Role of ventrolateral medulla in vasomotor regulation: a correlative anatomical and physiological study

Dampney, R.A.L.; Goodchild, Ann K.; Robertson, L.; Montgomery, William

doi:10.1016/0006-8993(82)90056-7

Cited by 308 publications

(91 citation statements)

References 29 publications

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“…[1][2][3][4] The rostral ventrolateral medulla (RVLM) is an important center for the regulation of sympathetic and cardiovascular activities. 5,6 After the initial report by Jannetta and Gendell in 1978, 7 several clinical studies have suggested an association between neurovascular contact (NVC) of RVLM and essential hypertension (EH). [8][9][10][11][12][13][14][15] Jannetta et al 16,17 have reported that MVD of RVLM decreases blood pressure (BP) in hypertensive patients with NVC of RVLM.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of clonidine in patients with essential hypertension with neurovascular contact of the rostral ventrolateral medulla

et al. 2010

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The rostral ventrolateral medulla (RVLM) is an important center for regulation of sympathetic nerve activity. Several clinical studies have suggested an association between neurovascular contact (NVC) of RVLM and essential hypertension. Microvascular decompression (MVD) of RVLM decreases blood pressure (BP) in hypertensive patients with NVC of this region. Therefore, MVD could be a useful therapeutic strategy to reduce BP in these patients. However, as MVD is an invasive procedure, it is worthy to seek useful antihypertensive agents for hypertensive patients with NVC. It is reported that sympathetic nerve activity is elevated in patients with hypertension accompanied by NVC of RVLM. It is anticipated that sympatholytic agents could be effective in lowering BP in these patients. In this study, we investigated the efficacy of clonidine, an a2 adrenergic agonist, in essential hypertensives with NVC of RVLM. Thirty consecutive essential hypertensive patients with NVC and 30 consecutive essential hypertensive patients without contact were treated with clonidine for 4 weeks, and decreases in BP and plasma norepinephrine levels were compared between the two groups. Decreases in BP and plasma norepinephrine levels were significantly greater in patients with NVC than in those without contact. These results suggest that clonidine exhibits significantly greater reductions of BP and sympathetic nerve activity in essential hypertensive patients with NVC compared with those without contact of the rostral ventrolateral medulla.

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Section: Introductionmentioning

confidence: 99%

Efficacy of clonidine in patients with essential hypertension with neurovascular contact of the rostral ventrolateral medulla

et al. 2010

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“…1,2 After the initial report by Jannetta and Gendell in 1978, 3 several clinical studies have suggested an association between neurovascular compression (NVC) of the RVLM and essential hypertension (EH). [4][5][6][7][8][9][10] We have reported that magnetic resonance imaging (MRI) with a high-resolution matrix revealed a significantly higher incidence of NVC of the RVLM in EH patients as compared with those with secondary hypertension or normotensive patients, although the degree of organ damage from hypertension was not significantly different between the two groups of hypertensive patients.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of an L- and N-type calcium channel blocker in hypertensive patients with neurovascular compression of the rostral ventrolateral medulla

et al. 2009

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The rostral ventrolateral medulla is an important regulation center of sympathetic nerve activity. Several clinical studies have indicated a possible association between essential hypertension and neurovascular compression of the rostral ventrolateral medulla. We have found that patients with essential hypertension and neurovascular compression of the rostral ventrolateral medulla by adjacent arteries have increased sympathetic nerve activity and that microvascular decompression of the rostral ventrolateral medulla normalizes blood pressure and sympathetic nerve activity. Although sympatholytic agents are expected to lower blood pressure in these patients, this remains to be clarified. In this study, we evaluated the effect of cilnidipine, a calcium channel blocker that blocks both vascular L-type and sympathetic N-type Ca 2+ channels in hypertensive patients with neurovascular compression. Using high-resolution magnetic resonance imaging, 46 patients with untreated essential hypertension were distributed into those with and without neurovascular compression of the rostral ventrolateral medulla. All patients were prescribed 10 mg of cilnidipine for 16 weeks. Office and home blood pressure, plasma norepinephrine and left ventricular mass index were measured by echocardiography before and after cilnidipine treatment, and changes were compared between the two groups. At baseline, plasma norepinephrine was significantly higher in patients with neurovascular compression. Decreases in office and home blood pressure, plasma norepinephrine and left ventricular mass index were significantly greater in patients with neurovascular compression. These results suggest that cilnidipine lowers blood pressure by inhibiting enhanced sympathetic nerve activity and reduces left ventricular mass in hypertensive patients with neurovascular compression of the rostral ventrolateral medulla.

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“…Centrally mediated hyperactivity of the sympathetic nervous system has been proposed as an "initiator" of early EHTN and may provide a major contribution to sustaining elevated blood pressure over the long term in some patients. Studies in animal models [1][2][3][4][5][6][7] have confirmed the presence of sympathoexcitatory bulbospinal neurons in the rostral ventrolateral medulla (RVLM) and their important role in the control of blood pressure. In humans, those neurons are thought to be in the retro-olivary sulcus (ROS), just anterior to the root entry zone of the glossopharyngeal and vagus nerves.…”

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confidence: 99%

Vascular Compression of the Rostral Ventrolateral Medulla in Sympathetic Mediated Essential Hypertension

et al. 2000

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Abstract-The pathophysiological factors of neurogenic or sympathetically mediated essential hypertension are unknown.Neurons close to the surface of the ventrolateral medulla (specifically, in the retro-olivary sulcus [ROS]) are integrally involved in the control of blood pressure by means of efferent connections to presympathetic neurons in the spinal cord. It is hypothesized that vascular contact with the ROS is pathogenically involved in neurogenically mediated hypertension. We evaluated that theory in 20 subjects with uncomplicated stage 1 to stage 2 essential hypertension (EHTN) (18 of whom completed the study). The baseline supine plasma norepinephrine level served as an index of central sympathetic outflow. The response of blood pressure to clonidine was used as a surrogate marker for neurogenically mediated hypertension. We also examined the relationship between those markers and evidence of anatomic abnormalities in the area of the ROS that was provided by magnetic resonance imaging. A vessel contacted the left ROS in 5 of the 18 subjects. Those 5 subjects had higher plasma norepinephrine concentrations than did the 13 subjects without this vascular contact (358Ϯ46 versus 76Ϯ43 pg/mL, PϽ0.001). These 5 subjects also exhibited a significant depressor response to clonidine that tended to be greater than that seen in the 13 subjects without vascular contact (Ϫ20.6Ϯ3.2 versus Ϫ13.6Ϯ9 mm Hg). Both race and baseline mean blood pressure had only an independent effect on the depressor response to clonidine. The findings are consistent with the theory that vascular contact with the left ROS may contribute to neurogenically mediated "essential" hypertension in some patients. (Hypertension. 2000;36:78-82.)Key Words: hypertension, essential Ⅲ norepinephrine Ⅲ medulla oblongata Ⅲ clonidine Ⅲ sympathetic nervous system T he cause of essential hypertension (EHTN) remains unclear and is probably multifactorial. Centrally mediated hyperactivity of the sympathetic nervous system has been proposed as an "initiator" of early EHTN and may provide a major contribution to sustaining elevated blood pressure over the long term in some patients. Studies in animal models [1][2][3][4][5][6][7] have confirmed the presence of sympathoexcitatory bulbospinal neurons in the rostral ventrolateral medulla (RVLM) and their important role in the control of blood pressure. In humans, those neurons are thought to be in the retro-olivary sulcus (ROS), just anterior to the root entry zone of the glossopharyngeal and vagus nerves. 8 Several studies 9 -11 in which the results of magnetic resonance imaging (MRI) and autopsy were used have indicated an increased incidence of vascular compression of the left ventrolateral medulla (VLM) in patients with EHTN. However, the reported incidences have been inconsistent, as has been the laterality of vascular contact, and the exact location of vessel contact was not made clear. Moreover, microvascular decompression to relieve such vascular contact with the VLM has not been uniformly effective in normaliz...

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Role of ventrolateral medulla in vasomotor regulation: a correlative anatomical and physiological study

Cited by 308 publications

References 29 publications

Efficacy of clonidine in patients with essential hypertension with neurovascular contact of the rostral ventrolateral medulla

Efficacy of clonidine in patients with essential hypertension with neurovascular contact of the rostral ventrolateral medulla

Efficacy of an L- and N-type calcium channel blocker in hypertensive patients with neurovascular compression of the rostral ventrolateral medulla

Vascular Compression of the Rostral Ventrolateral Medulla in Sympathetic Mediated Essential Hypertension

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