Search

Experiments were done in alpha-chloralose anesthetized rats to investigate the effect of stimulating the intermediate region of the ventrolateral medulla (VLM) on the response of single units in nucleus of the solitary tract (NTS) that altered their rate of discharge during aortic baroreceptor stimulation. Of 178 units recorded within NTS, 65 responded orthodromically to VLM stimulation. An additional 16 units were activated antidromically by VLM stimulation. The interaction between the aortic depressor nerve and VLM orthodromic inputs was investigated in 38 units that received converging inputs from VLM and the aortic depressor nerve. A conditioning stimulus applied to VLM, regardless of whether the NTS unit was excited by (n = 13) or did not respond to (n = 9) VLM stimulation, decreased the excitatory response of the unit to aortic depressor nerve stimulation. These data suggest that VLM neurons are involved in the modulation of aortic baroreceptor afferent information at the level of the NTS and that this interaction of inputs in NTS may involve both postsynaptic and presynaptic mechanisms.

Renal nerves are thought to play an important role in cardiovascular regulation under both normotensive and hypertensive conditions. In the present study the effect of renal denervation on the changes in plasma renin activity (PRA) after aortic baroreceptor deafferentation (tADN) were investigated in the rat. Bilateral renal denervation did not alter arterial pressure (AP, 100 +/- 4 mmHg; 1 mmHg = 133.32 Pa), heart rate (HR, 363 +/- 12 bpm), or PRA (2.9 +/- 0.6 ng.mL-1.h-1) compared with the respective sham renal denervation values of 106 +/- 3 mmHg (AP), 385 +/- 13 bpm (HR), and 3.3 +/- 0.7 ng.mL-1.h-1 (PRA). On the other hand, bilateral tADN resulted in significant increases in AP, HR, and PRA. One and 3 days after tADN, AP was 130 +/- 4 and 127 +/- 6 mmHg, HR was 461 +/- 15 and 463 +/- 20 bpm, and PRA was 9.1 +/- 3.0 and 11.9 +/- 4.5 ng.mL-1.h-1, respectively. Renal denervation before tADN prevented the increases in AP and PRA, but it did not affect the increase in HR. These data indicate that renal denervation does not alter basal PRA in normotensive animals but prevents the increased renin release observed in neurogenic hypertension. These data suggest that the increased PRA may be one of several factors that contributes to the elevated AP after tADN.

The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 microA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.

Concentrations of noradrenaline, adrenaline, and dopamine were measured using a sensitive radioenzymatic assay in hypothalamic nuclei of rats 4 days after bilateral renal denervation. After renal denervation, catecholamine levels in several hypothalamic nuclei were found to be different from those of sham-operated animals. Noradrenaline was found to be increased in the supraoptic nucleus, adrenaline was increased in the paraventricular nucleus and lateral hypothalamic area, and dopamine was decreased in the supraoptic nucleus, medial preoptic nucleus and lateral hypothalamic area. These data suggest that afferent renal fibers influence the metabolism of hypothalamic catecholamines and that neural information originating in the kidney and transmitted to the hypothalamus is probably involved in physiological responses related to cardiovascular adjustments and body fluid balance.

It has recently been reported that stimulation of the region of the subfornical organ (SFO) elicits an increase in arterial pressure. However, the mechanisms and forebrain neural circuitry that are involved in this cardiovascular response have not been elucidated. The present study was done in urethane-anaesthetized rats to determine whether selective activation of SFO neurons elicit cardiovascular responses and whether these responses were mediated by a pathway involving the paraventricular nucleus of the hypothalamus (PVH). Stimulation sites which required the lowest threshold current (30 microA) to elicit a pressor response and at which the largest rise in mean arterial pressure (MAP; 22 +/- 2 mmHg) was elicited at a constant current intensity (150 microA) were histologically localized in the region of the SFO. Short (mean peak latency; 4 +/- 2 s) and long (mean peak latency; 61 +/- 8 s) latency increases in MAP were observed during and after electrical stimulation of the SFO, respectively. Cardiac slowing accompanied the short latency pressor response and cardioacceleration was observed in most (57%) of the cases to accompany the late pressor response. Microinjection of L-glutamate into the SFO consistently elicited cardiovascular responses qualitatively similar to those observed during electrical stimulation. Ganglionic blockade abolished the short latency increase in MAP and the accompanying bradycardia. However, the long latency pressor and cardioacceleratory responses were not altered by ganglionic blockade and adrenalectomy. Selective bilateral electrolytic or kainic acid lesions of the region of the PVH significantly attenuated the cardiovascular responses elicited by stimulation of the SFO. These data suggest that activation of neurons in the SFO elicit cardiovascular responses partially mediated by sympathetic outflow through a neural pathway involving the PVH.

In recent years a considerable amount of experimental evidence has suggested that forebrain structures are involved in the pathogenesis of high arterial pressure (AP). However, little is known about the location and function of these supramedullary structures in the hypertensive process. This report reviews a series of studies done to identify the location and to determine the contribution of some forebrain structures to both the development and maintenance of the elevated AP following selective aortic baroreceptor deafferentation (ABD). In the first series of studies, it was demonstrated that the elevated AP resulting from ABD was associated with increased metabolic activity in several forebrain structures: the paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus, nucleus circularis, median preoptic nucleus, subfornical organ (SFO), and central nucleus of the amygdala. In the second series, bilateral electrolytic lesions of the PVH were shown to prevent the development of and (or) reverse the elevated AP after ABD. Similarly, bilateral microinjections of the neurotoxin kainic acid into the PVH were shown to reverse the increased AP after ABD. In the final series, electrolytic lesions of the SFO were shown to attenuate the rise in AP after ABD and (or) to reduce the elevated AP to a level that remained above control values. Taken together, these data suggest that the PVH and SFO are components of a neuronal circuit involved in the hypertensive process following ABD, and that the SFO likely exerts its effect through the PVH.

Afferent renal nerves (ARN) are thought to be an important link in the pathogenesis of hypertension because of their influence on neuronal circuits involved in the control of arterial pressure and body fluid homeostasis. However, the central neural pathways involved in mediating ARN information have not been completely elucidated. In the present study, regions of the brainstem and forebrain, whose metabolic activity was altered after renal denervation, were functionally identified using hexokinase histochemistry in the rat. No differences in arterial pressure or heart rate were observed in either the 3-day or 13-day ARN-transected (tARN) animals compared with the respective sham ARN-transected (sARN) groups. Significant increases in the hexokinase reaction product were seen in the parvocellular component of the paraventricular nucleus of the hypothalamus, the supraoptic nucleus, the arcuate nucleus, the subfornical organ, the median preoptic nucleus, and the medial nucleus of the amygdala in both the 3-day and 13-day tARN animals. The bed nucleus of the stria terminalis was observed to have a significant decrease in hexokinase activity in the tARN groups, as were the caudal and medial aspects of the nucleus of the solitary tract. In the 3-day tARN group only, a significant decrease in hexokinase activity was observed in the region of the brainstem containing the A5 cell group, compared with sARN animals. The magnocellular component of the paraventricular nucleus of the hypothalamus and the lateral hypothalamus was seen to have increased hexokinase activity in the 13-day tARN animals only.(ABSTRACT TRUNCATED AT 250 WORDS)