Depressor Area Research Articles

Baroreceptor sensitive neurones in the anterior hypothalamus of the cat.

1. The activity of 372 neurones, located within or close to the hypothalamic depressor area, was recorded on raising the pressure within a vascularly isolated carotid sinus.2. When the intrasinusal pressure was raised abruptly to 200 mm Hg the activity of fifteen neurones was enhanced and of six inhibited.3. The neurones exhibiting excitation on baroreceptor afferent stimulation were broadly divisible into two groups. Nine neurones responded with a marked increase in discharge frequency, the other six responded with a ;burst-on' discharge with a minimum latency of 90 msec. Excitation in both cases was always within 500 msec of the presentation of the stimulus. No functional distinction has been drawn from these responses.4. Evidence has been obtained suggesting that the responses of both types of neurone showing excitation may be potentiated using a pulsatile rather than static stimulus.5. The role of the neurones in the integration of the carotid sinus baroreceptor reflex is discussed. It is suggested that the hypothalamic depressor area represents the rostral extension of the integrative centre for the reflex.

Bulbar inhibition of spinal and supraspinal sympathetic reflex discharges.

1. In chloralose anesthetized cats, the sympathetic reflex discharge was recorded from the renal sympathetic nerve. 2. The early-spinal and late-supraspinal sympathetic reflex discharges were elicited by single electrical stimulation of the thoracic dorsal roots. 3. Increased excitation of the baroceptor afferents produced by a rise of blood pressure after injection of noradrenaline caused strong inhibitition of the latesupraspinal reflex discharge. The early-spinal reflex discharge was only rarely affected. 4. Electrical stimulation of the medullary depressor area caused inhibition of the spinal and supraspinal reflex discharges. 5. It is concluded that spinal reflex pathways receive some inhibitory descending influences from the medulla oblongata.

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.

Changes in Cardiac Output upon Stimulation of the Hypothalamic Defence Area and the Medullary Depressor Area in the Cat

Folkow, B., B. Lisander, K. S. Tuttle and S. C:. Wang. Changes in cardiac output upon stimulation of the hypothalamic defenca araa and the medullary depressor area in the. cat. Acta physiol. scand. 1968. 72. 220–233. The hypothalamic defence area and the bulbar depressor area, with related hypothalamic sympatho-inhibitory structures, were topically stimulated while changes in cardiac output (C. O.). heart rate, stroke volume, central venous pressure and peripheral blood flow were studied in anesthetized-curarized cats and dogs. Defence area stimulation induced up to two-fold increases in C. O. and up to threefold increases in calculated work load for the left ventricle. The major part of the C. O. increase was directed to the skeletal muscles, where active cholinergic vasodilatation increased flow up to fivefold. Gastrointestinal and renal blood flows were promptly reduced and since this neurogenic flow reduction slightly prereded muscle vasodilatation, the C. O. increase could be preceded by a very brief phase of C. O. decrease. β-adrenergic blockade could reduce the threefold increase in left ventricular work load by 50–60 per cent by eliminating the sympathetic drive on the heart. Depressor area stimulations produced an often profound reduction in C. O., sometimes prereded by a brief C. O. increase. Flow resistance fell, especially so in skeletal musrles, where an initial flow increase coincided with the transient C. O. increase; further, blood was pooled within the capacitance section. Blood loss or raised venous transmural pressure greatly potentiated these changes so that imminent cardiovascular collapse could be induced by this central depressor stimulation. The mechanisms involved in the mentioned, diametrically opposite cardiovascular patterns are. discussed.

Changes in cardiac output upon stimulation of the hypothalamic defence area and the medullary depressor area in the cat.

AbstractFolkow, B., B. Lisander, K. S. Tuttle and S. C:. Wang. Changes in cardiac output upon stimulation of the hypothalamic defenca araa and the medullary depressor area in the. cat. Acta physiol. scand. 1968. 72. 220–233.The hypothalamic defence area and the bulbar depressor area, with related hypothalamic sympatho‐inhibitory structures, were topically stimulated while changes in cardiac output (C. O.). heart rate, stroke volume, central venous pressure and peripheral blood flow were studied in anesthetized‐curarized cats and dogs. Defence area stimulation induced up to two‐fold increases in C. O. and up to threefold increases in calculated work load for the left ventricle. The major part of the C. O. increase was directed to the skeletal muscles, where active cholinergic vasodilatation increased flow up to fivefold. Gastrointestinal and renal blood flows were promptly reduced and since this neurogenic flow reduction slightly prereded muscle vasodilatation, the C. O. increase could be preceded by a very brief phase of C. O. decrease. β‐adrenergic blockade could reduce the threefold increase in left ventricular work load by 50–60 per cent by eliminating the sympathetic drive on the heart. Depressor area stimulations produced an often profound reduction in C. O., sometimes prereded by a brief C. O. increase. Flow resistance fell, especially so in skeletal musrles, where an initial flow increase coincided with the transient C. O. increase; further, blood was pooled within the capacitance section. Blood loss or raised venous transmural pressure greatly potentiated these changes so that imminent cardiovascular collapse could be induced by this central depressor stimulation. The mechanisms involved in the mentioned, diametrically opposite cardiovascular patterns are. discussed.

Centrally evoked sympathetic discharge: a functional study of medullary vasomotor areas.

1. The medulla oblongata was stimulated electrically in decerebrate cats following bilateral vagotomy. Changes in splanchnic nerve discharge evoked by stimulation of pressor and depressor areas in the medulla are correlated with changes in arterial pressure. An interaction of baroreceptor afferents with the efferent sympathetic system at the level of the medulla and/or spinal cord is demonstrated. Evidence is presented which suggests that it is possible to alter activity selectively in a given division (splanchnic) of the sympathetic outflow.2. Evoked responses were categorized as follows:(a) Sustained splanchnic activation; an immediate increase in total splanchnic activity occurred with only a small, gradual decline in activity during the stimulation period. Mild stimulation (150-200 muA) raised systolic pressure by 60-80 mm Hg and stronger stimulation (300-400 muA) increased pressure by 100-150 mm Hg. When comparable pressor responses were elicited from points on either side of the mid line, splanchnic excitation was greater with homolateral stimulation (left side).(b) Unsustained splanchnic activation; an immediate increase in activity occurred which declined sharply as systolic pressure rose by 60-100 mm Hg during stimulation. Such a decline was attributed to the influence of baroreceptor afferents. Thus, if previous carotid occlusion was maintained during stimulation, the decline in activity was minimized although the pressor response increased. It is suggested that the structures yielding unsustained responses differ from those yielding sustained responses in their functional relation with the baroreceptor afferents.(c) Reduced splanchnic discharge during direct medullary stimulation; a partial or complete inhibition of splanchnic activity was obtained, which was sometimes accompanied by a 20-40 mm Hg reduction in systolic pressure. However, the direction and magnitude of the systemic pressure change were not as consistently related to the splanchnic response as they were during activation. Even if splanchnic efferent activity were elevated by carotid occlusion, stimulation still reduced discharge.

NEUROGENIC HYPERTENSION IN THE RAT.

Several techniques of radical denervation of the sino-aortic depressor areas were tried in order to produce a permanent neurogenic hypertension in the rat. The aortic depressor fibers were interrupted at the neck level by resecting the nerves which usually exhibit baroreceptor activity, namely, isolated aortic nerve, sympathetic, and laryngeal nerves. The carotid sinus was denervated by stripping the carotid bifurcation and painting with phenol. When the carotid bifurcation was resected bilaterally, in a one-stage operation, all rats showed symptoms of cerebral ischemia, dying shortly thereafter. Isolated denervation of the aortic baroreceptors was followed by a transitory hypertension. No changes in preasure were observed when only the carotid sinuses were denervated. A few rats in which the usual baroreceptor pathways were interrupted, except the superior laryngeal nerve, developed chronic hypertension. Yet, to obtain consistently permanent hypertension it was necessary to include in the denervation every baroreceptor route. A simple one-stage operation for complete sino-aortic baroreceptor denervation is described. This procedure was used in 140 rats that were then studied for periods up to one year. All the operated animals presented some degree of hypertension. Blood pressure measurements made during the first week showed even then that the rats were hypertensive. This observation suggests that in the rat no latent period for the appearance of neurogenic hypertension is present. Hypertension was permanent in 75% of the rats observed up to one year; blood pressure returned to normal values in the remaining 25%, usually after the third month. Extirpation of the adrenal medulla had no effect on the evolution of the hypertension in the denervated rats. Blood pressure was measured repeatedly in unanesthetized rats by tail plethysmography. Pressure values determined by this method, though 10 to 20 mm Hg lower, approximated the mean arterial pressure recorded directly from the femoral artery in normotensive and hypertensive rats. The hypertension in denervated rats included an increase of systolic as well as diastolic pressure. The heart rates of quiet hypertensive rats were within the normal range and, in general, no close correlation was observed between increases in blood pressure and elevations in heart rate. Normal rats have marked fluctuations in both pressure and heart rate when walking or when stimulated; these fluctuations were much greater in the neurogenic hypertensive animals. Moreover, the hypertensive rats showed large oscillations of blood pressure synchronous with respiratory movements particularly when the latter were slower and deeper than normal. The rats seemed to tolerate both the denervation and the hypertension very well. Histological examination of tissues from hypertensive rats showed myocardial hypertrophy and a thickening of the basement membrane of the glomerular capsule. The severity of the latter abnormality was closely associated with the duration of the hypertension.

CHANGES IN ELASTICITY OF PULMONARY REFLEXOGENIC AREA WITH SYMPATHETIC ACTIVITY.

The isolated rabbit sympathetic nerve-pulmonary artery preparation has been shown to be taken from a part of the pulmonary artery which contains a high concentration of adventitial sensory endings resembling those in the carotid sinus and aortic depressor area. Using this preparation the static bulk modulus of elasticity has been measured under a variety of circumstances. Sympathetic nerve stimulation, increased potassium ion concentration, and l-norepinephrine addition decreased the unstretched circumference of the artery, with increasing strain, increased and then decreased the elastic modulus of the arterial wall, and decreased the change in elastic modulus for any proportionate increase in circumference. Sodium nitrite had opposite actions. Angiotensin and pH changes between 7.0 and 8.1 had no effect on these measurements. A possible cause for some of the divergent conclusions found in the literature, and the relation of these experimental findings to the afferent activity of associated pressoreceptors is discussed.

Brain stem augmentation of cardiovascular activity.

Midpontile ischemic decerebration in vagotomized mesencephalic cats produced marked tachycardia and hypertension. Subsequent transection of the brain stem at or above the midpontile level did not affect the cardiovascular hyperactivity. Transection at the pontomedullary junction abolished the brain stem augmentation of heart rate and blood pressure. The results suggest the existence of a cardiovascular augmenter area in the caudal half of the pons and a cardiovascular depressor area in a more rostral portion of the brain stem.

Vasoconstrictor inhibition and vasodilator activation; two functionally separate vasodilator mechanisms in the skeletal muscles.

Summary.Vasodilatation in the skeletal muscles is produced by electric stimulation of a sinus nerve, a vagus nerve, the depressor area of the oblongate medulla or by activation of sympathetic vasodilator nerves.Destruction of the depressor area does not prevent the transmission of impulses in the bulbar sympathetic vasodilator tract.The depressor area and the bulbar part of the sympathetic vasodilator tract seem to be separate anatomical and functional entities. The writers have been unable to activate the two vasodilator mechanisms simultaneously, a fact that is regarded to support the conception that they form two independently operating mechanisms.The expenses of this investigation were partly defrayed by a grant from the Swedish Medical Research Council to one of us (B. U.) which is gratefully acknowledged.

TONIC AND REFLEX FUNCTIONS OF MEDULLARY SYMPATHETIC CARDIOVASCULAR CENTERS

TONIC AND REFLEX FUNCTIONS OF MEDULLARY SYMPATHETIC CARDIOVASCULAR CENTERS