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

Abstract

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.

Comparison of Efficacy of Amlodipine and Cilnidipine on Left Ventricular Hypertrophy amongst Hypertensive Patients

“…Another study showed that in hypertensive patients with neurovascular compression of the rostral ventro-lateral medulla (increased sympathetic nerve activity), Cilnidipine reduces left ventricular mass [44], these two studies are corroborative with present study. A significant reduction in left ventricular mass index with relatively short course of Amlodipine [45], in the patients with concentric LVH, Amlodipine treatment produced significant regression in hypertrophy [46], as well as Amlodipine caused significant reduction in LV Mass and RWT coincides with present study [47].…”

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

“…We have found that cilnidipine, a calcium Efficacy of clonidine in hypertension T Sakuma et al channel antagonist that blocks not only L-type channels but also Ntype channels and inhibits SNA by inhibiting the release of NE from the peripheral sympathetic nerve endings, reduces BP and plasma NE more significantly in untreated EH with NVC than in those without NVC of RVLM. 30 Accordingly, it is possible that any antihypertensive agent that reduces SNA activity may decrease BP especially in hypertensive patients with NVC of RVLM. To test this hypothesis, clinical studies examining the effects of other sympatholytic agents such as a-blockers and b-blockers are also needed, and if this hypothesis is confirmed, it will become necessary to evaluate hypertensive patients for the presence of NVC of RVLM before deciding the treatment for hypertension.…”

Hypertension in patients with cranial nerve vascular compression syndromes and comparison with a population-based cohort

“…Morimoto et al [26][27][28] and Aota et al 2 found in their studies that patients with essential AH and NC of the RVLM have increased sympathetic nerve activity and that MVD of the RVLM normalizes blood pressure and sympathetic nerve activity. Sympatholytic agents decreased blood pressure significantly more in hypertensive patients with RVLM compression than in hypertensive patients without RVLM compression.…”

“…Compression of this center might yield a heightened sympathetic tone, leading to AH. 2,7,12,25,29,35 Jannetta et al [17][18][19] demonstrated that microvascular decompression (MVD) of the RVLM could normalize or improve a raised blood pressure. Because the RVLM is close to the origin of the facial nerve, vessel loops originating from the vertebral/basilar arteries might be responsible for multiple neurovascular compressions (NCs), inducing both hemifacial spasms (HFSs) and AH.…”

“…2,12,[17][18][19][23][24][25][26]28,42 The RVLM is the brainstem cardiovascular center that regulates systemic control of blood pressure. Compression of this center might yield a heightened sympathetic tone, leading to AH.…”