Parabrachial pons mediates hypothalamically induced renal vasoconstriction

The role of the parabrachial region of the dorsal rostral pons (PB) in mediating control of renal blood flow and of systemic arterial blood pressure was investigated in nine cats anesthetized with chloralose-urethan. Electrical stimulation through electrodes placed stereotaxically in lateral and medial positions in the hypothalamus (LH and MH) in PB and in ventrolateral reticular formation (VLRF) of each cat elicited pronounced systemic arterial pressor responses and renal vasoconstrictions. Stimulation parameters were adjusted so that renal flow responses elicited from each site were equal. Following a unilateral lesion in the PB, responses of renal vasoconstriction induced by hypothalamic stimulation were attenuated, but responses of arterial pressure were not altered. Stimulation of the VLRF, posterior to the lesion, consistently produced undiminished systemic pressor responses and renal vasoconstriction throughout the durations of the experiments excluding decay of renal vascular responsiveness. Thus, the data suggest that pathways mediating renal vasoconstriction in response to hypothalamic stimulation was discrete and pass through the parabrachial region, whereas pathways mediating systemic vasoconstriction in response to hypothalamic stimulation are distinct or less compact.     

The paramedian reticular nucleus: a site of inhibitory interaction between projections from fastigial nucleus and carotid sinus nerve acting on blood pressure

1. The interaction between the pressor response to electrical stimulation of the fastigial nucleus (FN), the fastigial pressor response (FPR), and the depressor response to electrical stimulation of the carotid sinus nerve (CSN) was examined in paralysed anaesthetized cats.2. Blood pressure responses evoked by electrical stimulation of the FN and the CSN were mutually inhibitory and summed algebraically.3. The FPR was augmented after denervation of buffer nerves. Lesions of the FN did not alter the depressor response to stimulation of the CSN.4. Bilateral electrolytic lesions of the paramedian reticular nucleus abolished both the FPR and the CSN depressor response without altering base line pressure.5. With micro-electrode recording neurones were discovered within the paramedian reticular nucleus which responded to electrical stimulation of the FN or the CSN. These neurones were polysynaptically excited by stimulation of either the FN or the CSN but rarely from both, and could be further subdivided into cells responding with either a single spike or a burst discharge.6. The interaction between the FN and the CSN projections to the paramedian reticular nucleus was examined by conditioning-test studies. Eleven per cent of FN- and CSN-units were inhibited by conditioning stimulation of the heteronymous input. The interaction was exclusively inhibitory and observed only in units with latencies > 4 msec and having burst responses. The latency for inhibition was > 20 msec, peaked around 100 msec and lasted up to 300 msec.7. We conclude that the FRP is buffered by baroreceptors and that there is a mutually inhibitory interaction between projections from the FN and the CSN acting on sympathetic vasomotor neurones. The paramedian reticular nucleus appears to be an important site for the interaction.8. The findings support the view that interneurones mediating pressor and depressor responses are intermixed within the medial reticular formation of the medulla.     

Role of atrial natriuretic peptide in the development of arterial hypertension in patients with pubertal hypothalamic syndrome

The role of a depressor factor, atrial natriuretic peptide, in the development of arterial hypertension in adolescents with pubertal hypothalamic syndrome was studied in 52 patients and 13 healthy males aged 13–24 years. The duration of disease was 2–11 years. Radioimmunological methods were used to measure plasma atrial natriuretic peptide, plasma renin activity, and serum aldosterone. Patients with borderline arterial hypertension were found to have a significant reduction in their atrial natriuretic peptide levels, and this correlated directly with the renin-aldosterone system, demonstrating insufficiency of the depressor system in patients with pubertal hypothalamic syndrome and the involvement of atrial natriuretic peptide in the development of arterial hypertension, along with disturbances in the functional relationship between atrial natriuretic peptide and the renin-aldosterone system. This article was presented at the III All-Russian Congress of Endocrinologists. Samara Medical University. Translated from Problemy éndokrinologii, Vol. 43, No. 4, pp. 21–22, July–August, 1997.     

Changes in intracranial pressure and arterial blood pressure following electric stimulation to restricted regions in the cat brainstem

The brainstem of anesthetized cats was electrically stimulated to examine the changes in the intracranial pressure (ICP). There were pressor and depressor sites, which preferentially produced an immediate increase and decrease in ICP in association with the arterial pressor and depressor responses, respectively. A preferential increase in ICP was also observed by stimulation of some depressor sites. The stimulus-induced ICP responses were usually different from the secondary ICP changes due to nonneurogenic alteration of arterial blood pressure (BP) as evoked by arterial bleeding and infusion of saline solution; the stimulus-induced increase in ICP was greatly enhanced when the stimulation to the pressor sites was applied at lowered BP levels and at moderately elevated ICP levels. In addition, when a gradual elevation in ICP was spontaneously observed with the lowering of the BP level, the pressor site-induced increase in ICP exceeded 70-100 mmHg at the peak plateau-like waves, regardless of the magnitude of accompanying arterial pressor response. We propose that the stimulus-induced ICP responses cannot be explained merely by the metabolic changes, the decreased intracranial compliance, and the secondary transmural action on the intracranial space of the arterial pressor and depressor responses. A neurogenic mechanism that directly affects intracranial blood diameter may be involved in the ICP responses, especially those observed at a lower BP level, in addition to extracranic action of sympathetic and parasympathetic nerve activities.     

Sympathetic hyperresponsiveness to hypothalamic stimulation in young hypertensive rats.

The possible occurrence of central sympathetic dysfunction during development of spontaneous hypertension was studied by recording aortic pressure and sympathetic nerve activity concurrently during electrical stimulation of the posterior hypothalamus in 9-wk-old Kyoto-Wistar rats. Even at this early age, basal levels for both measurements were already elevated significantly in those with spontaneous hypertension. Increases in sympathetic neural firing induced by graded hypothalamic stimulation were always followed by corresponding increases in blood pressure; magnitude of both effects was appreciably larger in spontaneously hypertensive than in normotensive rats, as was the vasodepression caused by blocking autonomic ganglia with pentolinium. By contrast, pressor responses to injected norepinephrine were almost equal thereby suggesting that cardiovascular reactivity was unaltered and that enhanced responsiveness to hypothalamic stimulation was directly due to the concomitant increase in sympathetic nerve activity. Although the exact site from which sympathetic hyperactivity originates was unidentified, our results support the interpretation that sympathetic mechanisms involving the posterior hypothalamus participate in elevating blood pressure during development of spontaneous hypertension in rats.     

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.     

Hypothalamic afferent projections of the aortic nerve

Responses of neurons in the anterior, middle, and posterior hypothalamus to electrical stimulation of the aortic nerve were studied. Two groups of neurons were distinguished in the pressor zones of the hypothalamic region. Changes in the discharges of one group of neurons preceded a fall of arterial pressure in response to stimulation of the aortic nerve. Changes in activity of the other group of neurons occurred after the fall of blood pressure. It is concluded that excitation evoked by stimulation of the aortic depressor nerves and afferent influences from the baroreceptors of the blood vessels arriving during the depressor response spread to neurons of the supraoptic, paraventricular, and ventromedial nuclei of the hypothalamus, the anterior and lateral hypothalamic field, and the supramamillary region.P. K. Anokhin Institute of Normal Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Yudaev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 6, pp. 643–646, June, 1977     

Excitatory projections from the anterior hypothalamus to periaqueductal gray neurons that project to the medulla: a functional anatomical study

The present study was designed to investigate the organization of excitatory projections from regions of the anterior hypothalamus that are known to co-ordinate autonomic and sensory functions to medullo-output neurons in the periaqueductal gray. The induction of Fos protein was used to identify neurons in the periaqueductal gray that were activated synaptically by chemical stimulation at sites in the anterior hypothalamus from which either increases or decreases in arterial blood pressure were evoked (pressor sites and depressor sites, respectively). This was combined with retrograde tracing using fluorescent latex microspheres from sites in the medulla. When compared to control animals, neuronal activation at pressor sites in the anterior hypothalamus evoked Fos-like immunoreactivity in significantly more neurons in all but one sub-division of the periaqueductal gray (P at least < 0.05). The majority of Fos-positive neurons following a pressor response were located in the caudal half of the periaqueductal gray where significantly more neurons contained Fos-like immunoreactivity in lateral than in any other sub-division (P < 0.01). In all but two of 14 subdivisions of the periaqueductal gray, the numbers of neurons that expressed Fos-like immunoreactivity following stimulation at depressor sites in the anterior hypothalamus were not significantly different from controls. When neuronal activation at pressor or depressor sites in the anterior hypothalamus was combined with retrograde tracing from the rostral ventrolateral medulla, nucleus raphe magnus and/or nucleus raphe obscurus the majority of double-labelled neurons were located in the caudal half of the periaqueductal gray. Comparisons between the numbers of double-labelled neurons that resulted from different combinations of hypothalamic and medullary injection sites revealed that neuronal activation at pressor sites in the anterior hypothalamus combined with retrograde tracing from the rostral ventrolateral medulla resulted in the greatest numbers of double-labelled neurons. The identification of double-labelled neurons indicates that medullo-output neurons in the periaqueductal gray receive excitatory inputs predominantly from pressor compared to depressor sites in the anterior hypothalamus. These results are discussed in relation to the roles of the different longitudinal columns of the periaqueductal gray, and the organisation of their projections to the medulla, in the co-ordination of autonomic and sensory functions.     

Participation of adrenal hormones in the genesis of arterial hypertension of hypothalamic origin

Continuous electrical stimulation for many hours of hypothalamic negative emotiogenic centers (the ventromedial nuclei) evoked persistent arterial hypertension with a characteristic phasic dynamics of adrenal secretory activity in waking, immobilized rabbits. Bilateral extirpation of the adrenals lowered the original level of the mean arterial pressure and inhibited the development of persistent arterial hypertension. Stimulation of the above-mentioned hypothalamic structures for many hours in adrenalectomized rabbits, in conjunction with administration of hydrocortisone and adrenalin, evoked persistent arterial hypertension again. After administration of hydrocortisone and adrenalin separately to adrenalectomized rabbits, stimulation of the ventromedial hypothalamic nuclei for many hours resulted in only a transient rise of blood pressure. It is concluded that an essential role in the formation of persistent arterial hypertension in rabbits during continuous stimulation of the hypothalamic negative emotiogenic centers for many hours is played by activation of adrenal cortical and medullary hormones.Department of Normal Physiology and Interclinical Hormonal Laboratory, I. M. Sechenov First Moscow Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 4, pp. 399–402, April, 1976.     

Analysis of the reflex changes in the cardiovascular system following stimulation of the pericardial chemoreceptors. Report 2. The role of the heart and of various vascular fields in the development of the pressor reaction

Summary Acute experiments were staged on cats under urethane anesthesia. As demonstrated, stimulation of pericardial chemoceptors by nicotine solution caused various arterial pressure changes: depressor, pressor or depressor-pressor reaction. As demonstrated in report 1,in effecting the pressor reaction the leading role was played by the vessels of the lungs, which deposited the blood as well as by decelerated cardiac rhythm. Stimulation of the pericardial chemoceptors by the nicotine pressor reaction was accompanied by reduction of the strength of cardiac conditions and often sistance of the vessels of the spleen, small intestine, kidneys, pelvic area and of extremities always increases. In experiments with temporary exclusion of various vascular areas from the general circulation it was shown that the main role in the rise of arterial pressure belonged to the vessels of the small intestine and of the spleen. Bilateral section of the splanchnic nerves and adrenalectomy eliminated the indicated pressor reaction. Participation of the hurnoral link in effecting this reaction was demonstrated in experiments on the isolated frog hearts.A rise in arterial pressure in depressor-pressor reaction, which is a reflex compensation in response to the preceding arterial pressure reduction, is connected with the stimulation of the baroceptors of the sinocarotid and aortic zones and the effect from them on adrenal secretion.(Presented by Active Member AMN SSSR P. S. Kupalov) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 55, No. 1, pp. 12–17, January 1963     

Differential cardiovascular changes as a function of stimulation electrode site in rabbit hypothalamus

Twenty chronically prepared, unanesthetized rabbits received both high-frequency (200 pulse/sec), short pulse-train (1.0 sec) and relatively low-frequency (25 pulse-sec), long pulse-train (10 sec) electrical stimulation of the hypothalamus. High-frequency, short pulse-train stimulation elicited a pressor response and bradycardia at all 27 electrode sites. In contrast, three other cardiovascular response patterns were obtained following low-frequency, long pulse-train stimulation. These latter patterns reflected a medial-lateral organization of autonomic function within the hypothalamus. Whereas all 15 lateral hypothalamic placements yielded depressor responses, 7 of 12 medial hypothalamic placements yielded pressor responses and tachycardia. Cardiovascular changes following administration of selective autonomic blocking agents (e.g., phentolamine, propranolol, methylatropine) suggest that high-frequency, short pulse-train stimulation elicited a pressor response followed by a reflexive bradycardia essentially mediated by an increase in vagal restraint. In contrast, the heart rate changes observed to low-frequency, long pulse-train stimulation all appear to have been importantly influenced by changes at the heart in beta-adrenergic activity.     

Classically Conditioned Blood Pressure Decreases Induced by Electrical Stimulation of Posterior Lateral Hypothalamus in Rabbits

An experimental group of 5 rabbits received 5 acquisition sessions during which repeated presentation of a 550 Hz tone for 10 sec as the conditioned stimulus (CS) was always followed immediately by 25 pulse per sec, 10 sec train-duration stimulation of the posterior lateral hypothalamus as the unconditioned stimulus (US). A control group of 5 rabbits received random presentations of the CS and US. The unconditioned responses (URs) to intracranial stimulation consisted of tachycardia and a depressor response; conditioned responses (CRs) consisted of depressor responses unaccompanied by systematic changes in heart rate. Neither systematic heart rate nor blood pressure responses occurred to the CS in the control group. The present results contrast with those of previous studies in rabbits in which higher frequency, shorter pulse-train hypothalamic stimulation as US induced a pressor response and reflexive bradycardia as URs, and bradycardia unaccompanied by blood pressure changes as CRs. It is concluded that hypothalamic stimulation as US permits more than one cardiovascular response pattern to be studied under controlled conditions during classical conditioning.     

Functional organization of the bulbar vasomotor center

Summary Experiments were carried out on cats under urethane anesthesia. A study was made of pressor and depressor points in the reticular formations of medulla oblongata. The vasomotor effects were recorded by local stimulation with electric current with different parameters of retangular impulse. The data obtained show the following: 1) there was no strict space division between the groups of neuronal elements with pressor and depressor function: both of them were present in all the formations studied; however, the pressor ones were more frequently encountered in the rostrolateral, whereas depressor — in the mediocaudal formations; 2) both types of neuronal elements, some of which when stimulated provoked only a pressor, while others - only a depressor effect, possess different specialized functions and their excitability in response to the parameters of the stimulating current differed: diverse frequency optimums, length of the current impulse, and intensity thresholds. Neuronal elements within each type also differed by their excitability; 3) alteration of the functional state of the neuronal elements by local polarization and reflexly led to changes of their excitability, which could have different directions in the neuronal elements with pressor and depressor function.(Presented by Active Member AMN SSSR V. V. Parin) Translated from Byullenten' Éksperimental'noi Biologii i Meditsiny, Vol. 55, No. 4, pp. 3–9, April, 1963     

Electroencephalographic changes in hypo- and hypertensive responses to hypothalamic stimulation

Changes in cortical and subcortical electrical activity during hypo- and hypertensive vascular responses to electrical stimulation of the hypothalamus were investigated before and after injection of the monoamine oxidase inhibitor vetrazin, in experiments on rabbits anesthetized with urethane. Vetrazin completely blocked the hypertensive response and its electroencephalographic manifestation but had no effect on hypotensive hypothalamic responses. The results are interpreted from the standpoint of differences in the neurochemical mechanisms of hypothalamic pressor and depressor responses.Department of Normal Physiology, I. M. Shechenov First Moscow Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 5, pp. 528–531, May, 1976     

Analysis of hemodynamic responses to hypothalamic stimulation in waking animals

Experiments on waking cats showed that electrical stimulation of protective zones of the hypothalamus leads to development of hypertension and inhibits baroreceptor reflexes. In animals with divided carotid sinus and aortic nerves, threshold hypothalamic stimulation leads to the appearance of depressor responses, whereas above-threshold stimulation evoked depressor-pressor responses. It is suggested that depression of baroreceptor reflexes is one of the mechanisms of the development of hypertension in response to hypothalamic stimulation.Department of Experimental Physiology and Pharmacology, Central Research Laboratory, I. P. Pavlov First Medical Institute, Leningrad. (Presented by Academician of the Academy of Medical Sciences of the SSSR N. P. Bekhtereva.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 9, pp. 281–283, September, 1979.     

The hypothalamus and hypertension

Most forms of hypertension are associated with a wide variety of functional changes in the hypothalamus. Alterations in the following substances are discussed: catecholamines, acetylcholine, angiotensin II, natriuretic peptides, vasopressin, nitric oxide, serotonin, GABA, ouabain, neuropeptide Y, opioids, bradykinin, thyrotropin-releasing factor, vasoactive intestinal polypeptide, tachykinins, histamine, and corticotropin-releasing factor. Functional changes in these substances occur throughout the hypothalamus but are particularly prominent rostrally; most lead to an increase in sympathetic nervous activity which is responsible for the rise in arterial pressure. A few appear to be depressor compensatory changes. The majority of the hypothalamic changes begin as the pressure rises and are particularly prominent in the young rat; subsequently they tend to fluctuate and overall to diminish with age. It is proposed that, with the possible exception of the Dahl salt-sensitive rat, the hypothalamic changes associated with hypertension are caused by renal and intrathoracic cardiopulmonary afferent stimulation. Renal afferent stimulation occurs as a result of renal ischemia and trauma as in the reduced renal mass rat. It is suggested that afferents from the chest arise, at least in part, from the observed increase in left auricular pressure which, it is submitted, is due to the associated documented impaired ability to excrete sodium. It is proposed, therefore, that the hypothalamic changes in hypertension are a link in an integrated compensatory natriuretic response to the kidney's impaired ability to excrete sodium.     

Somatosensory and hypothalamic inhibitions of baroreflex vagal bradycardia in rats

Somatosensory and forebrain mechanisms inhibiting arterial baroreflexes were investigated in chloraloseurethane anesthetized and artificially ventilated rats. Electrical stimulation of the sciatic nerve (ScN) and the hypothalamic pressor area (HP) suppressed baroreflex vagal bradycardia (BVB) and hypotension provoked by electrical stimulation of the aortic depressor nerve (ADN). Suppression of BVB was more marked, but inhibitory potencies of ScN and HP were not different. These two inhibitions were considered to have a functional implication in common, since both were accompanied by increase in hindlimb vascular conductance. A variety of experiments were conducted to localize the target site of ScN and HP inhibitions of BVB. Either ScN or HP stimulations was without effect on antidromic compound spike potentials along ADN evoked by microstimulation of the nucleus tractus solitarius (NTS), precluding the possibility of these inhibitions being presynaptic. Both ScN and HP stimulation suppressed ADN-induced field potentials in the NA region which provoked vagal bradycardia upon microstimulation, but failed to affect ADN-induced responses, either field or unitary, in the NTS region. Antidromic unitary responses in the NA region to vagus cardiac branch stimulation were suppressed by ScN and HP stimulations in NTS-lesioned rats. Intracisternal bicuculline, a GABA antagonist, was found to abolish both ScN and HP inhibitions of BVB, while intracisternal muscimol, a GABA agonist, eliminated bradycardia. These findings suggest that somatosensory and forebrain inhibitions of BVB occur principally at the preganglionic cell level and are probably mediated by a GABAergic mechanism.     

Circulating angiotensin II attenuates the sympathetic baroreflex by reducing the barosensitivity of medullary cardiovascular neurones in the rat

Chronic intravenous angiotensin II (Ang II) has been widely used to establish centrally mediated hypertension in experimental animals, and disruption of Ang II activity is a frontline treatment for hypertensive disease. However, the acute central actions of circulating Ang II are poorly understood. We examined the effects of intravenous pressor doses of Ang II on autonomic activity in anaesthetized rats under neuromuscular blockade, and compared baroinhibition evoked by Ang II pressor ramps to equipressor responses evoked by phenylephrine (PE). Baroinhibition of splanchnic sympathetic nerve activity was attenuated during Ang II trials compared with PE, and rats remained sensitive to electrical stimulation of the aortic depressor nerve at higher arterial pressures during Ang II trials. This was not due to a direct effect of Ang II on aortic nerve baroreceptors. In a separate series of experiments, we provide direct evidence that bulbospinal barosensitive neurones in the rostral ventrolateral medulla are differentially sensitive to pressure ramps evoked by Ang II or PE vasoconstriction. Nineteen out of 41 units were equally sensitive to increased arterial pressure evoked by Ang II or PE. In 17 of 41 units, barosensitivity was attenuated during Ang II trials, and in five of 41 cases units that had previously been barosensitive increased their firing rate during Ang II trials. These results show, for the first time, that circulating Ang II acutely modulates central cardiovascular control mechanisms. We suggest that this results from activation by Ang II of a central pathway originating at the circumventricular organs.     

The role of the solitary and paramedian reticular nuclei in mediating cardiovascular reflex responses from carotid baro- and chemoreceptors

1. With dye-filled micro-electrodes single neurones in the medulla of anaesthetized paralysed cats were identified which: (a) fired rhythmically in synchrony with or were modulated by the cardiac cycle, and which ceased firing with occlusion of the ipsilateral common carotid artery (carotid sinus baroreceptor neurones); (b) were excited by stimulation of carotid body chemoreceptors by close intra-arterial injection of lobeline into the thyroid artery (carotid body chemoreceptor neurones).2. Twelve carotid baroreceptor neurones were identified, in thirty-three cats, nine of which were localized in the intermediate area of the nucleus of the solitary tract (NTS) within 1 mm ahead of or behind the obex; three units were located either in the parahypoglossal area or the dorsal portion of the paramedian reticular nucleus (PRN).3. Of the twenty-one carotid chemoreceptor neurones which were identified, thirteen were localized in the NTS, three in the parahypoglossal area and four in the dorsal PRN.4. Bilateral lesions of the paramedian reticular area of medulla destroying the PRN, abolished or reversed the depressor response to electrical stimulation of myelinated fibres of the carotid sinus nerve (CSN), attenuated the depressor response to carotid sinus stretch and augmented the pressor response to chemoreceptor stimulation by lobeline. Such lesions did not significantly alter the reflex heart rate responses.5. Small lesions of the NTS within an area 1 mm rostral to the obex abolished all reflex blood pressure and heart rate responses to electrical stimulation of the CSN or natural stimulation of carotid baro- or chemoreceptors.6. Baroreceptors and chemoreceptors of the CSN project both to the intermediate zone of the NTS and to more medial areas of the medulla, particularly the dorsal PRN and parahypoglossal area.7. The PRN serves to mediate the reflex depressor, but not cardio-vagal, response from myelinated baroreceptors and buffers the pressor responses from chemoreceptors; it may serve as an important area integrating cardiovascular activity descending from forebrain, brain stem and cerebellum with baroreceptor reflexes.8. Cardiovascular reflex responses arising from non-myelinated baroreceptors and all chemoreceptors are mediated by neurones in the intermediate area of the NTS.     

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.