Modification of the reflex response to stimulation of carotid sinus baroreceptors during and following stimulation of the hypothalamic defence area in the cat

1. The effects of stimulation of the hypothalamic defence area on carotid sinus baroreceptor reflexes have been investigated by examining the cardiovascular responses to a 15 sec period of increased pressure within the vascularly isolated carotid sinus before, during, and immediately following a 25 sec period of hypothalamic stimulation.2. Identification of the hypothalamic defence area was based on the occurence of atropine-sensitive muscle vasodilatation. Electrode positions were confirmed by histological examination.3. During hypothalamic stimulation the reflex fall in blood pressure resulting from a rise in sinus pressure was found to be undiminished whether sinus pressure was raised at the onset or at the 10th sec of hypothalamic stimulation.4. By contrast, in at least half the cats in which a reflex bradycardia could be evoked from the sinus, this bradycardia was largely if not completely suppressed during hypothalamic stimulation. This suppression of reflex bradycardia occurred when sinus pressure was raised at the onset as well as at the 10th sec of stimulation.5. During the first 5 sec after hypothalamic stimulation the hypotensive response to an increase in carotid sinus pressure was much reduced; on the other hand the reduction in heart rate was exaggerated, sometimes to a very marked degree.6. The results suggest that stimulation of the hypothalamic defence area can modify baroreceptor reflexes and that this modification can include selective alterations in the various components of the reflex response.     

Differentiated Interaction between the Hypothalamic Defence Reaction and Baroreceptor Reflexes

As the interrelationship of autonomic patterns involving cortico-hypothalamic and bulbar levels is of general interest, the interaction between the hypothalamic defence reaction and the homeostatic baroreceptor reflexes was explored in cats with respect to cardiac as well as vascular effects. The results suggest, in conformity with Hilton's observations (1963), that defence area stimulation suppresses the baroreceptor reflex inhibition of the heart. On the other hand, the baroreceptor influence on vasoconstrictor fibre discharge was largely the same, whether defence area stimulations were performed or not. This had important haemodynamic consequences, especially for muscle blood flow, since the reflex inhibition of regional constrictor fibre tone could greatly enhance the cholinergic vasodilatation. Therefore such a differentiated interaction between oppositely directed central and reflex autonomic mechanisms has the consequence that the baroreceptor reflexes, rather than damping the defence reaction, act in synergism with it with respect to net haemodynamic effects; some further implications of this are dealt with in the subsequent paper (Kylstra and Lisander 1969).     

Extent of Engagement of Various Cardiovascular Effectors to Alterations of Carotid Sinus Pressure

Reflex adjustments of blood pressure, heart rate, skeletal muscle and renal resistance vessels to changes in intrasinusal pressure were recorded and the respective sinus pressure—reflex response curves plotted. In this way one could evaluate whether the various individual reflex arcs, which together constitute the baroreceptor reflex control of the circulation, display “threshold” response and maximal sensitivities, respectively, at identical sinus pressures.—The curves describing the blood pressure, muscle and renal resistance vessel responses were found to follow identical courses, while the heart rate response curve was displaced to the right of the others. This discrepancy is, however, in all probability a mere consequence of the peculiar neuro-effector characteristics in the heart. The individual components of the baroreceptor reflex, therefore seem to be recruited simultaneously when the sinus pressure is increased, and there is thus nothing to indicate that afferents from low and high “threshold” baroreceptors, respectively, are preferentially distributed to different neuron pools in the bulbar cardiovascular centres.—A displacement of the response curves to the right was observed when a) non-pulsating sinus pressures were used instead of pulsating, b) sinus pressures alterations were induced by lowering the pressure from higher levels instead of elevating it, c) arterial PCO₂ was increased.     

The baroreceptor reflex and the cardiovascular changes associated with sustained muscular contraction in the cat

Summary In decerebrate unanaesthetised cats the cardiovascular effects of raising the pressure in a blind sac preparation of a carotid sinus on one side were examined at rest and during sustained contractions of hind-limb muscles. During a tetanic contraction the absolute value of the blood pressure and heart-rate components of the baroreceptor reflex response were not significantly changed from those at rest. The curve relating heart-rate and mean blood pressure, during carotid sinus distension, was similar at rest and when the muscles of the hind-limb were contracting tetanically, although each value of heart-rate was greater, suggesting a resetting of the baroreceptor reflex. By contrast, in the same experiments, suppression of the baroreceptor reflex changes in heart-rate and blood pressure could be demonstrated during the increases of blood pressure and heart-rate elicited by electrical stimulation of limb nerve. It was concluded that the increases in blood pressure and heart-rate elicited by the afferent discharge from muscles during sustained contraction are buffered to some extent by the baroreceptors, though their inhibitory effect is incomplete under these conditions.     

Differentiated Interaction between the Hypothalamic Defence Area and Baroreceptor Reflexes

In experiments on cats, the interaction between the oppositely directed hypothalamic defence reaction and the baroreceptor reflexes was analysed with particular regard to the effects on aortic blood flow, left ventricular work load and muscle blood flow. Because of their differentiated interaction — suppression of the baroreceptor reflex effect on the heart with preservation of the reflex modulation of the vascular bed (Djojosugito et al. 1969) — the baroreceptor reflex so modifies the primary defence reaction, with its intense neurogenic drive on the heart, that a greater cardiac output is gained for a given left ventricular work load. This particularly favours muscle blood supply. It follows that such a differentiated interaction between two basically opposite autonomic patterns causes them to act in synergism with respect to efficient cardiovascular performance in states of emergency.     

Arterial baroreceptor reflex function during elevation of intracranial pressure

The ability of the arterial baroreceptor reflex to buffer the blood pressure responses elicited by increasing the intracranial pressure (ICP) has been studied in chloralose anesthetized cats. Standardized elevations of ICP induced pressor responses of similar magnitude irrespective of whether the baroreceptor inhibitory activity was high or very low. When ICP was elevated baroreceptor activation induced a reflex reduction of flow resistance and blood pressure, but never to the same levels obtained when ICP was normal. Thus when ICP was elevated there was an upward displacement of the curve relating carotid sinus pressure to mean arterial blood pressure.     

Bradycardia evoked by hypothalamic stimulation in the rabbit: Dependence upon the arterial blood pressure

The spinal cord was transected in adult New Zealand White rabbits anaesthetized with urethane plus chloralose. The level of transection was in the mid-cervical region. The animals were then ventilated mechanically and the arterial blood pressure was maintained with an intravenous infusion of noradrenaline solution. Stimulation of the hypothalamus 1–2 mm lateral to the third ventricle and 1.5–3 mm dorsal to the mammillary nuclei, in a region known to evoke pressor responses and bradycardia in normal anaesthetized rabbits, never evoked pressor responses in the spinally transected rabbits. Bradycardia was evoked only when the mean arterial blood pressure was maintained above 44–49 mmHg. At higher pressures stimulation evoked a greater bradycardia and the relationship between bradycardia and pressure was approximately linear over much of the range of pressures tested (up to 116 mmHg).Because the threshold mean arterial blood pressure at which hypothalamic stimulation evoked bradycardia was similar to the threshold pressures reported in the literature for baroreceptor activation in the rabbit and because the curve of bradycardia:pressure was similar to published curves of baroreceptor and baroreflex activity against blood pressure, it is concluded that the bradycardia evoked by hypothalamic stimulation in the rabbit is mediated by a neural pathway in the hypothalamus that can increase the gain of the cardio-inhibitory baroreceptor reflex.     

The pontomedullary area integrating the defence reaction in the cat and its influence on muscle blood flow

1. In anaesthetized cats the effects were investigated of electrical stimulation of regions in the caudal mesencephalon, pons and medulla on muscle blood flow, skin blood flow and arterial blood pressure.2. It was found that within the dorsal part of the well known pressor area there is a narrow strip, 2.5 mm lateral from the mid line, starting ventral to the inferior colliculus and ending in the medulla close to the floor of the IV ventricle, from which vasodilatation in skeletal muscles is selectively obtained. This strip is quite separate from the more ventral, efferent pathway for active vasodilatation running from the hypothalamic and rostral mesencephalic ;defence centre'.3. As in the case of the hypothalamic and rostral mesencephalic ;defence centre', the muscle vasodilatation obtained from the caudal strip is accompanied not only by a rise of arterial blood pressure, but also by tachycardia, vasoconstriction in the skin, pupillary dilatation and piloerection.4. Stimulation, restricted to the caudal strip, via implanted electrodes in unanaesthetized animals, produced a behavioural response resembling the defence reaction. The strip, therefore, is probably a caudal extension of the ;defence centre'.5. Unlike the vasodilatation elicited from the more rostral part of the ;defence centre' in the hypothalamus and mesencephalon, the muscle vasodilatation obtained on stimulation of the caudal strip was resistant to atropine, but was blocked by guanethidine.6. It is suggested that during naturally occurring defence reactions in the normal animal the ponto-medullary area is activated together with the hypothalamo-mesencephalic area, inhibition of vasoconstrictor tone then accompanying activation of the vasodilator nerve fibres in skeletal muscle.     

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

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

Aspects of the Central Integration of Arterial Baroreceptor and Cardiac Ventricular Receptor Reflexes in the Cat

The possible central integrative mechanisms, responsible for the earlier reported, differentiated reflex engagement of the renal and muscle vessels and the heart from cardiac ventricular receptors and arterial baroreceptors, respectively, were analyzed in atropinized cats. The reflex renal vessel, muscle vessel and heart rate responses, expressed as per cent of maximum, to graded activations of arterial baroreceptors (sinus pressure variations) and stimulations of ventricular receptor afferents in the cardiac nerve were systematically compared. Cardiac nerve stimulation with low frequencies was found to elicit more pronounced reflex renal vessel responses than muscle vessel and heart rate responses. In contrast, elevations of sinus pressure induced equally pronounced renal and muscle vessel responses. High frequency cardiac nerve stimulation elicited maximal reflex renal vessel responses, but only submaximal effects on muscle vessels and heart rate, while intense baroreceptor stimulation induced maximal reflex effector responses throughout. The submaximal heart rate response to cardiac nerve stimulation is probably due to a simultaneous activation of excitatory afferents. On the other hand, the less pronounced muscle than renal vessel responses when the cardiac nerve was stimulated probably reflect a relatively sparse innervation of muscle vasomotor neurons by ventricular receptor afferents, which seem instead to be preferentially oriented towards renal vasomotor and, possibly, cardiac motor neurons.     

Aspects of the central integration of arterial baroreceptor and cardiac ventricular receptor reflexes in the cat.

The possible central integrative mechanisms, responsible for the earlier reported, differentiated reflex engagement of the renal and muscle vessels and the heart from cardiac ventricular receptors and arterial baroreceptors, respectively, were analyzed in atropinized cats. The reflux renal vessel, muscle vessel and heart rate responses, expressed as per cent of maximum, to graded activations of arterial baroreceptors (sinus pressure variations) and stimulations of ventricular receptor afferents in the cardiac nerve were systematically compared. Cardiac nerve stimulation with low frequencies was found to elicit more pronounced reflex renal vessel responses than muscle vessel and heart rate responses. In contrast, elevations of sinus pressure induced equally pronounced renal and muscle vessel responses. High frequency cardiac nerve stimulation elicited maximal reflex renal vessel responses, but only submaximal effects on muscle vessels and heart rate, while intense baroreceptor stimulation induced maximal reflex effector responses throughout. The submaximal heart rate response to cardiac nerve stimulation is probably due to a simultaneous activation of excitatory afferents. On the other hand, the less pronounced muscle than renal vessel responses when the cardiac nerve was stimulated probably reflect a relatively sparse innervation of muscle vasomotor neurons by ventricular receptor afferents, which seem instead to be preferentially oriented towards renal vasomotor and, possibly, cardiac motor neurons.     

Comparison of the reflex vasomotor responses to separate and combined stimulation of the carotid sinus and aortic arch baroreceptors by pulsatile and non-pulsatile pressures in the dog

1. In the anaesthetized dog the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. When the vasosensory areas were perfused at non-pulsatile pressures within the normal physiological range of mean pressures, the reflex reduction in systemic vascular resistance produced by a given rise in mean carotid sinus pressure was significantly greater than that resulting from the same rise of aortic arch pressure.3. On the other hand, when the vasosensory areas were perfused at normal pulsatile pressures and within the normal physiological range of mean pressures, there was no difference in the size of the reflex vascular responses elicited by the same rise in mean pressure in the carotid sinuses and in the aortic arch.4. Whereas the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in pulse pressure, those evoked by the aortic arch baroreceptors through changes of mean pressure are only weakly affected by modifications in pulse pressure. Evidence for this was obtained from single stepwise changes of mean pressure in each vasosensory area during pulsatile and non-pulsatile perfusion, and from curves relating the mean pressure in the carotid sinuses or aortic arch and systemic arterial perfusion pressure.5. The vasomotor response elicited by combined stimulation of the carotid sinus and aortic arch baroreceptors was greater than either response resulting from their separate stimulation.6. When the mean perfusion pressures in the two vasosensory areas are changed together, the curve relating mean pressure to systemic arterial pressure during pulsatile perfusion of the areas is considerably flatter than that for non-pulsatile perfusion.7. Increasing the pulse pressure in the carotid sinuses or aortic arch caused a decrease in systemic vascular resistance, the response elicited from the carotid sinuses being the larger.8. Altering the phase angle between the pulse pressure waves in the carotid sinuses and aortic arch had no effect on systemic vascular resistance.9. In both vasosensory areas, increasing the pulse frequency caused a reduction in systemic vascular resistance.     

Interaction between the Hypothalamic Defence Reaction and Cardiac Ventricular Receptor Reflexes

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

Cardiovascular effects elicited from the ventral surface of medulla oblongata in the cat

Cardiovascular adjustments induced by topical application of drugs on a restricted area on the ventral surface of the medulla oblongata, corresponding to the caudal part of the rostral chemoreceptor area and the intermediate area, have been studied in chloralose-anesthetized cats. Topical application of GABA or glycine on these structures resulted in blood pressure fall, bradycardia, vasodilatation in the kidney and the skeletal muscles and also depression of respiration. Similar responses except for a slight tachycardia occurred with application of physostigmine. Application of GABA resulted in a marked attenuation of the reflex vasoconstrictor responses to removal of arterial baroreceptor restraint (carotid occlusion), particularly in the kidney, and to disappearance of the reflex renal vasodilatation to baroreceptor stimulation. The findings suggest that GABA application leads to a general diminution of the tonic vasomotor neuron activity, and with regard to renal vasomotor neurons a virtual cessation. Atropine methylnitrate application induced blood pressure rise, increased peripheral resistance in both skeletal muscle and kidney and a strongly potentiated renal vasoconstrictor response to carotid occlusion. The results indicate that the studied superficial medullary structures play an important role for the maintenance of tonic vasomotor neuron activity, especially renal.Deceased January 1980     

Participation of the anterior hypothalamus in the baroreceptor reflex

1. On the basis of discrete electrical stimulation in the pre-optic region and anterior hypothalamus of anaesthetized cats, a depressor area has been defined, stimulation of which elicits a fall of arterial blood pressure of 30-50 mm Hg and a bradycardia of some 25%, caused by inhibition of sympathetic vasomotor tone and by vagal activation respectively. These are accompanied by a reduction in rate and depth of respiration.2. The depressor area, from which this pattern of response is elicited, lies ventral and caudal to the anterior commissure, and extends caudally in the dorsal hypothalamus, dorsal to the fornix.3. The pattern of response elicited from identified points in the depressor area was shown to be indistinguishable from that to baroreceptor afferent stimulation.4. A lesion destroying the hypothalamic depressor area bilaterally reduced the response to baroreceptor afferent stimulation. Lesions in the medullary depressor area which spared a large part of the nucleus of the tractus solitarius also reduced, but did not abolish, the baroreceptor reflex response. The two lesions combined abolished the reflex.5. It is concluded that the whole brain-stem depressor area, from the hypothalamus through the mid-brain to the medulla, constitutes a functional unit which integrates the response to baroreceptor afferent stimulation.     

Studies on the central integration of excitatory chemoreceptor influences and inhibitory baroreceptor and cardiac receptor influences.

Experiments were performed on cats to explore the integrated cardiovascular responses when excitatory (chemoreceptor) and inhibitory (baroreceptor or cardiac receptor) influences are simultaneously presented to the medullary cardiovascular areas. At a given sinus pressure in the low or medium pressure range, the systemic blood pressure and the vascular resistance were higher when the chemoreceptors were stimulated, while a high, pulsating sinus pressure, i.e.a strong baroreceptor stimulation, could suppress completely even an intense chemoreceptor activation. Thus, the set point and the gain of the baroreflex were increased by a concomitant chemoreceptor activation. These effects are compatible with a simple, mutual 'summation' of excitatory and inhibitory influences on a common population of central vasomotor neurons. The reflex vasodilator effects elicited via vagal cardiac afferents were found to be more effectively suppressed by a concomitant chemoreceptor stimulation than were the baroreceptor effects, provided a primary chemoreceptor response (bradycardia) was at hand, while the heart rate responses were essentially uninfluenced by the prevailing chemoreceptor activity. This chemoreceptor suppression of the reflex vasodilatation from cardiac receptors, which may be of great importance in hypoxic situations, e.g. during a dive, suggests a more complex, neuronal interaction between the two reflex mechanisms in the CNS.     

Carotid baroreflex regulation of vascular resistance in high-altitude Andean natives with and without chronic mountain sickness

We investigated carotid baroreflex control of vascular resistance in two groups of high-altitude natives: healthy subjects (HA) and a group with chronic mountain sickness (CMS), a maladaptation condition characterized by high haematocrit values and symptoms attributable to chronic hypoxia. Eleven HA controls and 11 CMS patients underwent baroreflex testing, using the neck collar method in which the pressure distending the carotid baroreceptors was changed by applying pressures of -40 to +60 mmHg to the chamber. Responses of forearm vascular resistance were assessed from changes in the quotient of blood pressure divided by brachial artery blood velocity. Stimulus-response curves were defined at high altitude (4338 m) and within 1 day of descent to sea level. We applied a sigmoid function or third-order polynomial to the curves and determined the maximal slope (equivalent to peak gain) and the corresponding carotid pressure (equivalent to 'set point'). The results showed that the peak gains of the reflex were similar in both groups and at both locations. The 'set point' of the reflex, however, was significantly higher in the CMS patients compared to HA controls, indicating that the reflex operates over higher pressures in the patients (94.4 +/- 3.0 versus 79.6 +/- 4.1 mmHg; P < 0.01). This, however, was seen only when subjects were studied at altitude; after descent to sea level the curve reset to a lower pressure with no significant difference between HA and CMS subjects. These results indicate that carotid baroreceptor control of vascular resistance may be abnormal in CMS patients but that descent to sea level rapidly normalizes it. We speculate that this may be explained by CMS patients having greater vasoconstrictor activity at altitude owing to greater hypoxic stimulation of chemoreceptors.     

Barosensory cells in the nucleus tractus solitarius receive convergent input from group III muscle afferents and central command

Some neural mechanism must prevent the full expression of the baroreceptor reflex during static exercise because arterial blood pressure increases even though the baroreceptors are functioning. Two likely candidates are central command and input from the thin fiber muscle afferents evoking the exercise pressor reflex. Recently, activation of the mesencephalic locomotor region, an anatomical locus for central command, was found to inhibit the discharge of nucleus tractus solitarius cells that were stimulated by arterial baroreceptors in decerebrated cats. In contrast, the effect of thin fiber muscle afferent input on the discharge of nucleus tractus solitarius cells stimulated by baroreceptors is not known. Consequently in decerebrated unanesthetized cats, we examined the responses of barosensory nucleus tractus solitarius cells to stimulation of thin fiber muscle afferents and to stimulation of the mesencephalic locomotor region, a maneuver which evoked fictive locomotion. We found that electrical stimulation of either the mesencephalic locomotor region or the gastrocnemius nerve at current intensities that recruited group III afferents inhibited the discharge of nucleus tractus solitarius cells receiving baroreceptor input. We also found that the inhibitory effects of both gastrocnemius nerve stimulation and mesencephalic locomotor region stimulation converged onto the same barosensory nucleus tractus solitarius cells. We conclude that the nucleus tractus solitarius is probably the site whereby input from both central command and thin fiber muscle afferents function to reset the baroreceptor reflex during exercise.     

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

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

Studies on the Central Integration of Excitatory Chemoreceptor Influences and Inhibitory Baroreceptor and Cardiac Receptor Influences

Experiments were performed on cats to explore the integrated cardiovascular responses when excitatory (chemoreceptor) and inhibitory (baroreceptor or cardiac receptor) influences are simultaneously presented to the medullary cardiovascular areas. At a given sinus pressure in the low or medium pressure range, the systemic blood pressure and the vascular resistance were higher when the chemoreceptors were stimulated, while a high, pulsating sinus pressure, i.e. a strong baroreceptor stimulation, could suppress completely even an intense chemoreceptor activation. Thus, the set point and the gain of the baroreflex were increased by a concomitant chemoreceptor activation. These effects are compatible with a simple, mutual ‘summation’ of excitatory and inhibitory influences on a common population of central vasomotor neurons. The reflex vasodilator effects elicited via vagal cardiac afferents were found to be more effectively suppressed by a concomitant chemoreceptor stimulation than were the baroreceptor effects, provided a primary chemoreceptor response (bradycardia) was at hand, while the heart rate responses were essentially uninfluenced by the prevailing chemoreceptor activity. This chemoreceptor suppression of the reflex vasodilatation from cardiac receptors, which may be of great importance in hypoxic situations, e.g. during a dive, suggests a more complex, neuronal interaction between the two reflex mechanisms in the CNS.