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At least 19 recordsLinked to original sources

PubMed2004

Inverse association between prostate cancer and the use of calcium channel blockers.

Calcium channel blockers block calcium signal-mediated apoptosis. It is hypothesized that the use of these drugs may be associated with the development of cancer. This study investigated the association between daily use of calcium channel blockers and prostate cancer in a community-based cohort of men who participated in a longitudinal study of lower urinary tract symptoms. Study subjects were men ages 40 to 79 years by January 1, 1990, and were randomly selected from Olmsted County in Minnesota. At baseline, participants underwent an interview to determine all medications taken on a daily basis, including calcium channel blockers and to elicit a family history of prostate cancer. During follow-up, all men with a histological diagnosis of prostate cancer were identified through patient self-report and by a review of the complete medical record. Over 12,668 person years of follow-up, 15 (6.8%) of 220 calcium channel blocker users and 120 (10.5%) of 1142 nonusers developed prostate cancer (P = 0.09; odds ratio, 0.62; 95% confidence interval, 0.36-1.10). With adjustment for age and family history of prostate cancer, the risk (odds ratio, 95% confidence interval) of prostate cancer was 0.55 (0.31-0.97) in calcium channel blocker users compared with nonusers. In analyses stratified by family history of prostate cancer, the risk of prostate cancer was 0.45 (0.23-0.88) in men without a family history and 2.64 (0.82-8.47) in men with a family history of prostate cancer (P = 0.006). These findings suggest an association between prostate cancer and daily use of calcium channel blockers that varies by family history of prostate cancer.

Adult↗

PubMed1987

Inhibition of platelet-activating factor binding to human platelets by calcium channel blockers.

Calcium channel blockers may impair cell activation either by inhibiting calcium influx or by inhibiting agonist binding. Because of this dual action of calcium channel blockers and because of the close relationship between calcium influx and platelet-activating factor (PAF) binding to platelets the current studies examined the effect of calcium channel blockers on PAF binding to washed human platelets. Diltiazem and verapamil inhibited aggregation by PAF in a dose-dependent manner with 50% inhibition at 2.8 +/- 1.4 X 10(-5) M diltiazem (mean +/- SD, n = 5) and 4.2 +/- 2.0 X 10(-5) M verapamil. Both channel blockers also inhibited PAF binding in a dose-dependent manner with 50% inhibition at 4.7 +/- 2.5 X 10(-5) M diltiazem and 6.3 +/- 1.2 X 10(-5) M verapamil. Analysis of the mechanisms of inhibition of binding indicate both competitive and non-competitive effects of the channel blockers. Scatchard analysis of PAF binding in the presence of different fixed concentrations of either diltiazem or verapamil revealed that these agents both increased PAF receptor number and decreased the receptor binding affinity. Lineweaver-Burke analysis of the same data revealed a family of lines which intersect to the right of the ordinate. The channel blockers also dissociated previously-bound PAF from platelets. The current studies indicate that calcium channel blockers inhibit platelet activation by PAF by more than one mechanism and suggest that the PAF receptor may be closely associated with calcium channels.

Adult↗

PubMed1997

Vascular smooth muscle cell migration, atherosclerosis, and calcium channel blockers.

Calcium channel blockers have been studied widely for their potential ability to retard or even reverse atherosclerosis. Several potential cellular mechanisms have been proposed, including interactions with vascular smooth muscle cells: migration, inhibition of proliferation, or both. This paper reviews some of the signaling events involved in smooth muscle cell migration, including changes in intracellular calcium, and the inhibition of cell migration by calcium channel blockers. Finally, there is a discussion of preliminary experiments on human vascular smooth muscle cell migration using amlodipine.

Amlodipine↗

PubMed1998

[Tissue selectivity of calcium channel blockers].

Calcium channel blockers are also termed calcium antagonists or calcium entry blockers. The use of calcium antagonists for the management of hypertension is well established. Their control of vascular tone is related to their interaction with the alpha 1 subunit of L-type calcium channels. This interaction is not simple since prolonged depolarisation promotes the inactivated state of the channels resulting in a change of affinity which is different for various molecules so far considered. The isoforms of alpha 1 subunits and the duration of the stimulus required to activate heart or vessels are important parameters to be considered with the nature of the molecule. Those parameters influence the vascular selectivity which is quantified as the ratio of the concentrations required to reduce by 50% the contraction of heart and of vessels. This selectivity is an important component in the therapeutic action. Another component of this action is the prevention of structural changes noted in heart and arteries. As well as lowering blood pressure, calcium channel blockers have also been found to exert blood pressure independent effects. For instance, they reduce cardiac and vascular hypertrophy and avoid renal damage. In the stroke-prone rat, such protective effects are accompanied by reduction of the salt-dependent overexpression of the gene of endothelin-1 and of fetal genes associated with cardiac hypertrophy. This paper summarizes available information about those components and discuss their significance.

Animals↗

PubMed2000

Regulation of the renal basolateral transport system for organic anions by calcium channel blockers.

Calcium channel blockers have been reported to exert multiple effects on renal tubular function. Therefore, the effects of the calcium channel blockers nifedipine and verapamil on the cellular uptake of tritiated para -aminohippuric acid (PAH) into microdissected non-perfused rabbit kidney S2 proximal tubule segments were investigated to study a possible influence of calcium channel blockers on renal PAH transport. Since the tubules were entirely collapsed, the accumulated radioactivity overwhelmingly reflects the transport across the basolateral membrane. Tubular PAH accumulation was increased by 1 and 10 microm verapamil, and by 1 microm nifedipine, but it was unaffected by lower or higher concentrations of these calcium channel blockers. The increase in PAH accumulation caused by 1 microm nifedipine or 10 microm verapamil was independent from changes in intracellular Ca(2+) and inhibited by staurosporine (1 and 10 n m) a potent inhibitor of protein kinase C (PKC). Our results indicate that the calcium channel blockers nifedipine and verapamil increase the transport of organic anions across the basolateral membrane of proximal tubules, probably by an activation of PKC. Furthermore, the increased tubular PAH transport may disturb the estimation of the renal PAH-clearance.

Adenosine Triphosphate↗

PubMed2001

Risk of suicide in users of beta-adrenoceptor blockers, calcium channel blockers and angiotensin converting enzyme inhibitors.

AIMS: To examine the risk of suicide in users of beta-adrenoceptor blockers, calcium channel blockers, and angiotensin converting enzyme inhibitors. METHODS: We conducted a cohort study based on linkage of a population-based prescription registry in North Jutland County, Denmark, and the nationwide Death Registry. From 1989 to 1995 there were 58 529 users of beta-adrenoceptor blockers, calcium channel blockers, and angiotensin converting enzyme inhibitors. The mortality rates from suicides in the cohort members were compared with the rates in the general population. RESULTS: One hundred and four suicides occurred in the cohorts. The standardized mortality ratio for suicide in users of beta-adrenoceptor blockers was 1.6 (95% confidence interval: 1.2-2.1), in users of calcium channel blockers 1.2 (95% confidence interval: 0.8-1.7), and in users of angiotensin converting enzyme inhibitors 1.2 (95% confidence interval: 0.7-1.8). In users of beta-adrenoceptor blockers, the risk of suicide was increased during the first 12 months after the start of therapy, standardized mortality ratio 2.1 (95% confidence interval: 1.2-3.5). There was a trend in the standardized mortality ratio of suicide from 0.9 (95% confidence interval: 0.4-1.9) in users of beta-adrenoceptor blockers with low lipid solubility, to 1.6 (0.8-2.8) and 2.7 (1.7-4.1) in users of beta-adrenoceptor blockers with medium and high lipid solubility, respectively. CONCLUSIONS: Users of medium and high lipid soluble beta-adrenoceptor blockers may have an increased risk of suicide. Users of calcium channel blockers and angiotensin converting enzyme inhibitors do not seem to have a significantly increased risk of suicide.

Adrenergic beta-Antagonists↗

PubMed1989

Esophageal blood flow in the rabbit: response to calcium channel blockers.

Calcium channel blockers have recently been added to the therapeutic regimen for patients who have chest pain of esophageal origin. Although relief of symptoms has been reported, this has not always been associated with changes in esophageal contraction pressures or luminal pH. Myoischemia has been proposed as one possible mechanism for esophageal chest pain. We have investigated the effect of the calcium channel blockers verapamil, nifedipine, and diltiazem on esophageal blood flow in the rabbit model. Esophageal blood flow was measured three times in each rabbit with use of the radiolabeled microsphere technique after a 30-minute continuous infusion of (1) saline solution (baseline), (2) a low dose, and (3) a high dose of each agent. Esophageal mucosal blood flow significantly decreased with nifedipine but was unchanged with verapamil and diltiazem. Esophageal muscle blood flow significantly increased--approximately 100% after administration of each of the calcium channel blockers. Thus esophageal muscle blood flow is enhanced after administration of calcium channel blockers, and this may be one therapeutic mechanism of the calcium channel blockers in the relief of esophageal chest pain in some esophageal diseases.

Animals↗

PubMed1997

Cell-cycle arrest in G0/G1 phase of growth factor-induced endothelial cell proliferation by various calcium channel blockers.

Calcium channel blockers cause antiproliferative effects on various cells in culture. Since angioneogenesis is a crucial step in the development of tumor growth, we examined the influence of different calcium channel blockers on human umbilical arterial endothelial cell (HUAEC) growth. Cell growth was measured by cell count, by [3H]thymidine incorporation, and by a 5-bromo-2-deoxyuridine (BrdU-incorporation immunofluorescence assay. Cell-cycle analysis was performed by flow cytometric analysis. Nifedipine, isradipine, diltiazem, and verapamil dose-dependently inhibited the basic fibroblast growth factor (bFGF)-induced [3H]thymidine incorporation. Fifty micromolars of nifedipine, isradipine, diltiazem, and verapamil completely inhibited bFGF-induced proliferation of HUAEC. Ten micromolars of each calcium channel blocker abolished the bFGF-induced increase in cell count. Five micromolars of isradipine completely blocked the bFGF-induced BrdU incorporation. Stimulation of HUAEC with bFGF (50 ng/ml) for 24 h caused a 2-fold increase in cells that entered S and G2+M phase in comparison with control cells. Five micromolars of isradipine abolished this effect completely. We conclude that calcium channel blockers are able to inhibit cell proliferation by a cell-cycle arrest in G0/G1 phase.

Calcium Channel Blockers↗

PubMed1992

Calcium channel blockers.

Calcium channel blockers are widely used in the treatment of ischemic heart disease, hypertension, and supraventricular tachycardia. The prototype agents, verapamil, nifedipine, and diltiazem, represent three classes of calcium channel blockers, each of which has different pharmacologic effects. Nifedipine and the other dihydropyridines primarily are vasodilators and have no clinical effects on cardiac conduction or contractility. Diltiazem and verapamil also are vasodilators, but they possess, to varying degrees, negative inotropic, chronotropic, and dromotropic effects. Side effects of these drugs are relatively rare and usually not serious, with the exception of potential conduction disturbances and heart failure in patients with underlying cardiac disease. To assess patients taking these medications and provide the necessary teaching, the nurse needs an understanding of the pharmacologic properties, clinical indications, and potential adverse effects of the various drugs.

Calcium Channel Blockers↗

PubMed1991

Comparative clinical pharmacology of calcium channel blockers.

Calcium channel blockers are effective antihypertensive agents, both as initial monotherapy and in combination with other antihypertensive agents. These drugs are also effective in the treatment of chronic, stable angina, variant angina and supraventricular arrhythmias. Drugs in this class have different affinities for calcium channels in vascular smooth muscle, cardiac muscle, cardiac sinus and atrioventricular node. They are all useful in hypertension and angina, but only verapamil and diltiazem are also useful in the control of heart rate and supraventricular arrhythmias. Nimodipine may control vascular spasm following subarachnoid hemorrhage. Calcium channel blockers have also been used in the treatment of migraine headache and Raynaud's phenomenon.

Calcium Channel Blockers↗

PubMed1992

Interventions that beneficially influence the evolution of coronary atherosclerosis. The case for calcium channel blockers.

Calcium channel blockers have been shown to retard the development of atherosclerosis in rabbits fed cholesterol-rich diets. The mechanism accounting for this effect is controversial but may be by stimulation of cholesteryl ester hydrolase activity in smooth muscle cells, by amelioration of hypercholesterolemia-induced endothelial dysfunction, or by inhibition of smooth muscle cell proliferation and migration. The effect of calcium channel blockers on the evolution of coronary atherosclerosis in humans has been assessed in two clinical trials. In the Montreal Heart Institute trial, nicardipine did not influence the overall rate of progression and regression; however, nicardipine-treated patients experienced significantly less progression of minimal lesions, defined as stenoses of < or = 20% severity. In the International Nifedipine Trial on Antiatherosclerotic Therapy, nifedipine had no effect on overall progression and regression but reduced the rate of appearance of new coronary lesions. These studies constitute a potentially important new approach to the management of coronary atherosclerosis.

Animals↗

PubMed1986

Differentiation of calcium entry blockers into calcium channel blockers and calcium overload blockers.

The heterogeneity of the several subgroups of calcium-antagonistic drugs requires a rigid and well-defined differentiation of this type of agents. From the chemical point of view verapamil-like drugs, dihydropyridines, benzothiazepines and diphenylalkylamines should be distinguished. Among these largely different groups no obvious relationship between chemical structure and calcium-antagonistic activity can be recognized. Irrespective of the chemical classification all above-mentioned compounds inhibit the entry of calcium into cells. However, from a pharmacological point of view a distinction should be made between calcium channel blockers and calcium overload blockers. Calcium channel blockers selectively and competitively inhibit the transmembranous slow inward current, which is carried by calcium ions both in cardiac tissues and in vascular smooth muscle under physiological conditions. However, calcium overload blockers only inhibit the overload of the cell with calcium ions, which occurs under pathological, ischemic conditions. Finally, a survey is given of the various subtypes of calcium-antagonistic drugs with respect to their organ specificity and therapeutic applicability.

Animals↗

PubMed1997

Pharmacological aspects of calcium channel blockers.

Calcium channel blockers (CCBs) inhibit voltage-dependent L-type calcium channels. This leads to vascular smooth muscle relaxation and negative inotropic and chronotropic effects in the heart. The latter are counteracted in vivo by a vasodilatation-triggered, baroreceptor-mediated reflex increase in sympathetic tone, resulting in indirect cardiostimulation. The mean vascular/cardiac effect ratios of the first-generation CCBs-verapamil, nifedipine, and diltiazem-are relatively low and amount to approximately 3, 10, and 3, respectively. The pharmacokinetic properties of verapamil, nifedipine, and diltiazem are similar. The drugs are almost completely absorbed after oral administration, but their bioavailability is reduced because of first-pass hepatic metabolism. The onset of action of verapamil, nifedipine, and diltiazem, at least in immediate-release formulations, is relatively fast (0.5-2 hours), and their elimination half-lives range from 2 to 7 hours. The second-generation CCBs (e.g., amlodipine, felodipine, and nisoldipine) have a slower onset of action (due to either intrinsic properties of the drug or a slow-release formulation), a longer duration of action, and greater vascular/cardiac effect ratios. These features may provide therapeutic benefits, for example, a less pronounced increase in sympathetic tone and reflex tachycardia, and reduced likelihood of negative inotropic effects. These agents can therefore probably be used in patients with left ventricular dysfunction.

Calcium Channel Blockers↗

PubMedDate not supplied

Immunosuppressive properties of calcium channel blockers.

Calcium channel blockers are extensively used for their beneficial effects on the cardiovascular system. Solid organ transplant recipients commonly have cardiovascular disease and are often treated with these agents. Research demonstrates that calcium antagonists may have beneficial effects in this population that are independent of their effects on the cardiovascular system. Indeed, both in vitro and in vivo studies suggested that they may possess immunosuppressive properties. Their actions at the cellular level in both the afferent and efferent arms of the immune system indicate that alone, as well as in combination with cyclosporine, these agents possess immunosuppressive properties that may potentially benefit the transplant population.

Animals↗

PubMed2000

A suicide attempt with an oral calcium channel blocker.

Calcium channel blockers are widely used in all-aged populations. The drugs are generally safe in therapeutic dosage, but severe side effects with elevated intake are increasingly described, mainly in adult patients. We report an adolescent girl who intentionally ingested an overdose of nifedipine.

Adolescent↗

PubMed2005

[Clinically significant drug-drug and drug-food interactions associated with calcium channel blockers].

Calcium channel blockers have been widely used for treatment of hypertension, angina pectoris, arrhythmia, and other heart diseases. Nowadays, combination therapy is widely common for these diseases. However, combination therapy is associated with increasing risks of pharmacokinetic or pharmacodynamic drug-drug interaction, and therefore clinicians should pay attention to prevent it. Furthermore, in addition to drug-drug interactions, we need to be cautions for drug interaction with food and drink including health-food and supplement.

Calcium Channel Blockers↗

PubMed1991

Improved outcome of cadaveric renal transplantation due to calcium channel blockers.

Calcium channel blockers (CCB) administered to recipients of cadaveric renal transplants have been shown to improve graft function, decrease the incidence of delayed function, prevent acute cyclosporine toxicity, and lessen the number of rejection episodes in the first several weeks posttransplant. In order to determine whether CCB provide a similar long-term benefit, a retrospective analysis of 83 first cadaveric renal transplants performed in 1987 and 1988 was performed. The clinical course of 17 patients who were discharged and maintained on CCB therapy for 1 year was compared with that of 24 patients who never received CCB during the same 1-year period. The remaining 42 patients were excluded for failing to meet these inclusion criteria. The two groups were similar with respect to age, sex, cold ischemia time, degree of sensitization, HLA matching, DR matching, and DR mismatching. The no CCB group did receive a significantly greater number of pretransplant transfusions. In the 1 year of follow-up, graft loss in the CCB group was less than in the no CCB group (1/17, 5.9% vs. 6/24, 25%). There was a striking decrease in the percentage of first rejection episodes in the CCB group as compared with no CCB therapy (35% vs. 83%, P less than 0.005). In addition, a similar decrease in second rejection episodes was found in the CCB group (18% vs. 33%, P less than 0.05). The two groups also were compared with respect to graft function. Despite similar serum creatinine levels at 1 month (CCB 1.8 mg% vs. no CCB 2.2 mg%, P = 0.37) and 1 year (CCB 1.7 mg% vs. no CCB 2.4 mg%, P = 0.19), the CCB group had a significantly higher glomerular filtration rate at 1 month (53.9 vs. 38.7, P less than 0.05) and 1 year (57.0 vs. 35.0, P less than 0.001) as measured by clearance of radiolabeled iothalamate. These results suggest that the short-term improvements noted in both graft function and rejection episodes with CCB are maintained for the first year posttransplant. More importantly, CCB use results in improved 1-year graft survival.

Adult↗

PubMed1988

Side effects of calcium channel blockers.

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)

Calcium Channel Blockers↗