1,721,234 research outputs found
Calcium channel blockers in cardiovascular pharmacotherapy
No full textThis paper summarizes the pharmacological properties of calcium channel blockers (CCBs), their established therapeutic uses for cardiovascular disorders and the current improvement of their clinical effects through drug combinations. Their identification resulted from study of small molecules including coronary dilators, which were named calcium antagonists. Further experiments showed that they reduced contraction of arteries by inhibiting calcium entry and by interacting with binding sites identified on voltage-dependent calcium channels. This led to the denomination calcium channel blockers. In short-term studies, by decreasing total peripheral resistance, CCBs lower arterial pressure. By unloading the heart and increasing coronary blood flow, CCBs improve myocardial oxygenation. In long-term treatment, the decrease in blood pressure is more pronounced in hypertensive than in normotensive patients. A controversy on the safety of CCBs ended after a large antihypertensive trial (ALLHAT) sponsored by the National Heart, Lung, and Blood Institute. There are two main types of CCBs: dihydopyridine and non-dihydropyridine; the first type is vascular selective. Dihydropyrines are indicated for hypertension, chronic, stable and vasospastic angina. Non-dihydropyridines have the same indications plus antiarrythmic effects in atrial fibrillation or flutter and paroxysmal supraventricular tachycardia. In addition, CCBs reduced newly formed coronary lesions in atherosclerosis. In order to reach recommended blood pressure goals, there is a recent therapeutic move by combination of CCBs with other antihypertensive agents particularly with inhibitors acting at the level of the renin-angiotensin system. They are also combined with statins. Prevention of dementia has been reported in hypertensive patients treated with nitrendipine, opening a way for further studies on CCBs' beneficial effect in cognitive deterioration associated with aging
Is the Combination Between Beta-blockers and Calcium-antagonists Appropriate in the Management of Angina-pectoris
No full textPharmacological Basis of the Classification of Calcium-antagonists
No full textIn this brief account of Ca antagonists, I have attempted to illustrate similarities and differences among selective Ca antagonists. Four typical pharmacological profiles may be recognized by taking into account studies at molecular, cellular and tissular levels. This gives a rational basis for understanding that all calcium antagonists do not show identical therapeutic actions
Antioxidant effects and the therapeutic mode of action of calcium channel blockers in hypertension and atherosclerosis.
No full textDrugs currently known as calcium channel blockers (CCB) were initially called calcium antagonists because of their ability to inhibit calcium-evoked contractions in depolarized smooth muscles. Blocking the entry of calcium reduces the active tone of vascular smooth muscle and produces vasodilatation. This pharmacological property has been the basis for the use of CCBs in the management of hypertension and coronary heart disease. A major question is whether drugs reducing blood pressure have other effects that help prevent the main complications of hypertension, such as atherosclerosis, stroke, peripheral arterial disease, heart failure and end-state renal disease. Experimental studies that focus on this question are reviewed in the present paper
Drug-induced cardionecrosis.
No full textCardiotoxicity may be defined as a drug action producing abnormalities in cardiac function, such as transitory disturbances or rhythm, conduction or contractility. Clearance of the drug is followed by recovery of the initial function. Cardionecrosis is the irreversible consequence of cardiotoxicity. Its appearance depends not only upon the toxicological potency of a given compound but may also depend upon the pathophysiological state of the heart. Therefore, two main categories may be recognized considering the influence of this state. Drugs may act on the processes controlling cellular structure such as protein biosynthesis in the case of antibiotics of the anthracycline group. Drugs may act at the level of metabolic regulation through a membranal or an intracellular action; in this case, the functional state of the heart plays a major role. This is mainly observed with sympathomimetics and with drugs interacting with the function of catecholamines. The cardiotoxicity observed in such conditions mimics the action of anoxia or of ischemia. The main determinant of the cardiac lesion is probably the disturbance of cellular calcium metabolism. This situation may be prevented (or treated) by the use of calcium entry blockers (calcium antagonists). A great part of this report will deal with the second group of drugs, because of their potential importance as a chemical hazard for the population and because of a possible preventive protection by calcium entry blockers (calcium antagonists)
New insights into the therapeutic mechanism of action of calcium channel blockers in salt-dependent hypertension: their interaction with endothelin gene expression.
No full textIt appears that the beneficial action of calcium channel blockers (CCBs) in hypertension may be related to short-term and long-term effects. This paper summarises pharmacological studies aiming to characterise those effects. The primary consequence of the short-term effects is the decrease of blood pressure related to a selective interaction of CCBs with calcium channels in hypertensive vessels. The long-term effects may additionally control the disease through prevention of end organ damage, accompanying the interaction of CCBs with the pathways, leading to the re-expression of embryonic genes and to the overactivation of type I collagen gene, which are amplified by a high-salt diet. ET-1 and tumour growth factor beta-1 could be among the main factors activating those pathways. The processes leading to overexpression of those factors and to tissue remodelling may be controlled by lacidipine, independent of the reduction of blood pressure
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