal to that of the afferent nerve twig, abolished the depression of afferent chemoreceptor discharge caused by electrical stimulation; on washing the procaine away electrical stimulation once more induced depression of chemoreceptor discharge.2. The depressant effect of efferent stimulation on carotid chemoreceptor activity was still seen during complete carotid glomeral ischaemia. Atropine given by close intra-arterial injection to the carotid body did not affect the depressant influence of efferent sinus nerve stimulation on carotid body chemoreceptor discharge.3. Stimulation of the sinus nerve efferents usually increased carotid body blood flow. Close arterial injection of atropine abolished this effect.4. The responses of glomeral blood flow and carotid chemoreceptor activity to efferent stimulation of the cut sinus nerve were not temporally related. It seems improbable that the depressant effect of such stimulation on chemoreceptor discharge was due to alterations of glomeral blood flow.5. Stimulation of the peripheral end of the cervical vagus in atropinized cats reduced chemoreceptor activity recorded in the ipsilateral aortic nerve.     

Effect of cervical sympathetic nerve stimulation on canine carotid sinus reflex.

In the chloralose-anesthetized dog the carotid sinus on one side of the neck was isolated vascularly. Pressure in the isolated sinus [carotid sinus pressure (CSP)], electrocardiogram, and systemic arterial pressure were recorded. Both vagosympathetic trunks were cut and the contralateral common carotid artery was occluded or the contralateral sinus nerve was cut to reduce reflex buffering of arterial pressure changes. By varying CSP from 50 to 250 mmHg the full range of the reflex response was examined. Electrical stimulation of the peripheral end of the cut ipsilateral cervical sympathetic nerve brought about a rapid decrease in mean arterial pressure (MAP) and heart rate (HR) at lower CSPs, no change in these variables at midrange CSPs, and a gradual increase at higher CSPs, such that the gain of the reflex was reduced (1.89 +/- 0.19 to 1.33 +/- 0.15 mmHg/mmHg). The decrease in MAP and HR at lower CSPs implies an increase in baroreceptor activity whereas the converse would appear to occur at higher CSPs. These responses attained a maximum value at low stimulus frequencies (less than 10 Hz).     

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.     

Rabbit cardiovascular responses to aortic nerve stimulation at fixed carotid pressure.

In pentobarbital-anesthetized rabbits with aortic nerves cut, reflex heart rate and mean arterial pressure (MAP) changes were quantified in response to maximal central stimulation of the left aortic nerve (LANS) before and during steady-state changes in isolated carotid intrasinus pressure (ISP). To distinguish possible vagally mediated cardiopulmonary influences, responses were measured before and after vagotomy. Changes in MAP observed by altering ISP within +/- 15 mmHg of the equilibrium pressure (EP) were linear and inversely correlated to changes in ISP, with a slope of approximately 3 both before and after vagotomy (r greater than or equal to 0.929, P less than 0.05). The peak fall in MAP during LANS was dependent upon ISP. The change in the MAP responses to LANS for each mmHg change in ISP ranged from 1.7 with vagi intact to 1.3 after vagotomy. Heart rate was unaltered by isolation of the carotid sinus and was independent of the small changes in ISP between +/- 15 mmHg of EP. These results indicate that blood pressure changes elicited by the aortic baroreflex are extremely sensitive to the degree of carotid sinus compensation. Thus, to assess the sensitivity of any arterial reflex area, the existing level of compensation by other barosensitive areas must be known.     

Reflex discharge patterns of cardiac vagal efferent fibres

1. Unit activity was recorded from single and few fibre preparations in a cardiac branch of the right vagus nerve of the cat.2. Increases in blood pressure mediated solely by the right carotid sinus nerve produced bradycardia when all other nerves to the heart had been cut. Myelinated fibres in the cardiac branch of the right vagus nerve were reflexly activated by the same procedure.3. The fibres were silent when blood pressure was below 140-150 mm Hg. As the pressure began to rise, they discharged phasically with the cardiac cycle. At pressures greater than 180 mm Hg, the discharge was continuous attaining maximum rates of 40/sec.4. Stimulation of carotid body chemoreceptors also reflexly excited these fibres, as did stimulation of baroreceptors in both the left carotid sinus and aortic arch. Afferent fibres in the left vagus discharging in response to changes in blood pressure reflexly excited the cardiac efferent fibres. Increases in phrenic motoneurone discharge coincided with inhibition of these fibres. Electrical stimulation of the glossopharyngeal nerve also produced inhibition.     

Studies of Blood-pressure Regulation IV. The Effects of Impulse Train Stimulation of the Carotid-sinus Nerves

The effect of sinus nerve stimulation on the blood pressure and heart rate was studied in dogs. Electrical stimulation of the sinus nerves of both sides was given both in the form of 2 types of intermittent impulse trains and as impulses of constant frequency. The intermittent impulse bursts, which were synchronized with the ECG, comprised 5–50 imp which coincided with systole (150 ms). Comparisons were made between stimulation with a constant frequency and the intermittent types, with the same number of impulses per cardiac cycle. It was found that the maximal blood pressure reduction was already reached at 5–10 imp per cardiac cycle. The difference between stimulation with a constant frequency and the intermittent types, with the same number of impulses per cardiac cycle, is negligible as regards blood pressure reduction but the intermittent type has a greater effect on the heart rate. Sinus nerve stimulation in massive haemorrhage and the influence of the amplitude of the stimulation signal were also studied.     

The contribution of alterations in cardiac output to changes in arterial pressure reflexly evoked from the carotid sinus in the rabbit.

1. The reflex cardiovascular effects of changes in pressure within the vascularly isolated carotid sinus were examined in seventeen anaesthetized rabbits. The opposite sinus was denervated and both aortic nerves were divided, 2. Comparison of the mean values at sinus pressures of 40 and 200 mmHg showed a large reduction in systemic arterial pressure from 126 to 58 mmHg and a moderate reduction in heart rate, from 287 to 253 beats min-1. Cardiac output, measured by thermal dilution, showed only a small change, a fall from 160 to 148 ml. min-1 kg-1. 3. By contrast with this reduction in cardiac output of just over 7%, total peripheral resistance, derived by dividing mean arterial pressure by cardiac output, was halved, falling from 0-48 to 0-41 mmHg ml.-1 min kg. 4. Thus in the anaesthetized rabbit changes in cardiac output make only a small contribution to the changes in systemic pressure evoked by alterations in carotid sinus pressure. Changes in total peripheral resistance are principally responsible for the effect on systemic pressure. 5. Though the changes in output of the heart were small, there were considerable changes in the work done by the left ventricle which was approximately halved when carotid sinus pressure was raised from 40 to 200 mmHg.     

Interaction between carotid sinus baroreceptor and aortic nerve pressor reflexes in the dog

In dogs anesthetized with morphine-chloralose, strong, low-frequency (2 Hz) electrical stimulation of the aortic nerve (AN) causes pressure in the perfused hindlimbs to rise. This pressor response is followed by a large depressor phase upon cessation of stimulation. Simultaneous stimulation of the ipsilateral carotid sinus nerve (CSN) with intermittent trains of stimuli enhanced the AN pressor response by 113%. Similar stimulation of the contralateral CSN had little effect on the AN pressor response. Constant-frequency stimulation of the ipsilateral CSN also failed to enhance this response. Possible mechanisms of the interaction between these antagonistic reflexes were investigated. The results suggest that the augmentation of the AN pressor response results from a central neuronal interaction between these antagonistic reflexes.     

An analysis of the inhibition of phrenic motoneurones which occurs on stimulation of some cranial nerve afferents

1. Inhibition and excitation of spontaneous phrenic nerve discharges in response to stimulation of the sinus, glossopharyngeal, aortic and superior laryngeal (SLN) nerves has been investigated in cats.

2. The inhibition, in response to a single shock, had a latency of 5-10 msec and lasted for 20-40 msec; the response to SLN stimulation was the most prolonged.

3. Excitation of phrenic motoneurones also occurred and was seen either before or after the end of the inhibition of the inspiratory burst and sometimes also during expiration.

4. Intravenous strychnine blocked the inhibition.

5. Intracellular recording from phrenic motoneurones showed that hyperpolarization was evoked by each nerve during the central phrenic depolarizing potential (CPDP) but only rarely in the interval between these potentials.

6. When the CPDP was suppressed, hyperpolarization could sometimes be evoked.

7. There were no changes in amplitude or time course of hyperpolarization during the passage of current through the cell membrane. No change in membrane conductance could be shown by passing current pulses.

8. Raising the pressure in the carotid sinus also depressed phrenic activity and evoked a hyperpolarization whilst the CPDP was suppressed.

9. Inspiratory interneurones in the brain stem were suppressed by nerve stimulation and by a rise in carotid sinus pressure.

10. Expiratory interneurones in the brain stem were both excited and suppressed by electrical stimuli and unaffected by a change in carotid sinus pressure.

     

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.     

The relative roles of the aortic and carotid sinus nerves in the rabbit in the control of respiration and circulation during arterial hypoxia and hypercapnia

1. The respiratory and circulatory effects of graded arterial hypoxia, alone or with superadded hypercapnia, were studied in four groups of unanaesthetized rabbits including normal animals and those with selective section of the aortic nerves, selective section of the carotid sinus nerves and section of both sets of nerves.

2. When measured 2-4 days after selective section of the carotid sinus nerves the resting respiratory minute volume and arterial P_O2 were lower and the P_CO2 higher than normal. These effects were not observed after selective section of the aortic nerves. Selective aortic nerve section, and selective carotid sinus nerve section each produced a similar increase in the resting arterial pressure and heart rate, but were without effect on the resting cardiac output.

3. During arterial hypoxia reflex respiratory and circulatory effects ascribable to arterial chemoreceptor stimulation (hyperventilation, bradycardia, vasoconstriction) were mediated for the most part through the carotid sinus nerve. In animals with only the aortic nerves intact the circulatory response was determined largely by the opposing effects of aortic baroreceptor reflexes and the local peripheral dilator action of hypoxia.

4. The circulatory effects of hyperventilation induced by hypercapnia during arterial hypoxia, in animals with both aortic and carotid sinus nerves cut were small.

5. The results suggest that relatively few chemoreceptor fibres originate from the aortic region in the rabbit, though the carotid sinus and aortic nerves both contain baroreceptor fibres.

     

Effect of Carotid Sinus Stimulation on Cardiac Output and Peripheral Vascular Resistance during Changes in Blood Volume Distribution in Man

In ten healthy subjects (mean age 29.6 years) the hemodynamic response to carotid sinus stimulation (neck suction - 40 mmHg) was studied under control conditions and during peripheral pooling of blood (lower body negative pressure). Heart rate, arterial and central venous pressure, cardiac output and forearm blood flow were measured. The time sequence of the heart rate response was studied separately in six healthy subjects. During control conditions, carotid sinus stimulation induced a significant decrease in arterial pressure and heart rate. The blood pressure decrease mainly reflected a reduction in cardiac output, total peripheral vascular resistance being essentially unchanged. However, in the skeletal muscle, represented by a forearm segment, vascular resistance decreased significantly. During lower body negative pressure (LBNP) the same stimulation of the carotid sinus induced a significantly greater fall in mean arterial pressure even though the reduction in cardiac output was slightly smaller on the average than in the control condition. The heart rate increased, probably secondary to a time dependent increase in heart rate elicited by the continuous LBNP stimulus. Total peripheral vascular resistance decreased significantly during LBNP, the reaction likewise differing significantly from that in the control condition. Thus the augmented blood pressure response was due to a more pronounced vasodilatation when the carotid sinus was stimulated during lower body negative pressure. The results indicate that the hemodynamic changes elicited by carotid sinus stimulation are modified by changes in the distribution of blood volume and in the tone of resistance vessels.     

Evidence for central reorganization of ventilatory chemoreflex pathways in the cat during regeneration of visceral afferents in the carotid sinus nerve

There are two sets of peripheral arterial chemoreceptors in the cat, the carotid bodies innervated by the carotid sinus nerve and the aortic bodies with afferents in the aortic depressor nerves. Reflex stimulation of ventilation in response to hypoxia is abolished acutely after interrupting the sensory pathway from the carotid body chemoreceptors in the cat even though the reflex pathway from the aortic body chemoreceptors is intact. However, in chronically maintained preparations, there is a restoration of the hypoxic response which is mediated by the aortic chemoreflex pathway. It was proposed that restoration was due to a ‘central reorganization’ of chemoreflex pathways which followed interruption of the sensory pathway from the carotid bodies and that the reorganization enhanced the efficacy of the aortic ventilation chemoreflex. This proposal was tested in the present experiments by measuring reflex ventilatory and cardiovascular responses to electrical stimulation of the sensory nerves containing aortic and carotid chemoreceptor afferents following bilateral interruption of carotid sinus nerves and carotid body resection. Responses measured acutely (1–6 h) after interruption were compared with those measured 60–80 and 110–140 days later. At 60–80 days, a chemoreflex response (increase in tidal volume of ventilation) to stimulation of the interrupted carotid sinus sensory pathway was markedly attenuated while the response to stimulation of the uninterrupted pathway in aortic depressor nerves was enhanced. At 110–140 days, the tidal volume response to carotid sinus nerve stimulation was greatly enhanced while the aortic depressor nerve response declined from the elevated level. There were significant but less pronounced changes in the response of other ventilatory and cardiovascular variables to aortic depressor nerve and carotid sinus nerve stimulation.The results support the idea that there is a ‘central reorganization’ of chemoreflex pathways which is reflected functionally by changes in the efficacy of reflexes evoked from aortic depressor nerve and carotid sinus nerve. The changes are analagous to those occurring in somatic reflexes during regeneration of sensory nerves. It is suggested that the changes in efficacy of carotid sinus nerve reflexes are due to a degenerative loss of synapses of the central projections of interrupted carotid sinus nerve sensory axons (degenerative atrophy) and subsequent regenerative like changes (regenerative proliferation) in the central projections. The changes in the efficacy of aortic depressor nerve reflexes may be attributed to formation of new synapses by converging central projections of this uninterrupted pathway (reactive synaptogenesis) and subsequent regression of the newly formed synapses.     

Effect of pentobarbital anesthesia on hypotension after 10% hemorrhage in the dog.

The effect of pentobarbital anesthesia, 30 mg.kg body wt-1, on the rapidly acting arterial pressure control system was studied on splenectomized dogs chronically instrumented with catheters for pressure measurement and hemorrhage and with a flow probe for measurement of aortic flow. The dogs were subjected to 10% hemorrhage in 30 s under conscious and anesthetized states before and after denervation of the carotid sinus nerves (CS) and/or the vagi (V). In the intact nerve condition, arterial pressure fall (delta AP) at 1-2 min after hemorrhage was 8.0 +/- 1.3 (mean +/- SE) mmHg in conscious dogs and 9.4 +/- 2.0 mmHg in dogs under anesthesia. There was no significant difference between these delta APs or other pairs of delta APs in conscious and anesthetized states at any stage of denervation. As long as the CS reflex was intact, heart rate and total peripheral resistance increased in response to hemorrhage as in the intact condition. In conclusion, the pentobarbital anesthesia had little effect on the rapidly acting arterial pressure control system as far as its capacity to restore mean arterial pressure after the brief 10% hemorrhage is concerned.     

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.