Monosynaptic Excitatory Connection from the Rostral Ventrolateral Medulla to Sympathetic Preganglionic Neurons Revealed by Simultaneous Recordings

Oshima, Naoki; Kumagai, Hiroo; Onimaru, Hiroshi; Kawai, Akira; Pilowsky, Paul M.; Iigaya, Kamon; Takimoto, Chie; Hayashi, Kôichi; Saruta, Takao; Itoh, Hiroshi

doi:10.1291/hypres.31.1445

Cited by 37 publications

(29 citation statements)

References 41 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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“…[7][8][9][10][11][12][13][14]17,18 The protocols of the experiments were approved by the Institutional Review Board of Keio University School of Medicine, Tokyo, and were in accord with the National Guidelines for the Conduct of Animal Experiments. With the animals under deep ether anesthesia, the brainstem-spinal cord was isolated together with other organs (including the heart, carotid sinuses and aorta), which were maintained intact ( Figure 1).…”

Section: General Preparationsmentioning

confidence: 99%

“…[7][8][9][10][11][12][13][14] In an earlier study, 9 we performed whole-cell recordings of rostral ventrolateral medulla (RVLM) neurons and classified them into three types according to their discharge patterns. We have also demonstrated monosynaptic connections between neurons in the RVLM and sympathetic pre-ganglionic neurons by simultaneous recording using the same preparation.…”

Section: Introductionmentioning

confidence: 99%

“…We have also demonstrated monosynaptic connections between neurons in the RVLM and sympathetic pre-ganglionic neurons by simultaneous recording using the same preparation. 13 Furthermore, we identified a monosynaptic (axonal) projection extending from the caudal end of the ventrolateral medulla to the inter-mediolateral cell column using optical imaging and recorded the electrical transmission using a motion picture. 12 In the present study, we developed a modified brainstem-spinal cord preparation in which the aortic arch, carotid sinuses and baroreceptor afferent nerves remained intact.…”

Section: Introductionmentioning

confidence: 99%

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Baro-excited neurons in the caudal ventrolateral medulla (CVLM) recorded using the whole-cell patch-clamp technique

et al. 2011

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Caudal ventrolateral medulla (CVLM) neurons have important roles in the regulation of sympathetic nerve activity and blood pressure through their tonic inhibition of rostral ventrolateral medulla neurons. As few reports have demonstrated CVLM neuronal activity using the whole-cell patch-clamp technique, we attempted to find neurons in the CVLM that are depolarized by the stimulation of baroreceptors. To record the membrane potentials of the neurons in the CVLM, we developed a modified brainstem-spinal cord preparation that enabled us to change the pressure exerted on the aortic arch and carotid sinuses. We were able to identify neurons in the CVLM in which they were depolarized and the action potential (AP) frequency was increased upon baroreceptor stimulation. We referred to these neurons as baro-excited CVLM neurons. When these preparations were superfused with an angiotensin-II (Ang-II) solution, the frequency of the APs increased in 10 of the 14 baro-excited CVLM neurons. Superfusion with a low-Ca 2+ , high-Mg 2+ solution abolished the APs in all seven baro-excited CVLM neurons, suggesting that the baro-excited CVLM neurons did not fire spontaneously. When the preparation was superfused with a low-Ca 2+ solution, 6 of the 7 baro-excited CVLM neurons did not respond to Ang-II superfusion. We for the first time found the baro-excited CVLM neurons, which depolarized pressure dependently but may not fire spontaneously. As Ang-II did not change the activity of the CVLM neurons during superfusion with a low-Ca 2+ , high-Mg 2+ solution, the presynaptic neurons may be mandatory for the Ang-II-induced activation of postsynaptic baro-excited CVLM neurons.

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Monosynaptic Excitatory Connection from the Rostral Ventrolateral Medulla to Sympathetic Preganglionic Neurons Revealed by Simultaneous Recordings

Cited by 37 publications

References 41 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

Baro-excited neurons in the caudal ventrolateral medulla (CVLM) recorded using the whole-cell patch-clamp technique

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