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用于高血压初始治疗的钙拮抗剂。

Calcium antagonists for initial therapy of hypertension.

作者信息

Frohlich E D

机构信息

Alton Ochsner Medical Foundation, New Orleans, LA 70121.

出版信息

Heart Lung. 1989 Jul;18(4):370-6.

PMID:2663785
Abstract

A new class of antihypertensive agents has emerged for clinical consideration in the initial treatment of hypertension. These calcium antagonists are rapidly absorbed and reduce arterial pressure very promptly by antagonizing the pathophysiologic hallmark of the disease: an increased vascular resistance. Moreover, in reducing arterial pressure by means of arteriolar dilation, these agents do so without expanding intravascular volume and without inordinately stimulating the heart through reflex mechanisms. Vascular resistance is reduced in each of the major target organs of the disease: the heart, brain, and kidney. Reduction of coronary vascular resistance should be of particular value in patients with increased myocardial oxygen demands (e.g., with coronary arterial disease or with ventricular hypertrophy). Reduction of renal vascular resistance should be especially valuable for patients with renal functional impairment as a result of hypertensive vascular disease or with associated renal parenchymal diseases. In this respect, these agents reduce renal vascular resistance while maintaining glomerular filtration rate and reducing renal filtration fraction; these changes should reduce glomerular hyperfiltration and may inhibit promotion of glomerulosclerosis. Diltiazem may be of particular value because it may produce these effects while increasing renal blood flow. Clearly these agents reverse cerebral constriction and might be expected to improve blood flow to the brain; however, further study is anticipated and necessary.

摘要

一类新型抗高血压药物已出现,可供临床考虑用于高血压的初始治疗。这些钙拮抗剂吸收迅速,通过拮抗该疾病的病理生理特征——血管阻力增加,能非常迅速地降低动脉血压。此外,通过小动脉扩张来降低动脉血压时,这些药物不会增加血管内容量,也不会通过反射机制过度刺激心脏。在该疾病的每个主要靶器官(心脏、大脑和肾脏)中,血管阻力都有所降低。对于心肌需氧量增加的患者(如患有冠状动脉疾病或心室肥大),降低冠状动脉血管阻力应具有特别的价值。对于因高血压血管疾病或相关肾实质疾病导致肾功能损害的患者,降低肾血管阻力应特别有价值。在这方面,这些药物在降低肾血管阻力的同时,能维持肾小球滤过率并降低肾滤过分数;这些变化应能减少肾小球超滤,并可能抑制肾小球硬化的进展。地尔硫䓬可能具有特别的价值,因为它在增加肾血流量的同时可能产生这些效果。显然,这些药物能逆转脑动脉收缩,有望改善脑血流量;然而,预计还需要进一步研究且这是必要的。

相似文献

1
Calcium antagonists for initial therapy of hypertension.用于高血压初始治疗的钙拮抗剂。
Heart Lung. 1989 Jul;18(4):370-6.
2
Pathophysiology of hypertension: effects of calcium antagonists on heart and kidney.高血压的病理生理学:钙拮抗剂对心脏和肾脏的影响
J Cardiovasc Pharmacol. 1989;13 Suppl 1:S11-7.
3
[Calcium antagonists in cardiovascular disease. Clinical evidence from morbidity and mortality trials].[心血管疾病中的钙拮抗剂。发病率和死亡率试验的临床证据]
Drugs. 2000;59 Spec No 2:25-37.
4
Renal protection in essential hypertension: how do angiotensin-converting enzyme inhibitors compare with calcium antagonists?原发性高血压的肾脏保护:血管紧张素转换酶抑制剂与钙拮抗剂相比如何?
J Am Soc Nephrol. 1990 Nov;1(5 Suppl 2):S80-7.
5
Renal protection with calcium antagonism in essential hypertension.
Clin Invest Med. 1989 Oct;12(5):300-4.
6
Nephroprotection by antihypertensive agents.抗高血压药物的肾脏保护作用。
J Cardiovasc Pharmacol. 1994;24 Suppl 2:S55-64.
7
[Retrospective studies and prospects of therapy for hypertension].[高血压治疗的回顾性研究与展望]
Herz. 1995 Dec;20(6):370-89.
8
Place of calcium antagonists in the treatment of hypertension.钙拮抗剂在高血压治疗中的地位。
Cor Vasa. 1990;32(2 Suppl 1):2-11.
9
Renal haemodynamic and protective effects of calcium antagonists in hypertension.钙拮抗剂在高血压中的肾脏血流动力学及保护作用
J Hypertens. 1995 Dec;13(12 Pt 1):1363-75.
10
Renal vascular effects of calcium channel blockers in hypertension.钙通道阻滞剂在高血压中的肾血管效应。
Am J Hypertens. 1990 Dec;3(12 Pt 2):305S-312S.

引用本文的文献

1
Physician adherence to hypertension treatment guidelines and drug acquisition costs of antihypertensive drugs at the cardiac clinic: a pilot study.心脏科诊所医生对高血压治疗指南的遵循情况及抗高血压药物的购药成本:一项试点研究。
Patient Prefer Adherence. 2012;6:101-8. doi: 10.2147/PPA.S27223. Epub 2012 Jan 31.
2
Comparison of the efficacy and safety of once-daily versus twice-daily formulations of diltiazem in the treatment of systemic hypertension. The Canadian Multicenter Diltiazem-CD Hypertension Trial Group.
Cardiovasc Drugs Ther. 1995 Jun;9(3):413-20. doi: 10.1007/BF00879030.