Effects of morphine on somatocardiac sympathetic reflexes in spinalized cats

The effects of morphine on sympathetic reflexes, recorded in the inferior cardiac nerve, to myelinated A and unmyelinated C afferent stimulation were tested in 17 acutely spinalized cats. Stable sympathetic A and C reflexes of short latency (approximately 30 ms and 140 ms in the case of the ulnar nerve, respectively) could be recorded in the inferior cardiac sympathetic nerve to stimulation of somatic A and C afferents in the ulnar and upper thoracic intercostal nerves, ipsilaterally. Spinal sympathetic A reflexes, which were primarily evoked from stimulation of A delta afferent fibers, could be elicited from more segmental levels than could sympathetic C reflexes. Additionally, smaller reflexes, only from A afferent fiber activation, were identified from stimulations on the contralateral side of the body. Small doses of morphine (0.02 mg kg-1, i.v.) proved to be ineffective at altering sympathetic A and C reflexes, while somewhat larger doses (0.2 mg kg-1, i.v.) produced a clear 62% decrease in C reflexes and a 33% decrease in A reflexes, Dosages of 1 and 2 mg kg-1 severely depressed both A and C reflexes. All of the above effects of morphine administration were completely and immediately reversible by naloxone (i.v.). The results are discussed with regard to the effects of morphine on sympathetic A and C reflexes in CNS intact, anesthetized cats.     

Organ-localized hypothalamic-stimulated vasculature changes in the cat

Stimulation of specific lateral hypothalamic targets in a cat model induces vascular and/or cardiac changes. Evidence is presented that these may consist of discretely localized sympathetically mediated changes taking place in just one or two organs. Morever, following stimulation of either one of two adjacent lateral hypothalamus sites, pressor effects are induced that superficially look similar, but prove to be mediated by different pathways. To investigate possible synapsing at sympathetic ganglia, e.g. in superior cervical or stellate ganglia, 50 µg atropine methyl nitrate, a ganglionic blocker, was applied directly to the ganglia. This was shown to potentiate the pressor effects, in some cases when applied to the superior cervical ganglia, in others to stellate ganglia, presumably by blockade of a ganglionic attenuating mechanism. The contributions made by different sympathetic nerves to the lateral hypothalamus-induced pressor effect were analysed. Stimulation of one of the lateral hypothalamus sites (TAR.I) in eight cats induced a pressor effect that was abolished by severing a nerve branch, from the superior cervical ganglia laterally, shown to innervate neck muscle vasculature. In another group of nine cats stimulation of TAR.II induced a pressor effect abolished by cutting a branch from the superior cervical ganglia medially, shown to be destined to the vasculature of pharyngeal muscles and possibly lower respiratory tract. The hypothesis that central control via the sympathetic nervous system is responsible for differential organ specific regulation of blood flow to individual organs is discussed.     

Comparative study of sympathetic and parasympathetic discharges in the autonomic nerves during stimulation of different structures of the cat hypothalamus

Simultaneous recordings of hypothalamo-parasympathetic and hypothalamo-sympathetic evoked discharges in anesthetized cats demonstrated that both parasympathetic discharges in the pelvic nerve and sympathetic discharges in the splanchnic nerve of the lowest threshold and shortest latency could be obtained from stimulation of the posterior hypothalamus. The focus of the maximal neuronal activated elicited by stimulation of afferent fibres of visceral nerves and the focus evoking maximal efferent reactions of parasympathetic and sympathetic nerves were located in the same region of the postero-lateral hypothalamus. It is supposed (as a working hypothesis) that convergent polysensory neurons of the hypothalamus are also polyeffector divergent elements of the hypothalamo-visceral reflex system.     

The involvement of the sympathetic nervous system in the centrogenic pressor and tachycardiac effects of prostaglandins E2 and F2 alpha in anaesthetised cats

The intracerebroventricular (i.c.v.) administration of prostaglandin E2 (PGE2, 1 micrograms) and prostaglandin F2 alpha (PGF2 alpha, 10 micrograms) produced prolonged pressor and tachycardiac responses in chloralose-anaesthetised cats. Phenoxybenzamine-pretreatment completely prevented the pressor response without altering the tachycardiac response, whereas propranolol intervention completely inhibited the tachycardiac response and also attenuated the pressor response. The pretreatment with pentolinium completely antagonised both the pressor and tachycardiac responses to i.c.v. PGE2 and PGF2 alpha. The results suggest that the centrally administered PGE2 and PGF2 alpha augment sympathetic outflow to the heart and vascular system and thereby cause excitatory cardiovascular responses in anaesthetised cats.     

Prolonged inhibition of rostral ventral lateral medullary premotor sympathetic neurons by electroacupuncture in cats

We have shown that electroacupuncture (EA) at the Neiguan-Jianshi (N-J) acupoints over the median nerve reduces myocardial ischemia by modulating the pressor response induced by application of bradykinin on the gallbladder. The present study was designed to investigate the neural substrate underlying the prolonged modulatory effect of EA on visceral afferent input into the rostral ventral lateral medulla (rVLM). Experiments were performed on ventilated anesthetized cats. Neuronal activity was recorded while either stimulating the splanchnic nerve or applying EA at the N-J acupoints. Thirty-three cells responsive to splanchnic nerve and median nerve stimulation were antidromically driven from the intermediolateral columns, T(2)-T(4), indicating their function as premotor sympathetic neurons. These neurons also received baroreceptor input demonstrating that they were cardiovascular sympathoexcitatory cells. Arterial pulse-triggered averaging and coherence analysis demonstrated a correlation between cardiac-related discharge activity with 2.8+/-0.3 Hz rhythms and arterial blood pressure. Stimulation (2 Hz, 1-4 mA, 0.5 ms) of the splanchnic nerve for 30 s evoked excitatory responses. These neuronal responses were reduced during and after 30-min stimulation of EA at the Neiguan-Jianshi acupoints. These splanchnic nerve-induced excitatory responses in neurons subjected to 30 min of EA were reduced by 68%. Iontophoresis of naloxone promptly reversed the EA-induced inhibitory effect by 52%. Neuronal activity in the rVLM induced by splanchnic nerve stimulation was reduced for 50 (or more) min after termination of EA in 7 of 12 rVLM neurons.Our results indicate that rVLM premotor sympathetic cardiovascular neurons receive convergent input from the gallbladder through the splanchnic nerve and N-J acupoints through the median nerves. Through an opioid mechanism, EA inhibits splanchnic nerve-induced excitatory responses of these rVLM neurons. Many of these neurons receiving convergent visceral and somatic input exhibit long-lasting inhibition by EA.     

Evidence for a central depressor action of postsynaptic alpha 1-adrenergic receptor antagonists

The effects of alpha-adrenergic receptor antagonists on sympathetic nervous discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor intact and denervated cats. Prazosin (50 microgram/kg, i.v.) produced a rapid fall in mean arterial pressure (MAP) and no significant change in heart rate (HR) in baroreceptor denervated cats. Prazosin administration was also associated with a prolonged inhibition of SND. Nerve activity was significantly reduced within 5 min of prazosin administration remained depressed throughout the 2 h observation period. Like prazosin, WB-4101 (0.5 mg/kg, i.v.) also produced significant reductions in MAP and SND. In addition, WB-4104 produced a transient bradycardia. The decreases in MAP and SND were reversed by piperoxane (0.5 mg/kg, i.v.). Both prazosin and WB-4101 inhibited the pressor response to i.v. norepinephrine. In baroreceptor intact cats, prazosin decreased MAP and SND, but did not affect HR. In contrast, phentolamine (1 mg/kg, i.v.) decreased MAP but increased SND and HR. These data indicate that the sympatholytic action of WB-4101 and prazosin results from a centrally mediated reduction in SND as well as a peripheral blockade of alpha-adrenergic receptors. These data further suggest that noradrenergic neurons normally facilitate the outflow of sympathetic nerve activity from the central nervous system.     

Sympathetic control of antral and pyloric electrical activity in the rabbit

The effects of section and stimulation of the sympathetic nerve trunk on gastric motility were investigated in conscious and decorticate rabbits. In conscious animals after section of the abdominal splanchnic nerve, rhythm of antral and pyloric bursts was enhanced, becoming more regular, and the period of arrest of the rhythmic bursts, which was usually observed at the end of inflation of the antrum in intact rabbits, was shortened to 33.6 +/- 4.0 s from 112.2 +/- 14.6 s observed before the sympathetic nerve transection. Adrenergic agonists, phenylephrine (100 micrograms/kg), clonidine (5 micrograms/kg) and salbutamol (1 mg/kg) inhibited antral and pyloric activity. In decorticate rabbits the major effect of stimulation of the peripheral or the central end of the thoracic sympathetic trunk was inhibition; this was seen both with the spontaneous and vagally induced e.m.g. activity of the antrum and pylorus. Inhibition induced by stimulation of sympathetic efferents was abolished by beta-blocking agents and that induced by stimulation of the sympathetic afferents disappeared after alpha-adrenergic block. Significance of a dual control of the gastric motility by the sympathetic nerve was discussed.     

Bilateral carotid occlusion and the sympathetic regulation of insulin secretion

After a 2-min bilateral carotid arterial occlusion (BCO) in puppies, a centrally originating, sympathetic discharge takes place which increases heart rate and blood pressure. We examined the specificity of this sympathetic neural outflow by determining whether it also caused a direct neurally mediated inhibition of insulin release from the pancreas. The effects of this BCO on portal venous insulin concentrations, as well as on heart rate and blood pressure, were examined during i.v. glucose infusions of 0 (saline), 5 and 15 mg/kg X min-1. To determine changes in splanchnic blood flow and to more closely estimate pancreatic insulin secretion rates, a major vein draining the pancreas, the gastroduodenal, was catheterized. Blood flows and the amount of insulin traversing this vein per min (insulin flow rate) were followed before, during and after BCO. BCO decreased portal vein insulin concentrations during i.v. glucose infusions of 5 and 15 mg/kg X min-1, but not when saline was infused. Since bilateral splanchnicotomy altered this result little and since BCO increased blood flow and the insulin flow rate in the gastroduodenal vein, it appears that the lower portal venous insulin concentrations during BCO are secondary, not to sympathetically induced decrease in insulin secretion rates but, to dilution of pancreatic effluent blood. We conclude that while BCO causes appropriate changes in heart rate and blood pressure, this central stimulus to the sympathetic system does not provide a direct neuroendocrine reflex change in insulin secretion. BCO alters portal venous insulin concentration indirectly, and the alteration depends on the plasma glucose concentration and an enhancement in the splanchnic blood flow.     

Importance of spinal noradrenergic pathways in cardiovascular reflexes and central actions of clonidine and alpha-methyldopa in the rabbit

We have examined in conscious rabbits the chronic effects of 6-hydroxydopamine (6-OHDA)-induced local lesions of the spinal noradrenaline (NA) pathways on (i) resting mean arterial pressure (MAP) and heart rate (HR), (ii) the nasopharyngeal pressor response, (iii) the sympathetic component of the baroreceptor-heart rate reflex (iv) the acute responses to intracisternal (i.c.) clonidine and alpha-methyldopa (alpha-MD), and (v) the acute NA release response produced by i.e. 6-OHDA. One month after injection of 6-OHDA (40 nmol in 4 microliters) into the first cervical spinal cord segment (C1), the NA content was reduced to 29% in C2, 45% in T4 and 61% in L3 with little non-specific damage. Basal MAP was 14% higher (P less than 0.05) than in sham-operated rabbits suggesting increased vasoconstrictor tone. Basal cardiac sympathetic tone was enhanced, but a corresponding increase in cardiac vagal tone resulted in little net effect on resting HR in the spinal NA-depleted group. Spinal NA lesions attenuated the nasopharyngeal pressor reflex by 27% in baroreceptor-intact rabbits and by 38% in sino-aortically denervated (SAD) animals. The lesion did not affect HR range, gain and BP50 of the sympathetic baroreflex. In SAD rabbits, the acute MAP responses to i.c. 6-OHDA (early hypotension, late hypertension) were not affected by spinal NA depletion, but the early fall in HR (cardiac sympathetic inhibition) was abolished. The hypotension produced by i.c. clonidine or alpha-MD was not affected by the lesion, probably because many of the NA terminals in the lower thoracic and upper lumbar cord were still intact. Our results suggest that intraspinal NA fibers have a tonic inhibitory action on spinal preganglionic vasoconstrictor and cardiac motoneurons. The spinal NA neurons affecting vasomotor tone (but not cardiac sympathetic tone) are in turn inhibited by higher vasomotor centers receiving projections from the arterial and trigeminal afferents and thereby participate in vasoconstrictor reflexes.     

Reciprocal and non-reciprocal action of the vagal and sympathetic nerves innervating the heart

Simultaneous recordings were made from vagal and sympathetic fibers innervating the heart in dogs anesthetized with chloralose. Reciprocal relationship between the two autonomic nerves was clearly seen in the baroreceptor reflex. Stimulation of chemoreceptors, however, evoked non-reciprocal responses of the two nerves; at the onset of the chemoreceptor reflex cardiac vagal and sympathetic discharges both increased, then, as baroreceptors became excited due to a pressor response, sympathetic nerve activity suddenly decreased while vagal discharges remained high, indicating the appearance of the reciprocal action typifying the baroreceptor reflex. Decrease in ventilatory volume and a slight increase in end-expired CO2 level augmented greatly both vagal and sympathetic discharges. As the phrenic-locked activity of the two nerves (i.e. the activity in vagus nerve occurs only in the absence of phrenic bursts while sympathetic discharges increase with phrenic bursts) increased, the alternate discharges between the two nerves became more conspicuous and the heart rate fluctuated with the respiratory (phrenic) rhythm. Thus, strong reciprocity between vagus and sympathetic can result in an oscillatory heart rate. When ventilatory volume was increased, both nerve activities decreased below control level. Mild hypoxia had similar effects to hypercapnia though changes in nerve activity were greater. When coactivation of vagal and sympathetic nerve was produced in reflex action, changes in vagal discharges occurred earlier and faster than in the sympathetic fibers. The magnitude of change in vagus activity was also far greater. The elimination of afferents in the vagi, the aortic and sinus nerves reduced cardiac vagal activity greatly. However, discharges were still present and occurred between phrenic bursts, indicating that the vagal "tone" is maintained centrally as well as peripherally by input from receptors in the cardiovascular system. The physiological significance of reciprocal and non-reciprocal control of vagal and sympathetic nerves innervating the heart was discussed.     

Alpha2 adrenoceptors modulate the nociceptive jaw-opening reflex in rats

The jaw-opening reflex in lightly anesthetized rats induced by intrapulpal (left maxillary) electrical tooth pulp stimulation and quantified by the electromyograms (threshold values) recorded from the ipsilateral digastric muscle was used as the experimental pain index. The threshold for the jaw-opening reflex was significantly elevated by clonidine (12.5 to 50 micrograms/kg, i.v.) and was inversely correlated with the frequency of stimulation. The analgesia elicited by clonidine was antagonized by pretreatment with the alpha 2-adrenoceptor antagonist yohimbine (1 mg/kg, i.v.). All doses of clonidine produced an initial transient pressor response followed by a sustained hypotension and bradycardia. However, there was no direct correlation between the antinociceptive and cardiovascular effects of clonidine. It is proposed that clonidine modulates jaw-opening reflex analgesia by specifically activating alpha 2-adrenoceptors.     

The involvement of the sympathetic nervous system in the centrogenic pressor and tachycardiac effects of prostaglandins E2 and F2α in anaesthetised cats

The intracerebroventricular (i.c.v.) administration of prostaglandin E₂ (PGE₂, 1 μg) and prostaglandin F_2α (PGF_2α, 10 μg) produced prolonged pressor and tachycardiac responses in chloralose-anaesthetised cats. Phenoxybenzamine-pretreatment completely prevented the pressor response without altering the tachycardiac response, whereas propranolol intervention completely inhibited the tachycardiac response and also attenuated the pressor response. The pretreatment with pentolinium completely antagonised both the pressor and tachycardiac responses to i.c.v. PGE₂ and PGF_2α. The results suggest that the centrally administered PGE₂ and PGF_2α augment sympathetic outflow to the heart and vascular system and thereby cause excitatory cardiovascular responses in anaesthetised cats.     

Efferent discharges of sympathetic and parasympathetic nerve fibers during increased intracranial pressure in anesthetized cats in the absence and presence of pressor response

Efferent discharges of the cervical sympathetic cardiovascular and vagal type 1 fibers in response to increased intracranial pressure (ICP) were simultaneously recorded in cats anesthetized with pentobarbitone and ventilated artificially. Sympathetic outflow of renal nerve fibers was also recorded in some animals. The type 1 fibers were assumed to be cardiac vagal fibers, from the response behavior such a pulse-synchronicity to respiratory and heart rhythm, reflex activation from arterial baroreceptors and reciprocal relationship of the activity to sympathetic ones during slower fluctuations of hemodynamic changes, and which occur spontaneously during Mayer waves. The vagal type 1 discharges increased to various amplitudes with increase in ICP and in the absence and the presence of pressor response. Efferent outflow of the renal and cervical sympathetic fibers frequently decreased with a moderate increase in ICP. There was a slight decrease or no apparent change in the blood pressure, and a higher elevation of ICP ensued. Heart rates decreased with increase in ICP, while the rate frequently increased with levels of ICP over about 120 mm Hg. Changes in the vagal and sympathetic discharges always began at a time before the initiation of cardiovascular response to the elevated ICP. However, when ICP was repeatedly increased, the increase in vagal discharges progressively decayed and was accompanied by vigorous sympathetic firings and a marked pressor response. The sympathetic outflow also decayed following the decrease in vagal activities. The present findings of changes in the vagal type 1 discharges demonstrate clear participation of parasympathetic as well as sympathetic nerve activity in the occurrence of cardiovascular responses to increased ICP. Changes in both these autonomic nerve responses may explain the initial fall in arterial blood pressure and pressor responses associated with bradycardia or tachycardia, at different levels of elevated ICP.     

Responses of T2-T4 spinal neurons to stimulation of the greater splanchnic nerves of the cat

Effects of electrical stimulation of the greater splanchnic nerves on T2-T4 spinal neurons were determined in 16 cats anesthetized with alpha-chloralose. Of 77 neurons responding to somatic stimuli, 65 (84%) were excited, inhibited, or both excited and inhibited by splanchnic input. Each of the splanchnic responsive cells also was responsive to electrical stimulation of cardiopulmonary sympathetic afferent fibers. All but one neuron with left splanchnic input also received input from the right splanchnic nerve. Short- and long-latency excitatory responses were observed after splanchnic stimulation. The cell response to splanchnic stimulation was greatly inhibited by a conditioning stimulus applied to the other splanchnic nerve. A similar, although weaker, interaction occurred between splanchnic and cardiopulmonary sympathetic afferent fibers. The activity of 17 cells was inhibited by repetitive stimuli applied to one or both splanchnic nerves. Cells were found in laminae I, IV, V, VII, and VIII. These data provide the first evidence for splanchnic modulation of upper thoracic dorsal horn neurons.     

Antiepileptic and prophylactic effects of tetrahydrocannabinols in amygdaloid kindled cats.

Acute administration of delta8-tetrahydrocannabinol (delta8-THC) or delta9-THC failed to affect partially developed or fully developed kindled amygdaloid seizures in cats. However, delta9-THC was quite effective in suppressing focal AD in the stimulated amygdala when administered very early in kindling, before the development of any clinical manifestations. This finding suggested that chronic administration of delta9-THC during kindling might block the process of seizure development, which was supported by the observation that three of four cats failed to kindle when treated with the drug. The cat that failed to be protected by delta9-THC was also insensitive to the general electroclinical effects of moderately high doses of delta9-THC. The prophylactic activity of delta9-THC is in contrast to the ineffectiveness of diphenylhydantoin, a drug whose anticonvulsant activity is often compared with that of THC.     

Evidence for sar1-ala8-angiotensin crossing the blood cerebrospinal fluid barrier to antagonize central effects of angiotensin II.

Injections of angiotensin II into the cerebral ventricles of the rat produces both a drinking and a pressor response. We have measured both responses simultaneously in conscious animals. The effect of saralasin acetate (P113), a specific angiotensin II competitive antagonist, has been studied on these angiotensin II induced responses. The results show that: (1) P113 given intravenously (i.v.) in doses of 500 ng/min or 1800 ng/min has no observable effect on 50 ng angiotensin given intraventricularly (IVT). At 72 mug/min, however, there was a 55% reduction in the drinking and pressor responses to 50 ng angiotensin II (IVT); (2) 500 ng of P113 given IVT abolished the effects of 50 ng angiotensin II also given IVT and (3) P113 given i.v. at all doses antagonized the pressor effects of angiotensin II (i.v.) responses. The data indicate that both the drinking and pressor responses to angiotensin II (IVT) injections are centrally mediated and show that when a high enough dose of P113 is given peripherally the central effects of angiotensin II can be reduced. This suggests that a fraction of the P113 injected i.v. may pass across the blood-CSF barrier. Since P113 has a similar structure to angiotensin II the results have implications for studies in which high peripheral doses of angiotensin II are used.     

Hypothalamic stimulation counteracts sympathetically mediated gastrointestinal inhibition in chloralose-anaesthetised cats

The inhibitory motor effect of the sympathetic gastrointestino-gastrointestinal (GI-GI) reflex was studied in cats with isolated innervated ileal (Thiry-Vella) loops. They were subjected to acute experiments under chloralose-gallamine anaesthesia where gastric volume, arterial blood pressure and heart rate were continuously monitored. The cervical vagi were sectioned and used for efferent stimulation. The hypothalamus was systematically explored by means of stereotaxically guided electrodes. When the abdomen was undisturbed, gastric contractile responses to central stimulation were virtually absent, regardless of whether a vagally induced tone was present or not. Distension of the isolated intestinal loop induced marked inhibition of vagally induced gastric tone, indicating activation of the GI-GI reflex. Under these conditions, about 17% of the hypothalamic points induced gastric excitation, due to withdrawal of sympathetic tone. The GI-GI reflex can thus be inhibited from diencephalic levels. This inhibition is not linked to any distinct cardiovascular 'pattern'.     

Cardiovascular effects of central administration of clonidine in conscious cats

The effects on arterial blood pressure and heart rate after an intracerebroventricular (i.c.v.) administration of clonidine were investigated using conscious normotensive cats. Injection of clonidine (5–10 μg; 5 μl; i.c.v.) elicited a decrease in mean arterial pressure (MAP) and heart rate (HR) in a dose-dependent manner. The highest dose of 10 μg of clonidine decreased MAP and HR by 39 ± 3 mmHg and 74 ± 5 b.p.m., respectively (n = 7). Pretreatment with yohimbine, the α₂-adrenoceptor antagonist (8 μg; 5 μl; i.c.v.) blocked the cardiovascular responses to a subsequent i.c.v. injection of 10 μg clonidine (n = 7). Furthermore, preadministration of cimetidine (100 μg; 5 μl; i.c.v.), the H₂ histamine receptor antagonist with imidazoline receptor activating properties, prevented the decreases in MAP and HR to a subsequent i.c.v. injection of 10 μg clonidine (n = 7). By contrast, pretreatment with the specific I₁ imidazoline receptor blocker, efaroxan (100–500 μg; 5 μl; i.c.v.), failed to inhibit the cardiovascular effects of an i.c.v. administration of 10 μg clonidine (n = 7). These results suggest that the effects of centrally administered clonidine on MAP and HR are probably not mediated through activation of the I₁ subtype of imidazoline receptors in conscious cats. However, the cardiovascular effects elicited by i.c.v. administration of clonidine appear to result from stimulation of central α₂-adrenergic or the H₂ histaminergic-like receptors.     

Precollicular decerebration reduces the pressor responses evoked by stimulation of rostral pons but not medulla in cats

In 30 cats under chloralose (40 mg/kg) and urethane (400 mg/kg) anesthesia, the ponto-medullary region involved in cardiovascular integration were stimulated by rectangular pulses (0.5 ms, 80 or 5 Hz, 100 to 200 μA) and/or by microinjection of sodium glutamate (Glu, 0.25–0.5 M, 70–200 nl). Changes of systemic arterial blood pressure (SAP) and renal sympathetic nerve activity (RNA) following stimulation were compared before and after precollicular decerebration. Precollicular decerebration itself resulted in an immediate but brief (5 to 15 min) hypotension with a decrease in SAP ranging from 40 to 100 mmHg. Stimulation of the lateral tegmental field (FTL) produced depressor responses. After precollicular decerebration, the stimulation induced depressor responses were either abolished or converted to mild pressor responses. Stimulation of the dorsal gigantocellular tegmental field-periventricular grey (dFTG-PVG) produced pressor responses. These responses were abolished after precollicular decerebration without exception. On the other hand, precollicular decerebration did not reduce pressor responses produced by stimulation of the ventrolateral medulla (VLM) and the dorsal medulla (DM). In 7 additional cats killed with an overdose of pentobarbital, the brain stem were processed for dopamine β-hydroxylase (DBH). The pressor areas of the VLM and DM were DBH positive, indicating the presence of norepinephrine, while the dFTG-PVG and FTL were not. These findings suggest that the depressor mechanism of the FTL and the pressor mechanism of the dFTG, but not of the VLM or DM depend on actions of the brain structures rostral to superior colliculi.     

Arterial hypertension elicited either by lesions or by electrical stimulations of the rostral hypothalamus in the rat

Bilateral anodal lesions performed with stainless steel electrodes placed either in the anterior medial (AMH) or lateral (ALH) hypothalamus, or in the ventromedial nucleus (VMH), induced in unrestrained rats the rapid development of arterial hypertension, tachycardia and death. Similarly placed cathodal lesions performed with platinum electrodes failed to elicit the cardiovascular syndrome. The electrical stimulation of the AMH, ALH or VMH caused an increase in the arterial blood pressure in anesthetized rats. This pressor response was characteristically biphasic and consisted of a sharp increase in arterial pressure at the onset of the stimulation, followed by a second elevation at the end of the stimulation. The hypertension evoked either by lesions or by stimulations of the hypothalamus, appeared to depend largely on a neurally mediated release of adrenal medullary catecholamines, and to some extent on the activation of the sympathetic vasoconstrictor fibers. Bilateral adrenalectomy, or adrenal demedullation, prevented the hypertension evoked by lesions, and selectively blocked the important secondary phase of the pressor response elicited by stimulation, but did not affect the primary phase. The latter was specifically eliminated by the destruction of the sympathetic vasomotor axons with 6-hydroxydopamine (6-OHDA). On the other hand, the tachycardia evoked by lesions or stimulations of the medial hypothalamus, resulted from an increase in sympathetic neural discharges to the heart, and it was abolished either by β-receptor blockade with sotalol or by chemical sympathectomy with 6-OHDA. In contrast, the tachycardia occurring after lesions of the lateral hypothalamus was entirely due to circulating adrenal medullary catecholamines and it was eliminated by adrenalectomy. It is concluded that acute hypertension and tachycardia produced by anodal lesions performed with stainless steel electrodes results from the excitation of the hypothalamus, possibly due to the irritative action of the metallic ions deposited at the lesion sites. The observations of cardiovascular responses entirely due to adrenomedullary secretions suggests that the control of the adrenal medulla is at least partially distinct from that of the sympathetic vasoconstrictor and cardiac fibers, at the rostral hypothalamic level.