Electrical stimulation at single sites in the rostral fastigial nucleus elicits hypertension, grooming, feeding, and attack behaviors in the cat. The stimulus intensity and availability of suitable goal objects determines the behavior. Bilateral lesions of the area fail to produce motor deficits. The rostral fastigial nucleus may be a cerebellar area for behavioral and autonomic regulation.

The effects of selective destruction of the catecholamine innervation of the nucleus tractus solitarii (NTS) on arterial pressure (MAP) and heart rate (HR) were examined in unanesthetized rats in which 6-hydroxydopamine (6-OHDA), 1 ;J, was injected bilaterally into the nucleus at the level of the obex. Control rats received 1 fil of vehicle or were uninjected. Baroreceptor reflex activity was tested by measuring the reflex bradycardia in response to graded doses of phenylephrine. 6-OHDA, 2 /ig, did not alter MAP or HR; 12 /ig, a dose producing necrosis of NTS, resulted in the development within 4-6 hours of fulminating arterial hypertension and tachycardia. 6-OHDA, 4 fig, produced an elevation of MAP which returned to control levels by 48 hours without changing HR. By 6 hours, however, the arterial pressure became extremely labile. Lability of MAP in the absence of hypertension or change of HR persisted for the longest period of observation, 2 weeks. Baroreceptor reflex activity remained, although the sensitivity of the reflex was depressed. 6-OHDA, 4 /ig, failed to produce histological damage to NTS. Biochemically, it resulted after 14 days in a reduction of the activity of dopamine /3-hydroxylase, a specific marker of noradrenergic and adrenergic neurons, to 40% of control without altering the activity of choline acetyltransferase, a marker of cholinergic neurons. We conclude that selective removal of a substantial portion of the catecholamine innervation of the NTS, mostly noradrenergic, results in persistent lability without elevation of arterial pressure. The results suggest that the catecholamine innervation of NTS modulates rather than mediates baroreceptor reflexes, serving to maintain arterial pressure within narrow limits.

: Respiratory and circulatory reflexes from the perfused heart and pulmonary circulation of the dog. Am J Physiol 165: [261][262][263][264][265][266][267][268][269][270][271][272][273][274][275][276][277] 1951 18. Lewin RJ, Cross CE, Rieben PA, Salisbury PF: Stretch reflexes from the main pulmonary artery to the systemic circulation. The MAP in the lesion group was 144 mm Hg (180% of control) during the day, and 96 mm Hg (120% of control) at night. The lability, measured by the standard deviation, during the day in the lesion group was 4 times greater than in the control group and at night there were no differences. The heart rate of the lesion group was always higher than that of the control group but the lability of both groups was the same. We conclude that lesions of the NTS produced labile hypertension, probably by disinhibition of sympathetic activity through central interruption of the baroreceptor reflexes. The higher, more labile arterial pressures during the day may be caused by uninhibited increases in sympathetic activity elicited by environmental stimuli that are present during the day and absent at night. The daily variation of pressure may also be caused by somatomotor activity or by a daily rhythm of sympathetic activity which is unmasked by the lesions.THE CENTRAL nervous system may play a critical role in the initiation of and/or maintenance of several models of experimental hypertension in animals 1 and possibly of essential hypertension in man.2 -3 Neurogenic hyperten- sion may result from an imbalance between systems in the brain which excite or inhibit sympathetic discharge. The imbalance could favor increased sympathetic discharge which would enhance vasoconstriction and consequently elevate the arterial pressure. Many attempts to produce animal models of experimental hypertension have aimed at increasing sympathetic discharge either by chronic electrical stimulation of the hypothalamus, by producing brain ischemia, by subjecting animals to stress, or by behavioral conditioning. -5 Hypertension results from these procedures but it lasts, at most, for only a few weeks.Other studies have attempted to produce experimental hypertension by withdrawing inhibition of sympathetic

Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial hypertension, tachycardia, hyperthermia, and increased locomotor activity, often leading to pulmonary edema and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial hypertension was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial hypertension, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial hypertension and pulmonary edema as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial hypertension following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that pulmonary edema is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.• In 1954, Maire and Patton (1) demonstrated that bilateral electrolytic lesions of the anterior hypothalamus (AH) result in the development of a syndrome of hyperactivity, hyperthermia, and fatal pulmonary edema in the rat. Although cardiovascular measurements were not made, Maire and Patton attributed the pulmonary edema to a neurogenically mediated shift of blood from the capacitance vessels into the pulmonary circulation (2). More recently, Doba and Reis (3, 4) have observed that fulminating pulmonary edema can also be produced in the rat by bilateral lesions of the nucleus tractus solitarii (NTS), a brainstem nucleus in the medulla oblongata serving as a site of termination of arterial baroreceptors. In this instance, the pulmonary edema is due to the rapid development of neurogenic arterial hypertension with a marked increase in total peripheral resistance leading to a reduction in cardiac output and myocardial failure. Thus, the possibility exists that the pulmonary edema observed by Maire and This work was supported by Grant NS 03346 from NINDS and Grant NGR-33-010-179 from NASA and by the Harris Foundation.Received September 11, 1974. Accepted for publication May 13, 1975. Patton (1,2) after lesion of the AH was secondary to the development of arterial hypertension.In the present study, we investigated the hemodynamic changes following placement of lesions in the AH in the rat. Such lesions produced pulmonary edema as a consequence of arterial hypertension, and the hypertension was due to a neurally mediated release of adrenomedull...

SUMMARY. 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 /S-adrenergjc 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. a-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. (Circ Res 54: 227-238, 1984)