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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Verapamil has been established as the drug of choice in the treatment of supraventricular dysrhythmias and is recognized as useful in the treatment of ischemic heart disease and hypertension. However, verapamil has not generally been considered helpful in the treatment of ventricular dysrhythmias. Five cases are reported in which verapamil was used to terminate a cycle of supraventricular tachycardia-mediated recurrent ventricular fibrillation that could not be suppressed by conventional antidysrhythmics such as lidocaine, procainamide, and bretylium, Proposed mechanisms of verapamil's beneficial effect in this usually fatal situation include (1) a reduction in oxygen consumption related to the reduction in heart rate, thereby raising the ventricular fibrillation threshold; (2) direct anti-ischemic effect; and (3) a direct antidysrhythmic effect. These proposed mechanisms are substantiated by clinical studies. On the basis of this observation, it is recommended that in a situation of supraventricular tachycardia-mediated recurrent ventricular fibrillation that cannot be terminated by conventional antidysrhythmics, the administration of verapamil should be considered.
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PMID:Terminating SVT-mediated recurrent ventricular fibrillation with verapamil. 317 Nov 18

Verapamil is an effective and relatively-safe antihypertensive drug. Serious adverse effects are uncommon and mainly have been related to the depression of cardiac contractility and conduction, especially when the drug is combined with beta-blocking agents. We report a case in which myocardial infarction coincided with the introduction of captopril and the withdrawal of verapamil in a previously asymptomatic woman with severe hypertension. Possible mechanisms that involve a verapamil-related increase in platelet and/or vascular alpha 2-adrenoreceptor affinity for catecholamines are discussed.
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PMID:Verapamil withdrawal as a possible cause of myocardial infarction in a hypertensive woman with a normal coronary angiogram. 317 79

A 56-year-old female patient on verapamil for hypertension experienced two episodes of jaundice, pruritus and upper abdominal pain with transaminase elevated up to six-fold and alkaline phosphatase up to four-fold when inadvertently re-challenged with the drug. Liver biopsy showed marked cholestasis. Verapamil can occasionally cause mixed cytotoxic-cholestatic liver injury.
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PMID:Liver injury due to verapamil. 318 62

The contractile reactivity to norepinephrine, methoxamine, and verapamil of the perfused mesenteric vascular bed from sinoaortic denervated (SAD) and sham-operated (SO) rats was studied 3 to 30 days after surgery. A gradual but incomplete reduction of arterial hypertension was observed in SAD rats throughout the study. The norepinephrine- and methoxamine-induced dose-response curves were similar in both SAD and SO groups on day 3, but shifted to the left on days 7 and 15 and demonstrated a tendency to shift to the right at 30 days. Verapamil-induced vasodilation was similar in both groups. Enhanced mesenteric vascular responsiveness to endogenous catecholamines could contribute to the increased vascular resistance.
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PMID:Contractile reactivity of the perfused mesenteric vascular bed from sinoaortic denervated rats to norepinephrine, methoxamine and verapamil. 322 49

Verapamil, a calcium-entry blocker, and sodium nitroprusside, a non-specific vasodilator, were infused into the blood-perfused hindlimbs of New Zealand genetically hypertensive rats (NZGH) and spontaneously hypertensive rats (SHR), two genetic models of hypertension, and their normotensive controls, New Zealand normotensive rats and Wistar-Kyoto rats (WKY). Vasodilator responses, measured as the falls in perfusion pressure from the initial values, were similar and increased in NZGH and SHR. The responses were strongly dependent on the initial level of perfusion pressure in each strain of rat. It is concluded that increased vascular resistance, rather than a qualitative difference in vasodilator mechanisms, accounts for the enhanced responses to verapamil and sodium nitroprusside in NZGH and SHR hindlimbs.
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PMID:Effect of verapamil and sodium nitroprusside on hindlimb vascular resistance in New Zealand genetically hypertensive and Japanese spontaneously hypertensive rats. 324 Dec 80

Calcium channel blocking drugs are a chemically heterogenous group, so it might be expected that their effects on vascular smooth muscle, cardiac contractility, and conduction tissue may differ. However, the majority of adverse reactions are predictable from their pharmacological actions and may be conveniently grouped in the following categories: 1) vasodilatation, 2) negative inotropic effects, 3) conduction disturbances, 4) gastrointestinal effects, 5) metabolic effects, and 6) drug interactions. Vasodilatory symptoms, namely, dizziness, headaches, flushing sensation, and palpitation, are more likely with nifedipine. Peripheral edema is also common with nifedipine, but the mechanism is uncertain. For a given degree of vasodilation, the greatest negative inotropic effect is seen with verapamil first, diltiazem second, and nifedipine last. Calcium channel blocking drugs are contraindicated in hypertensive patients with second and third degree heart block, sick sinus syndrome, and severe heart failure. Verapamil and diltiazem have a significant effect on cardiac conduction, whereas nifedipine, in therapeutic doses, does not. Local gastrointestinal symptoms, such as nausea and constipation, are common with verapamil. None of the calcium channel blocking drugs have been reported to adversely affect lipid or protein metabolism. However, nifedipine, verapamil, and diltiazem in high doses may inhibit liberation of insulin. The significance of this finding needs to be explored further in hypertensive diabetics. Serum digoxin levels have been shown to increase after administration of verapamil and nifedipine, but there is no evidence that this change has any clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Mar
PMID:Side effects of calcium channel blockers. 328 Apr 92

The availability of calcium antagonists has provided yet another therapeutic option in the management of hypertension. Calcium antagonists lower the blood pressure in hypertensive individuals while preserving the blood flow at the microcirculatory level. While all the available calcium antagonists are effective in the treatment of hypertension, they differ in their hemodynamic and pharmacologic actions. Nifedipine appears to be suitable for immediate treatment of severe hypertension and for chronic treatment of uncomplicated or refractory hypertension. In some but not all patients, co-administration of a beta-blocker is necessary to blunt reflex tachycardia. This problem is less likely with the tablet/long-acting formulation of nifedipine. Verapamil and diltiazem are useful as initial therapy for chronic mild-to-moderate hypertension. They are as effective as other first-line drugs in the treatment of uncomplicated hypertension. The heart rate with verapamil or diltiazem does not change or is slightly reduced, thus contrasting with nifedipine. Experience to date suggests that calcium antagonists do not cause adverse biochemical effects and in this respect are superior to diuretics and certain beta-blockers. Currently, verapamil is available as a sustained release preparation. In the near future, nifedipine or diltiazem may also be available in the long acting formulation to permit simplicity and to enhance patient compliance in the treatment of hypertension.
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PMID:Calcium antagonists in the treatment of hypertension. An overview. 328 42

The antihypertensive effect and possible adverse effects of verapamil were assessed in 30 Thai patients with mild to moderate hypertension. All patients had normal blood chemistry evaluations and electrocardiograms. After a 4-week placebo period, 80 mg of verapamil was given 2 times a day for 8 weeks. Blood pressure and pulse rate were recorded both in supine and standing positions every 2 weeks. Verapamil decreased blood pressure significantly both in supine and standing positions. The pulse rate was not significantly affected. The most common adverse effect was constipation. No vivid dreams or breathlessness were reported. The blood chemistry and electrocardiograms at the end of the study period were not significantly changed. It is concluded that verapamil reduces blood pressure in mild to moderate hypertensive Thai patients.
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PMID:A multicenter study of verapamil in systemic hypertension in Thailand. 351 11

Many studies have confirmed that the treatment of mild and moderate hypertension reduces mortality and morbidity from cardiovascular accidents and cardiac and renal failure; more recent studies suggest that there is some beneficial effect on ischemic heart disease. The harmful metabolic effects of some hypotensive agents on serum potassium, magnesium, uric acid, glucose, renin and lipids might reduce the beneficial effect of controlling raised blood pressure. Also, the adverse effects associated with most antihypertensive drugs have decreased quality of life and, possibly, compliance in many patients. In assessing the value of newer antihypertensive agents, other effects of the drugs must be taken into account. The calcium-channel antagonist verapamil produces a dose-dependent reduction in blood pressure with little postural effect. There is little change in heart rate and the major antihypertensive effect results from a decrease in peripheral vascular resistance, with no accompanying increase in cardiac output. In 75 patients followed for more than 1 year, tolerance to verapamil did not appear to develop, nor were there any significant changes in serum electrolytes or creatinine clearance. Fasting serum lipid levels were measured in 15 patients before and after 3 months of treatment with verapamil (80 to 160 mg, 3 times a day); there was no change in cholesterol, triglycerides or high-density lipoproteins. Verapamil is, therefore, an effective hypotensive agent with a rapid onset of action. Tolerance does not develop with prolonged use, nor does it appear to affect electrolytes or serum lipids adversely. Constipation appears to be its only limiting adverse effect.
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PMID:Long-term results with verapamil in essential hypertension and its influence on serum lipids. 351 14


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