Lesions Of Nucleus Tractus Solitarii Research Articles

Modulation of brown adipose tissue-mediated thermogenesis by lesions to the nucleus tractus solitarius in the rat

Given that relatively little is known regarding the central control of brown adipose tissue (BAT)-mediated thermogenesis the present study assessed whether the direct pharmacological stimulation of β- or α-adrenergic receptors located on the brown adipocytes would result in a typical thermogenic response following electrolytic lesions to the nucleus tractus solitarius (NTS). Bilateral electrolytic lesions to the NTS in the rat effectively disrupted the baroreceptor reflex arc. It was observed that the metabolic and temperature responses to either norepinephrine (1, 5, or 25 μg/kg/min) or to the β-agonist isoproterenol (0.5 μg/kg/min) were significantly attenuated in the NTS-lesioned rats relative to the control animals with an intact baroreflex. Conversely, the cardiovascular effects of norepinephrine or of the α-agonist phenylephrine (10 μg/kg/min) were enhanced in the NTS-lesioned animals. The results suggest that the functional capacity of the brown adipocytes was reduced following NTS lesions and points to an alteration in the ability of β-receptors to respond to pharmacological stimulation with a typical thermogenic response.

Crossover in baroreflex pathways controlling renal sympathetic nerve activity.

Experiments were performed to investigate the physiologic significance of the crossover of baroreceptor afferent input to the contralateral nucleus tractus solitarius (NTS) in terms of reflex control of renal sympathetic nerve activity and to determine the physiologic significance of neuronal crossover which may occur beyond the NTS. Experiments were done in 14 alpha-chloralose anesthetized rabbits. Baroreflex control of left renal nerve activity was determined from responses to phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. Under control conditions, the mean regression slope for changes in renal nerve activity (imp/sec/mmHg change in arterial pressure) was -2.2 +/- 0.5. After unilateral NTS lesion (n = 14) the gain of the reflex was -2.4 +/- 0.4 imp/sec/mmHg. Denervation of baroreceptors ipsilateral to the NTS lesion (n = 6) did not alter the regression slope (-2.7 +/- 0.5 imp/sec/mmHg), but interruption of the contralateral carotid and aortic baroreceptor afferent fibers (n = 8) markedly reduced the slope of the linear regression relationship from -2.4 +/- 0.3 to -1.1 +/- 0.3 imp/sec/mmHg. We interpret these data to suggest that baroreceptor afferent input exerts its major reflex influence via the ipsilateral NTS and that there is modest influence exerted by fibers which cross over to the contralateral side. In addition, since we recorded from the left renal nerves and alternated the side of the NTS lesion, we interpret our findings regarding a lesion in only one NTS to suggest that there is crossover in the baroreflex pathway beyond the NTS which permits the NTS on one side to exert an influence on the renal nerves on the contralateral side similar to that seen when the NTSs on both sides are intact.

Changes in plasma catecholamines and plasma renin activity during hypotension in conscious rats with lesions of the nucleus tractus solitarii

The purpose of the present study was to examine the effects of lesions of the nucleus tractus solitarii on the reflex control of sympathetic activity and renin release in the conscious rat. Two doses of the arteriolar vasodilator hydralazine (0.3 and 1 mg/kg, i.v.) were used to activate reflexively the sympathetic nervous system in nucleus tractus solitarii lesion and control rats. Administration of 1 mg/kg of hydralazine to the control rats caused mean arterial pressure to fall from 120 ± 2 mm Hg to 84 ± 2 mm Hg and elicited an 11.2-fold increase in plasma renin activity and a 2.7-fold increase in plasma norepinephrine concentration. Administration of 0.3 mg/kg of hydralazine caused the arterial pressure of the lesion group to fall from 118 ± 3 mm Hg to a comparable value of 85 ± 4 mmg Hg, but plasma renin activity and plasma norepinephrine concentration did not rise significantly. However, administration of 1 mg/kg of hydralazine to the lesion group caused arterial pressure to fall from 128 ± 6 mm Hg to 64 ± 2 mm Hg, in association with a 12.4-fold increase in plasma renin activity and a 1.6-fold elevation in plasma norepinephrine concentration. Atenolol, a β 1-adrenoceptor antagonist, blocked 70% of the rise in plasma renin activity caused by 1 mg/kg of hydralazine in both groups of rats. In addition, prior renal denervation also markedly attenuated the rise in plasma renin activity caused by hydralazine in the lesion group. Finally, electrical stimulation of the vagus nerves, which caused a large vasodepressor response in the control group, failed to lower the arterial pressure of the lesion group. Based on these observations, we conclude that in the conscious rat (1) nucleus tractus solitarii lesions eliminate the arterial baroreflexes as well as the the cardiopulmonary baroreflex, and (2) severe hypotension induces sympathetically mediated renin release in the apparent absence of arterial and cardiopulmonary baroreflex function.

Lesions of the AV3V region attenuate sympathetic activation but not the hypertension elicited by destruction of the nucleus tractus solitarius

Previous studies have implicated a functionally defined area of the forebrain, the anteroventral third ventricle (AV3V) region as being involved in the regulation of blood pressure and required for the expression of neurogenic hypertension. The present study re-examined the effect of AV3V lesion on hypertension caused by the destruction of the nucleus tractus solitarius (NTS), focussing on whether ablation of the AV3V region altered either the sympathoadrenal or vasopressin (VP) components of NTS hypertension. Bilateral electrolytic lesions of the NTS elicited acute severe hypertension in conscious, freely moving rats whether or not the animals had received AV3V or Sham lesions 14 days previously. Mean arterial pressure (MAP) measured 45 min following NTS lesion was 157 ± 6 mm Hg in AV3V + NTS lesioned rats and 161 ± 7 mm Hg in SHAM + NTS lesioned rats. Plasma VP levels were similarly elevated in the two groups of NTS lesioned animals, and the contribution of VP to the hypertensive response (as assessed by the decrease in arterial pressure in response to a VP pressor antagonist) was the same in both groups. In contrast, NTS lesion appeared to produce a lesser degree of sympathetic nervous system activation in AV3V lesioned rats, as evidenced by a substantially smaller increase in plasma norepinephrine (NE) levels. These results demonstrate that AV3V lesions do not attenuate or prevent NTS hypertension. However, AV3V lesions do appear to attenuate the sympathoadrenal activation caused by NTS lesions.

Peripheral pressor systems in hypertension caused by nucleus tractus solitarius lesions.

The roles of vasopressin, the sympathoadrenal system, and the renin-angiotensin system in the production of hypertension after bilateral destruction of the nucleus tractus solitarius (NTS) were examined in chloralose-anesthetized rats. Since the activity of the renin-angiotensin system is high in anesthetized rats, additional studies were performed in unanesthetized, freely moving rats to evaluate the role of the renin-angiotensin system in hypertension caused by NTS lesions. Hypertension produced by bilateral electrolytic NTS lesions in rats was accompanied by elevated plasma levels of vasopressin (approximately 7-fold), norepinephrine (greater than 10-fold), and epinephrine (greater than 10-fold), but not of plasma renin activity. These results suggest that this form of hypertension is due to increased sympathoadrenal activity and increased vasopressin release into plasma and that the renin-angiotensin system is not involved. In rats with NTS lesions, blockade of vasopressin or the sympathoadrenal system, but not the renin-angiotensin system, elicited an acute decrease in arterial pressure. However, blockade of either vasopressin or the autonomic nervous system before production of the lesions had no effect on the resulting hypertension, indicating that in the absence of either one of these systems bilateral NTS lesions still result in severe hypertension. Although the renin-angiotensin system does not normally contribute to this hypertension, it does appear to contribute to the elevation in blood pressure once the actions of vasopressin have been blocked. In rats pretreated with a vasopressin antagonist, plasma renin activity increased following NTS lesions and the angiotensin converting enzyme inhibitor captopril decreased blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Lesions of nucleus tractus solitarii globally impair cerebrovascular autoregulation.

We studied the effects of acute bilateral electrolytic lesions of the nucleus tractus solitarii (NTS) on regional cerebral blood flow (rCBF) and its autoregulation in rats anesthetized (alpha-chloralose, 40 mg/kg), paralyzed (tubocurarine), and artificially ventilated. rCBF or regional cerebral glucose utilization (rCGU) was measured 30 min after NTS lesions, by the 14C-iodoantipyrine technique or 2-deoxyglucose method, respectively. Cerebrovascular autoregulation was assessed in groups of 4-5 rats at three levels of arterial pressure (AP): 90, 125, and 140 mmHg. AP was lowered by hemorrhage or elevated by intravenous infusion of phenylephrine. NTS lesions did not alter rCBF at 125 mmHg (P greater than 0.05) but resulted in loss of autoregulation (P less than 0.05, analysis of variance). In contrast, lesions of the cuneate nucleus or transection of the baroreceptor afferents did not alter autoregulation. NTS lesions did not affect the reactivity of the cerebrovascular bed to hypercarbia (PaCO2 57.4 +/- 1; n = 5) or hypocarbia (PaCO2 24.4 +/- 1; n = 5) nor the rCGU in any brain regions (P greater than 0.05; n = 5). We conclude that lesions of the NTS impair cerebrovascular autoregulation. The effect is not due to changes in metabolism, nonspecific effects of the lesions, vasoparalysis, or interruption of the baroreceptor reflex arch. Neural pathways originating in or passing through the NTS can regulate the cerebrovascular autoregulation of the entire brain.

Medullary lesions eliminate ACTH responses to hypotensive hemorrhage.

The adrenocorticotropin (ACTH) response to hemorrhage (15 ml . kg-1 . 3 min-1) before and 30 min or 4 days after placement of bilateral electrolytic lesions of the nucleus tractus solitarius (NTS) were examined in anesthetized and in conscious rats. Two groups of rats were anesthetized with pentobarbital sodium (45 mg/kg). Femoral arterial and venous cannulas were placed acutely in the anesthetized group and chronically in the conscious group. Each rat received a hemorrhage 30 min before and 30 min after NTS lesions (in the anesthetized group) and 1 day before and 4 days after NTS lesions (in the conscious group). Plasma ACTH was determined before and 20 min after hemorrhage, and mean arterial blood pressure and heart rate were measured throughout. The baroreceptor reflex (bradycardia caused by a phenylephrine-induced rise in MABP) was determined 5 min before hemorrhage (in the anesthetized group) and 1 day before hemorrhage (in the conscious group) to assess the effectiveness of lesion. Hexamethonium was given to rats that developed hypertension postlesion and to sham-lesioned controls. Plasma ACTH did not increase after hemorrhage 30 min or 4 days after NTS lesions when compared with the other groups (sham, sham with hexamethonium, and missed lesion) and to prelesion controls. Also, lesions of the NTS had no effect on resting ACTH levels 4 days later. Mean arterial pressure and heart rate decreased during hemorrhage to similar extents before and after lesions in all groups. This study demonstrates that lesions of the NTS eliminate the ACTH response to hemorrhage immediately and 4 days after the lesions but have no effect on resting ACTH levels. The result suggests that the NTS is an essential part of the neural pathway for ACTH release after hemorrhage.

Cardiovascular and neuroendocrine responses to behavioral stress after central or peripheral barodenervation in rats

The cardiovascular and neuroendocrine responses to acute behavioral stress were evaluated in rats after disruption of the baro reflexes by electrolytic lesions of the nucleus tractus solitarii (NTS) or sinoaortic denervation (SAD). Rats with NTS lesions or SAD showed significantly greater increases in mean arterial pressure (MAP) and plasma norepinephrine (NE) concentrations than control rats during a single 30-min escape-avoidance test. In addition, the increases in MAP and plasma NE concentration of NTS lesion rats were significantly greater than those of SAD rats. However, NTS lesion raats showed no increase in plasma renin activity (PRA), as observed in the other groups. Thus, disruption of the baroreflexes by NTS lesions oraugments the arterial pressure and plasma NE responses to stress. Additionally, NTS lesions appeared to eliminate the neurons or fibers of passage participating in the sympathetically mediated increase in PRA.

Contribution of vasopressin to hypertension caused by baroreceptor denervation and nucleus tractus solitarius lesions in rats.

The purpose of this study was to examine, using pentobarbital-anesthetized rats, whether vasopressin contributes to hypertension caused by denervation of baroreceptors, in comparison to the contribution of vasopressin to hypertension caused by nucleus tractus solitarius (NTS) lesions. Bilateral baroreceptor denervation caused acute hypertension which was inhibited by intravenous injection of an antagonist of the vasoconstrictor action of vasopressin. Lesions of the NTS also produced an increased in blood pressure which was reduced by the vasopressin antagonist. The magnitude of the antagonist-induced hypotension was significantly greater in NTS hypertension than that in baroreceptor denervation hypertension. It is concluded, that in rats, vasopressin contributes to the neurogenic hypertension caused by baroreceptor denervation and NTS lesions. Thus, it appears that interruption of baroreceptor afferents at the NTS level is responsible for the vasopressin-mediated hypertension caused by NTS lesions but that it is not the only factor involved.

Arterial pressure and heart rate responses to calcium channel blockers administered in the brainstem in rats.

The study examined the possibility that organic calcium channel blockers alter autonomic nervous system function by acting on brainstem neurons. Intracisternal administration of diltiazem or verapamil produced dose-related decreases in arterial pressure and heart rate. Diltiazem administered by drop on the dorsal surface of the brainstem at the obex or microinjected directly into the nucleus tractus solitarius also decreased arterial pressure and heart rate. The responses were absent or markedly attenuated in rats previously treated with 6-hydroxydopamine or with bilateral electrolytic lesions of the nucleus tractus solitarius but were preserved in rats treated with atropine or with sham nucleus tractus solitarius lesions. Nifedipine or ethylene glycol-bis-(beta-aminoethyl ether)N,N'-tetraacetic acid administered on the dorsal surface of the brainstem at the obex decreased arterial pressure and heart rate. Vehicle, acid saline, or sucrose solution failed to alter arterial pressure or heart rate. These results suggest that organic calcium channel blockers produce excitation of the nucleus tractus solitarius neurons, directly or indirectly, which results in the withdrawal of sympathetic nervous activity and in the decrease in arterial pressure and heart rate. The results suggest that calcium ion plays an important role in maintaining integral function of neurons in the brainstem, particularly in the nucleus tractus solitarius.

Nucleus tractus solitarius lesions elevate pulmonary arterial pressure and lymph flow.

The effects of lesions of the nucleus tractus solitarius (NTS) on pulmonary vascular pressure and pulmonary lymph flow were investigated in 6 halothane-anesthetized sheep. After lesions of the NTS were created using bilateral thermocoagulation, pulmonary artery pressure rose to 150% of baseline and remained elevated for the 3-hour duration of the experiment. Systemic and left atrial pressures did not change. Pulmonary lymph flow doubled within 2 hours; the lymph-plasma protein ratio was unchanged from baseline. Sham NTS lesions and lesions lateral to NTS produced no changes. These experiments demonstrate that lesions of the central nervous system can alter pulmonary vascular pressures and transcapillary fluid flux independently of effects upon the systemic circulation. These findings may have relevance for the understanding of neurogenic pulmonary edema in humans.

Brain stem area with C1 epinephrine neurons mediates baroreflex vasodepressor responses.

In anesthetized, paralyzed rats, bilateral electrolytic lesions of rostral ventrolateral medulla (RVL) containing epinephrine neurons of the C1 group 1) abolished the reflex hypotension and bradycardia elicited by electrical stimulation of the left vagus nerve or stretch of the left carotid sinus and 2) reduced arterial pressure (AP) and heart rate (HR) to values comparable to spinal cord transection. Combined lesions of the right nucleus tractus solitarii (NTS) and left or right C1 area did not alter AP. However, lesions of right NTS combined with lesions or microinjection of kainic acid into the left, but not right, C1 area abolished vasodepressor reflexes. Vasodepressor reflexes were unchanged by midcollicular decerebration, bilateral lesions of the parabrachial complex of the pons, or (after right NTS lesions) by lesions of the raphe or other reticular areas of the left half of the medulla. We conclude that neurons of the RVL, possibly belonging to the C1 epinephrine group, mediate vasodepressor responses from arterial baro- and other cardiopulmonary receptors, the pathway may be via a direct NTS-RVL projection, neurons in the C1 area of RVL are necessary for maintaining resting levels of arterial pressure.

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Lesions of the nucleus tractus solitarius (NTS) were studied to determine whether they elevate plasma vasopressin levels and, if so, whether these elevated levels of vasopressin contribute to the hypertension caused by NTS lesions. Bilateral electrolytic lesions of the NTS caused acute, severe hypertension in rats anesthetized with chloralose and in conscious, freely moving rats. After placement of the NTS lesions there was a greater than tenfold elevation in plasma vasopressin levels. Administration of an antagonist of the vasoconstrictor action of vasopressin markedly diminished the hypertension in both conscious and anesthetized rats. Following ganglionic blockade with chlorisondamine, NTS lesions still elicited hypertension, and the magnitude of the hypertension was not different from that observed in rats not treated with chlorisondamine. The hypertension produced by lesions of the NTS in ganglionic-blocked rats was completely abolished by administration of a vasopressin antagonist. These results indicate that (1) NTS lesions elevate plasma vasopressin levels and (2) elevated plasma vasopressin contributes to the hypertension produced by such lesions.

Clonidine can lower blood pressure by inhibiting vasopressin release

The effect of clonidine on vasopressin release was studied in chloralose anesthetized rats which were made hypertensive by bilateral electrons of the nucleus tractus solitarii (NTS). NTS lesions elevated arterial pressure and plasma vasopressin levels, and both of these variable were returned toward baseline values by intravenous injection of clonidine (30 μg/kg). Furthermore, the ability of a vasopressin antagonist to lower arterial pressure in NTS hypertensive rats was markedly attenuated by clonidine treatment. In contrast, autonomic blockade (chlorisondamine, 2.5 mg/kg) in NTS lesioned rats did not reduce plasma vasopressin levels or the effect of the vasopressin antagonist on blood pressure. These data demonstrate that part of the antihypertensive effect of clonidine in NTS hypertensive rats is due to inhibition of vasopressin release into the circulation.

Chronic lability of the arterial blood pressure produced by electrolytic lesions of the nucleus tractus solitarii in the rat.

The purpose of this study was to assess the chronic effects of lesions of the nucleus tractus solitarii on the cardiovascular activity of rats. Arterial pressure and heart rate were recorded in conscious, unrestrained rats 7-216 days following placement of electrolytic lesions in the nucleus tractus solitarii. To assess the impact of environmental stimuli on the mean level and lability of the mean arterial pressure, cardiovascular activity was recorded under conditions of controlled and uncontrolled environmental stimulation. Nucleus tractus solitarii lesions abolished the reflex bradycardia to a phenylephrine-induced elevation in arterial pressure. A marked increase in the lability of the mean arterial pressure was produced with nucleus tractus solitarii lesions. The standard deviation of the mean arterial pressure, an index of lability, was 380% greater in rats with lesions than in control rats. The average mean arterial pressure, heart rate and heart rate variability were not significantly different between the lesion and control groups, regardless of the environmental conditions under which the measurements were made. Nucleus tractus solitarii lesions also greatly exaggerated the arterial pressure response to naturally occurring behaviors, such as eating and drinking. Vagal and beta-adrenergic blockade with methyl atropine and propranolol did not alter the average level or lability of the mean arterial pressure, although heart rate responses were similar in both groups. alpha-Receptor blockade with prazosin significantly lowered the mean arterial pressure in both lesion and control rats, but the decrease in mean arterial pressure was significantly greater in rats with nucleus tractus solitarii lesions (42 +/- 6 mm Hg, 38.5%) than in control rats (27 +/- 4 mm Hg, 23.2%). Prazosin also reduced the lability of the mean arterial pressure to control levels in rats with lesions. Thus, the chronic effects of nucleus tractus solitarii lesions in rats are to abolish the cardiomotor component of the baroreflexes and to produce extreme lability of the arterial pressure without altering the average level of the mean arterial pressure. Exaggerated blood pressure responses are seen in association with various behaviors. These effects are mediated primarily by changes in sympathetic discharge to the vasculature and are independent of the ambient level of environmental stimuli.

Role of adrenaline neurons of ventrolateral medulla (the C1 group) in the tonic and phasic control of arterial pressure.

We have sought to determine if adrenaline neurons of the C1 group are responsible for cardiovascular functions heretofore attributed to neurons in the rostral ventrolateral medulla. C1 neurons were identified in rat with antibodies to the adrenaline synthesizing enzyme, PNMT. These project to spinal cord wherein they selectively innervate the sympathetic columns. C1 neurons are also innervated by projections, mostly unilateral, from the nucleus tractus solitarii (NTS). Stimulation of the C1 area electrically, by local injection of the excitatory amino acid, L-glutamate, or with the GABA antagonist bicuculline, elevates arterial pressure (AP). Bilateral electrolytic lesions, microinjection of GABA, or administration of tetrodotoxin, in contrast, collapses AP to levels comparable to that of spinal cord transection. After lesions of one NTS, a lesion of the contralateral C1 area abolishes all reflex activity elicited by electrical or natural stimulation of baroreceptors on the side of C1 lesion without modifying resting AP. Lesions of axon bundles of PNMT neurons in the medulla also abolish baroreflexes after unilateral NTS lesions. C1 neurons appear to be the neurons mediating cardiovascular effects of application of drugs or cold to rostral portions of the ventrolateral medulla. We conclude adrenaline neurons of the C1 area represent the purportedly tonic vasomotor neurons of the rostral ventrolateral medulla and mediate the vasodepressor limb of reflexes arising from arterial baroreceptors and other cardiopulmonary afferents. Whether the tonic vasomotor response to stimulation of C1 neurons is dependent upon the release of adrenaline is not yet certain.

Lesions of epinephrine neurons in the rostral ventrolateral medulla abolish the vasodepressor components of baroreflex and cardiopulmonary reflex.

Epinephrine-containing neurons of the rostral ventrolateral medulla (RVL) (the C1 group of Hökfelt) in the rat are primarily unilaterally innervated by neurons in the nucleus tractus solitarius (NTS) and in turn project to autonomic spinal neurons. In this study, we investigated whether the C1 area of the RVL mediates the vasodepressor responses (VDR) induced by either electrical stimulation of the vagus nerve or carotid sinus stretch. In all experiments, C1 neurons were localized immunocytochemically with antibodies to phenylethanolamine N-methyltransferase (PNMT). Bilateral lesions of the C1 area decreased arterial pressure (AP) and heart rate (HR) to spinal cord transection levels and blocked the VDR induced by vagal stimulation and carotid sinus stretch. Combined lesions of the contralateral NTS and C1 area ipsilateral to the stimulated vagus nerve maintained AP and HR at normal levels, and totally blocked the VDR to vagal stimulation and carotid sinus stretch. Since projections from the vagus nerve to NTS are bilateral and those from NTS to C1 unilateral, the combined contralateral NTS/ipsilateral C1 lesions isolated and interrupted the ipsilateral NTS-C1 pathway and, therefore, blocked the baroreceptor reflex. The results are consistent with the hypothesis that neurons in the NTS synapsing in or projecting through the C1 area mediate the baro- and cardiopulmonary mechanoreceptor reflex.

Neurogenic hypertension produced by lesions of the nucleus tractus solitarii alone or with sinoaortic denervation in the dog.

The cardiovascular effects of bilateral lesions of the nucleus tractus solitarii (NTS) were compared with those of subsequent sinoaortic denervation in the same dogs. Destruction of the lateral but not the medial component of the NTS between + 0.5 and 3 mm anterior to the obex produces mild hypertension and tachycardia, not always sustained for more than 2 weeks. Rises in pressure were accompanied by increased lability which was not present regularly in all dogs but correlated with the baseline level of arterial pressure. On the other hand, sinoaortic denervation following lateral NTS lesions produced the first demonstration of fulminant hypertension in the dog, which led to death within hours. These data suggest that, while NTS lesions in the dog probably only partially interrupt central baroreceptor pathways, the addition of sinoaortic denervation completely disrupts baroreceptor inputs to the central nervous system, thus releasing central sympathetic outflow completely from baroreceptor inhibition.

Hemodynamic responses to bilateral lesions of the nucleus tractus solitarii in spontaneously hypertensive and normotensive rats.

Systemic and regional hemodynamic responses to bilateral lesions of the nucleus tractus solitarii (NTS) were studied in alpha-chloralose-urethane anesthetized American Wistar rats (NR), Wistar-Kyoto rats (WKY), and spontaneously hypertensive rats (SHR) by microsphere methods. After NTS lesions, arterial pressure rose by virtue of increased total peripheral resistance in each strain. Cardiac output was lower in NR and WKY, but not in SHR. In all strains, vasoconstriction was nonuniformly distributed among the systemic vasculatures: hepatosplanchnic, renal, and carcass (i.e. skin, skeletal muscle, bone, fat) vascular resistances were higher, but cerebral and coronary vascular resistance remained unchanged. There were some differences, however, in regional vascular responses to NTS lesions among these strains: carcass vasoconstriction was predominant in NR; it was less evident in SHR; and the WKY responses were intermediate. These results indicate that, although systemic hemodynamic responses were similar in these strains, and the reflex inhibition of central sympathetic outflow is not evidently deteriorated in SHR, the regional hemodynamics (i.e., hepatosplanchnic and renal vasculatures) in the SHR demonstrated greater arteriolar constriction.

Production of sustained hypertension by lesions in the nucleus tractus solitarii of the American foxhound.

The purpose of this study was to develop a model of sustained neurogenic hypertension in the dog. Thirteen female American foxhounds (mean arterial pressure 105 ± 12 mm Hg) with Indwelling arterial and venous cannulas were maintained on a constant 82 mEq/day sodium intake. After a control period of at least 10 days, under pentothal anesthesia and direct visualization, the animals had placement of bilateral electrical lesions of the nucleus tractus solitarii (NTS) at the level of the obex. After recovery from anesthesia, the dogs could be divided into two groups on the basis of blood pressure response. Group I (n = 6) developed sustained hypertension with an increase of mean arterial pressure of 25-35% above control values (p < 0.01) for 10 days after placement of the lesions. Group II (n = 7) had a transient increase of blood pressure on postoperative Day 1 but became nonnotensive for the subsequent 9 days of observation. The bemodynamic features of the dogs in Group I were increased total peripheral resistance, decreased cardiac output and slightly decreased heart rate; these changes were reversed to control by pbetolamine. Plasma renin activity, aldosterone concentration and blood pressure response to SQ20,881 were unchanged by NTS lesions. Group I dogs had sodium retention on postoperative Day 1, but no change in renal plasma flow or glomerular filtration rate was observed during the chronic hypertensive phase. One Group I dog remained hypertensive for 8 weeks. All dogs in Group I were hypertensive and all in Group II were nonnotensive at sacrifice. Histologic sections from Group I dogs showed complete cellular destruction of the nucleus and the tractus solitarius bilaterally at the obex. In Group II, unilateral or incomplete cellular destruction of the NTS at the obex, or bilateral NTS lesions caudal to the obex were present. Bilateral NTS lesions at the obex in the American foxhound result in sustained arterial hypertension characterized by increased peripheral sympathetic nervous system activity and lack of dependence on the renin-angiotensin-aJdosterone system. (Hypertension 1: 246-254, 1979)