Sympathetic activation and contribution of genetic factors in hypertension with neurovascular compression of the rostral ventrolateral medulla

ABSTRACT. Recent data suggest a causal relationship between essential hypertension and neurovascular compression (NVC) at the rostral ventrolateral medulla. An increase of central sympathetic outflow might be an underlying pathomechanism. The sympathetic nerve activity to muscle was recorded in 21 patients with hypertension with NVC (NVC+ group) and in 12 patients with hypertension without NVC (NVC− group). Heart rate variability, respiratory activity, BP, and central venous pressure at rest and during unloading of cardiopulmonary baroreceptors with lower-body negative pressure and during a cold pressor test were also measured. Resting sympathetic nerve activity to muscle was twice as high in the NVC+ group compared with the NVC− group (34 ± 22 versus 18 ± 6 bursts/min; P < 0.05). Resting heart rate (P = 0.06) and low- to high-frequency power ratio values (P = NS) (as indicators of cardiac sympathovagal balance) tended to be augmented as well in the NVC+ group. The sympathetic nerve activity to muscle response to the cold pressor test was increased in the NVC+ group versus the NVC− group (+15 ± 11 versus 6 ± 12 bursts/min; P = 0.05), but hemodynamic and sympathetic nerve responses to lower-body negative pressure did not differ between the two groups. It is concluded that NVC of the rostral ventrolateral medulla in patients with essential hypertension is accompanied by increased central sympathetic outflow. Therefore, these data support the hypothesis described in the literature: in a subgroup of patients, essential hypertension might be causally related to NVC of the rostral ventrolateral medulla, at least in part, via an increase in central sympathetic outflow.

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Activation of corticotropin-releasing factor receptors in the rostral ventrolateral medulla is required for glucose-induced sympathoexcitation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00291.2014 ◽

2014 ◽

Vol 307 (10) ◽

pp. E944-E953 ◽

Cited By ~ 14

Author(s):

Megan E. Bardgett ◽

Amanda L. Sharpe ◽

Glenn M. Toney

Keyword(s):

Energy Expenditure ◽

Neuronal Activity ◽

Rostral Ventrolateral Medulla ◽

Corticotropin Releasing Factor ◽

Glucose Infusion ◽

Neural Mechanisms ◽

Male Rats ◽

Ventrolateral Medulla ◽

Sympathetic Activation ◽

Gaba A

Energy expenditure is determined by metabolic rate and diet-induced thermogenesis. Normally, energy expenditure increases due to neural mechanisms that sense plasma levels of ingested nutrients/hormones and reflexively increase sympathetic nerve activity (SNA). Here, we investigated neural mechanisms of glucose-driven sympathetic activation by determining contributions of neuronal activity in the hypothalamic paraventricular nucleus (PVN) and activation of corticotropin-releasing factor (CRF) receptors in the rostral ventrolateral medulla (RVLM). Glucose was infused intravenously (150 mg/kg, 10 min) in male rats to raise plasma glucose concentration to a physiological postprandial level. In conscious rats, glucose infusion activated CRF-containing PVN neurons and TH-containing RVLM neurons, as indexed by c-Fos immunofluorescence. In α-chloralose/urethane-anesthetized rats, glucose infusion increased lumbar and splanchnic SNA, which was nearly prevented by prior RVLM injection of the CRF receptor antagonist astressin (10 pmol/50 nl). This cannot be attributed to a nonspecific effect, as sciatic afferent stimulation increased SNA and ABP equivalently in astressin- and aCSF-injected rats. Glucose-stimulated sympathoexcitation was largely reversed during inhibition of PVN neuronal activity with the GABA-A receptor agonist muscimol (100 pmol/50 nl). The effects of astressin to prevent glucose-stimulated sympathetic activation appear to be specific to interruption of PVN drive to RVLM because RVLM injection of astressin prior to glucose infusion effectively prevented SNA from rising and prevented any fall of SNA in response to acute PVN inhibition with muscimol. These findings suggest that activation of SNA, and thus energy expenditure, by glucose is initiated by activation of CRF receptors in RVLM by descending inputs from PVN.

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Compression of the Rostral Ventrolateral Medulla by a Vagal Schwannoma of the Cerebellomedullary Cistern Presenting with Refractory Neurogenic Hypertension: Case Report

Neurosurgery ◽

10.1227/01.neu.0000215991.01402.4f ◽

2006 ◽

Vol 58 (6) ◽

pp. E1212-E1212 ◽

Cited By ~ 4

Author(s):

Mahmoud H. Kamel ◽

Nassir H. Mansour ◽

Chris Mascott ◽

Kristian Aquilina ◽

Steven Young

Keyword(s):

Blood Pressure ◽

Case Report ◽

Cranial Nerves ◽

Pressure Control ◽

Jugular Foramen ◽

Rostral Ventrolateral Medulla ◽

Ventrolateral Medulla ◽

Neurovascular Compression ◽

Neurogenic Hypertension ◽

First Case

Abstract OBJECTIVE: The rostral ventrolateral medulla is thought to serve as a final common pathway for the integration of central cardiovascular information and to be important for the mediation of central pressor responses. An association between essential hypertension and neurovascular compression of the rostral ventrolateral medulla has been reported. This may be mediated by an increase in sympathetic tone. CLINICAL PRESENTATION: Schwannomas arising from the lower cranial nerves (Cranial Nerves IX-XI) are rare, constituting only 3% of all intracranial schwannomas unassociated with neurofibromatosis. The majority of these tumors present as jugular foramen lesions and, less commonly, they occur along the extracranial course of these nerves. An intracisternal location is extremely rare. Fewer than 15 cases of pathologically proven intracisternal vagal schwannomas in the absence of neurofibromatosis have been reported. INTERVENTION: We report a case of vagal schwannoma in the cerebellomedullary cistern causing distortion of the vagal root entry zone and presenting with refractory neurogenic hypertension. Total microsurgical excision of this tumor, arising from one of the rootlets of the vagus nerve, was achieved. Immediately postoperatively, blood pressure decreased markedly, and despite our effort to maintain the blood pressure with fluids, the patient developed a cerebral infarction in the watershed zone. CONCLUSION: We discuss the proposed mechanism of hypertension, and the perioperative management, stressing blood pressure control. A review of the literature regarding vagal schwannomas is also presented. To the best of our knowledge, this is the first case report of a cerebellomedullary cistern vagal schwannoma presenting with neurogenic hypertension.

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