Central sympathoinhibitory effects of calcium channel blockers

被引：26

作者：

Leenen F.H.H. ^{[1
]}

Ruzicka M. ^{[1
]}

Huang B.S. ^{[1
]}

机构：

[1] Hypertension Unit, University of Ottawa Heart Institute, Ottawa, ON, KIY 4W7

来源：

Current Hypertension Reports | 2001年 / 3卷 / 4期

基金：

加拿大健康研究院;

关键词：

Nifedipine; Amlodipine; Sympathetic Activity; Valsartan; Hydralazine;

D O I：

10.1007/s11906-001-0094-7

中图分类号：

学科分类号：

摘要：

It is generally assumed that the arterial vasodilation induced by inhibition of Ca2+ influx into vascular smooth muscle cells represents the main mechanism for the hypotensive effect of dihydropyridine calcium channel blockers. Increases in sympathetic tone have been related to activation of the arterial baroreflex by rapid lowering of blood pressure. This review highlights new findings in two areas. First, in animal studies, direct central administration of dihydropyridines such as nifedipine or amlodipine lowers sympathetic nerve activity and thereby blood pressure. Peripheral administration of nifedipine or amlodipine at low rates appears to result in gradual accumulation of drug in the central nervous system, and also causes lowering of sympathetic nerve activity and thereby lowering of blood pressure (rather than by arterial vasodilation). Second, in hypertensive humans treated with long-acting dihydropy-ridines and presumably little activation of the arterial baroreflex, some studies have demonstrated lowering of sympathetic activity (as assessed by plasma norepineph-rine), but others reported increases (as assessed by plasma norepinephrine or microneurography). This sympathoexci-tatory response may be due to activation of the renin-angiotensin system, particularly at higher doses. Copyright © 2001 by Current Science Inc.

引用

页码：314 / 321

页数：7

共 33 条

[1]

Julius S., Nesbitt S., Sympathetic nervous system as a coronary risk factor in hypertension, Cardiologia, 41, pp. 309-317, (1996)

[2]

Ruzicka M., Leenen F.H.H., Relevance of intermittent increases in sympathetic activity for adverse outcome on short-acting calcium channel antagonists, Hypertension: Pathophysiology, Diagnosis and Management, pp. 2815-2825, (1995)

[3]

Leenen F.H.H., Dihydropyridine calcium antagonists and sympathetic activity: Relevance to cardiovascular morbidity and mortality, Calcium Antagonists in Clinical Medicine, pp. 527-552, (1998)

[4]

Ishii K., Kano T., Kurobe Y., Ando J., Binding of [3H]nitrendipine to heart and brain memebranes from normotensive and spontaneously hypertensive rats, Eur J Pharmacol, 88, pp. 277-278, (1983)

[5]

Akaike N., Kostyuk P.G., Osipchuk Y.V., Dihydropyridine-sensitive low-threshold calcium channels in isolated rat hypothalamic neurons, J Physiol, 412, pp. 181-195, (1989)

[6]

Igelmund P., Zhao Y.Q., Heinemann U., Effects of T-type, L-type, P-type, and Q-type calcium channel blockers on stimulus-induced pre- and post-synaptic calcium fluxes in rat hippocampal slices, Exp Brain Res, 109, pp. 22-32, (1996)

[7]

Higuchi S., Takeshita A., Ito N., Et al., Arterial pressure and heart rate responses to calcium channel blockers administered in the brainstem in rats, Circ Res, 57, pp. 244-251, (1985)

[8]

Laurent S., Girerd X., Tsoukaris-Kupfer D., Et al., Opposite central cardiovascular effects of nifedipine and bay K 8644 in anaesthetized rats, Hypertension, 9, pp. 132-138, (1987)

[9]

Huang B.S., Leenen F.H.H., Sympathoinhibitory effects of central nifedipine in spontaneously hypertensive rats on high versus regular sodium intake, Hypertension, 33, pp. 32-35, (1999)

[10]

Murzenok P.P., Huang B.S., Leenen F.H.H., Sympatho-inhibition by central and peripheral infusion of nifedipine in spontaneously hypertensive rats, Hypertension, 35, pp. 631-636, (2000)

← 1 2 3 4 →