● 高血壓藥- 脈優- Amlodipine- Norvasc

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台灣常用的高血壓藥物 -- 脈優錠
高血壓藥物療效最好比較
         在高血壓的治療過程中，無論什麼辦法能把血壓控制血壓值在130至85之間，用量又最少，副作用又最低，服用要方便，療效又是最好!我想這是廣大高血壓患者的追求，很多患者也一直在琢磨尋找，什麼是治療高血壓最好的藥物呢?其實目前在國內外銷量最大的抗高血壓藥就是脈優錠。在國內外都是，只不過每個國家和地區用的不同配方而已，而脈優錠屬於港台地區的配方，無疑是最合適中國人的，是港台地區高血壓患者首選的。
脈優錠在港台地區
     在台灣販賣量最大！知名度最高！
     台灣人吃最多的是治療高血壓、高血糖和高血脂的藥物，去年吃掉323億台幣；十大健保藥物排名第一的是具有降血壓與保護心臟功效的“脈優錠”，已蟬聯八年冠軍寶座，一年就吃掉44億862萬元.
明星蕭淑慎道出自己是二尖瓣膜脫垂，常心悸、心痛，長期服用'脈優錠'(心血管用藥)。
60%的台灣人治療高血壓用脈優錠.
高血壓的治療順序
       治療高血壓是要先藥物穩定血壓!再控制飲食調理!要不很難穩定控制,藥只能控製而不能根除,在生活中需要解除很多不良的生活習慣.達到有規律的生活習慣.更有助於高血壓的治療.
注意飲食習慣
1. 維持理想體重：以穩定和緩的速度進行。
2. 健康飲食：多蔬果、少油脂、少吃高鈉食物（臘肉、鹹魚、鹹蛋、皮蛋、香腸、罐頭、肉丸、豆腐乳、醃菜、蛋糕西點、調味料等）。
3. 多運動：每日至少30分鐘有氧運動，如游泳、快走、慢跑、韻律操、土風舞、騎腳踏車。
4. 少暍酒，慢慢減少喝酒量：男性每天少於啤酒72OCC、高梁酒6OCC、紹興酒200CC、陳年紹興180CC、蔘茸酒100CC。體重較輕或女性，再減一半。
5. 戒菸：可以尋求專業醫療院所協助。
6. 放鬆心情，調適壓力，睡眠充足。
          高血壓也分為許多種的，藥也不是任意亂吃的，高血壓病人吃哪種好並且降壓也是個漫長的過程，並且還不能根治。所以平常多吃清淡的，多吃青菜。高血壓食療方葉菜類：芹菜、茼蒿、莧菜、汕菜、韭菜、黃瓜!等盡量多吃!水果類盡量多吃香蕉、火龍果、菠蘿、西瓜、橘、山楂、蘋果、獼猴桃、桑椹等等.
醫生的選藥建議
        國外最新臨床實證實明，若55歲以上高血壓病患同時倂有高血脂、糖尿病及抽菸者，使用新型鈣離子阻斷劑為基礎藥方，將比常規第一線藥物如常規利尿劑及乙型交感神經阻斷劑，更有效降低23%中風機率、11%死亡率，以及3成糖尿病發生機會。高雄義大醫院內科部部長吳造中醫師表示，40歲以上國人罹患高血壓高達2成左右，近每5人即有1人罹患，他並突顯，如何控制病情，除了基本衛教觀念外，採用何種藥物也是一大關鍵。心腦血管研究指出，過去臨床治療上，往往只能就血壓值下降與否來評估治療效果，不容易觀察出降血壓藥對於單一病患，在長期5年至10年間，預防並發症發生的效果。經過歐洲心臟醫學會最新發表近年來最大型的高血壓治療研究中顯示，鈣離子阻斷劑(脈優錠)、ACE抑製劑，會比一般常規用藥降血壓效果更顯著，能有效控制病情。

高血壓藥物 -- 脈優

脈優 (Amlodipine, Norvasc)

Amlodipine (脈優)
Amlodipine (Norvasc (Pfizer) and generics) (as besylate, mesylate or maleate) is a long-acting calcium channel blocker dihydropyridine (DHP) class used as an antihypertensive and in the treatment of angina pectoris. Like other calcium channel blockers, amlodipine acts by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance thereby reducing blood pressure; in angina, amlodipine increases blood flow to the heart muscle (although DHP-class calcium channel blockers are more selective for arteries than the muscular tissue of the heart (myocardium), as the cardiac calcium channels are not of the dihydropyridine-type).
Medical Uses
Amlodipine is used in the management of hypertension and coronary artery disease.

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.

Pharmacokinetics and Metabolism
The metabolism and excretion of amlodipine have been studied in healthy volunteers following oral administration of 14C-labelled drug. Amlodipine is well absorbed by the oral route with a mean oral bioavailability of approximately 60%. Renal elimination is the major route of excretion with about 60% of an administered dose recovered in urine, largely as inactive pyridine metabolites. The major metabolite identified was 2-([4-(2-chlorophenyl)-3-ethoxycarbonyl-5-methoxycarbonyl-6-methyl-2-pyridyl]methoxy) acetic acid, and this represented 33% of urinary radioactivity. Amlodipine concentrations in plasma declined with a mean half-life of 33 h, while elimination of total drug-related material from plasma was slower.