副作用最少的高血壓藥

降压药，一般情况下得长期服药，所以高血压患者最担心的就是长期服药带来的副作用，怎么才能减少和避免降压药的副作用，这里谈几点看法，参考。

1、联合用药

每一种降压药都有副作用，由于高血压机理的复杂性，在疗效上，也有局限性，所以现在最为流行的降压方式，是联合用药，即坎少了单味降压药物的副作用，在机理上又引入了中医“君臣佐使”排兵布阵的用药理念。临床上，中重度的高血压患者，首选的减毒增效的用药方式，就是联合用药。这是目前世界各国高血压指南力推的主要方式。

所以，如果您是一位中、重度的高血压，应该提醒您的医生，帮您制定一个联合用药的方案。

2、合理搭档

联合用药的时候，药物之间也讲究“最佳搭档”，搭档的原则，就是两种以上的降压药之间，应该形成优势互补、取长补短的组合效应。

首先，大的原则是非同一类降压药之间搭档，比如，钙离子拮抗剂与转换酶抑制剂之间的搭档，转换酶抑制剂与利尿剂之间的搭档。我们临床上，经常见到有的服用两种同一类的降压药，这是不合适的，如尼莫地平+硝苯地平等、氨氯地平+拜新同、依那普利+替米沙坦等，有的是患者自己胡乱随意吃的，也有的是医生帮助“开药”的，这显然是不合适的，就好像吃饭，“包子配稀粥”可以，如果“包子配水饺”，就让人尴尬了。

其次，搭配好药物之间的“反向”作用。例如，倍他乐克降压的同时减慢心率，而硝苯地平类在降压的同时加快心率，这两种药物配合“门当户对”。

所以，如果医生给您联合用药降压的时候，您也不妨讲讲这些浅显的原理，去分析一下，方案是否合理，觉得不妥，可以反馈给您的医生。

3、中西配伍

这是中医师的本事，某些恰当的患者，可以发挥中西药“配伍”的优势，例如，在辨证的原则指导下，利尿剂配伍二陈、地平类的配伍知柏地黄、天王补心丹或五苓散等，也可以有效的减轻西药的副作用。

4、知己知彼

有的西药的副作用出现，是出现在特殊人群的。例如利尿剂双克，可以引起血糖增高、尿酸增高，如果是一个糖尿病、通风患者，就尽量避免使用利尿降压药；有的患者，具有直立性头晕的历史，在降压药的选择上，尽量不要选择直接扩张血管的“地平类”的降压药。

所以，作为高血压患者，找医生看病的时候，尽量把您这些情况给医生说清楚。

5、小量开始

有的是第一次服用降压药，容易出现“首剂反应”，就是第一次服用降压药出现不适应的头晕、黒朦、心慌、潮红、出汗等现象，所以，所有第一次服用降压药的患者，服用降压药宜从小剂量开始，如氨氯地平从2.5毫克、硝苯地平缓释剂宜从10毫克、倍他乐克缓释剂宜从25毫克开始，然后根据反应和疗效，再逐渐增加到合适的治疗量。

所以，当您第一次被要求服用降压药的时候，记得这一条，也提醒医生，避免弯路。

6、远离杯物

戒酒是防治高血压的重要举措，同时也是减少降压药副作用的重要手段，很多降压药要通过肝脏这个“化工厂”来分解、解毒代谢，如果是“降压药+酒精”，等于加倍了肝脏的负担，尤其是脂肪肝等肝脏本身有毛病的患者朋友。

所以，当您服用降压药（化学品）时候，应该首先战胜自我、克服酒瘾。

7、未雨绸缪

一些药物的副作用标注的很清楚，服药过程中应该留意观察，一旦有副作用的苗头，应该及时找医生换药调整方案。例如服用北京零号出现的嗜睡、多梦、记忆力下降等，应该及时更换，有慢支、肺气肿的朋友，尽量避开服用引起咳嗽的普利类降压药。

所以，服用降压药，有些细节需要医患双方配合，患者自我多警惕一些，也能未雨绸缪。

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Contraindications
(1). Breast feeding
(2). Cardiogenic shock
(3). Unstable angina
(4). Aortic stenosis: Amlodipine causes vasodilation, which can result in reduced cardiac output in patients with severe aortic stenosis.
Adverse effects
Adverse side effects of the use of amlodipine may be:
● Very often: peripheral edema in 8.3% of users, fatigue in 4.5% of users
● Often: dizziness; palpitations; muscle-, stomach- or headache; dyspepsia; or nausea - in one in 100 users
● Sometimes: blood disorders, development of breasts in men (gynecomastia), impotence, depression, insomnia, tachycardia, or gingival enlargement - in one in 1,000 users
● Rarely: erratic behavior, hepatitis, jaundice - in one in 10,000 users
● Very rarely: hyperglycemia, tremor, Stevens–Johnson syndrome - in one in 100,000 users
The acute oral toxicity (LD50) of amlodipine in mice is 37 mg/kg.
Cautions
● Hepatic impairment
● Pregnancy
Interactions
● In patients with severe coronary artery disease, amlodipine can increase the frequency and severity of angina or actually cause a heart attack on rare occasions. This phenomenon usually occurs when first starting amlodipine, or at the time of dosage increase.
● Excessive lowering of blood pressure during initiation of amlodipine treatment can occur, especially in patients already taking another medication for lowering blood pressure. In rare instances, congestive heart failure has been associated with amlodipine, usually in patients already on a beta blocker.
● Amlodipine is primarily metabolyzed by the liver, via the cytochrome P450 isoenzyme CYP3A4. As a result, serum levels can potentially be affected by drugs which inhibit or activate CYP3A4. Grapefruit juice can inhibit the cytochrome P450 system, but the predicted interaction risk with amlodipine is low.
     The most recent study indicates that long-term use (10 yrs) of calcium channel blockers to control hypertension lead to a 10 fold increase in risk to develop breast cancer.
Mechanism of Action
     Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the movement of calcium ions into vascular smooth muscle cells and cardiac muscle cells. Experimental data suggest amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects, or decreased heart muscle contractility, can be detected in vitro, but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa = 8.6), and its interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect.
     Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure.
     Amlodipine also acts as a functional inhibitor of acid sphingomyelinase (FIASMA). Sphingomyelin is involved in signal transduction and apoptosis, or cell death.
    The precise mechanisms by which amlodipine relieves angina have not been fully delineated, but are thought to include:
Exertional angina -- In patients with exertional angina, amlodipine reduces the total peripheral resistance (afterload) against which the heart works and reduces the rate pressure product, so lowers myocardial oxygen demand, at any given level of exercise.
Vasospastic angina --Amlodipine has been demonstrated to block constriction and restore blood flow in coronary arteries and arterioles in response to calcium, potassium, epinephrine, serotonin, and thromboxane A2 analog in experimental animal models and in human coronary vessels in vitro. This inhibition of coronary spasm is responsible for the effectiveness of amlodipine in vasospastic (Prinzmetal's or variant) angina.