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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1992

Beta-blockers, calcium channel blockers and the sulfhydryl-ACE inhibitors demonstrate protection against free-radical-mediated injury of cardiovascular cells and membranes.

During reperfusion of previously ischemic cardiac tissue, oxygen-centered free radicals are generated and may result in peroxidative injury of cardiovascular cells and membranes. Since the occurrence of reperfusion injury in patients is unpredictable, particularly in those patients with chronic ischemic coronary artery disease, silent ischemia and those predisposed to significant coronary spasm, it would be advantageous to provide continuing therapy with antioxidant agents.

Adrenergic beta-Antagonists↗
PubMed1985

Basic cellular mechanisms of action of the calcium-channel blockers.

Calcium-channel blockers inhibit the entry of calcium ion (Ca++) into excitable cells, including those of coronary and peripheral arterial smooth muscle and the heart. The ability of these drugs to block Ca++ entry into cells inhibits the essential role of this cation as an intracellular messenger. The effects of calcium-channel blockers on the heart include a negative inotropic effect on the working myocardial cells of the atria and ventricles. Because the up-stroke of the action potential in these regions of the heart, and in the rapidly conducting cells of the His-Purkinje system, is due to a fast, sodium-dependent ionic current, calcium-channel blockers do not inhibit conduction in these cells. In the sinoatrial and atrioventricular (AV) nodes, on the other hand, depolarization is due primarily to a Ca++-dependent slow inward current; as a result, the calcium-channel blockers inhibit the sinus pacemaker and AV conduction. Because our knowledge of the molecular structure of the calcium channels in the heart and smooth muscle is rudimentary, little is known of the molecular mechanisms by which calcium-channel blockers inhibit Ca++ entry across the sarcolemmal membranes in these cells. It is apparent, however, that the actions of different members of this class of drugs on the sarcolemma are not the same. Indirect evidence indicates that some members of this class of drugs may interact with hydrophobic regions of the proteins that make up, or regulate, the calcium channels in the plasma membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1989

Potentiation of cocaine toxicity with calcium channel blockers.

Three calcium channel blockers were studied for efficacy in preventing seizures and death from cocaine intoxication. Rats were first pretreated with a test drug then subjected to high dose intraperitoneal cocaine. In this model, control animals developed seizures within six minutes, followed by death within ten minutes. Animals that were pretreated with diltiazem, nifedipine, or verapamil developed seizures significantly faster than controls, and at specific doses the death rate was higher than in controls for all three drugs. The potentiation of seizures and death by 2 mg/kg nifedipine pretreatment was further shown by challenge with three different doses of cocaine. This study fails to demonstrate a protective effect and suggests augmentation of cocaine toxicity by pretreatment with the three currently available calcium channel blockers. Several mechanisms by which calcium channel blockers may augment cocaine-induced toxicity are discussed.

Animals↗
PubMed1989

Cutaneous adverse reactions associated with calcium channel blockers.

The calcium channel blockers, nifedipine, verapamil, and diltiazem, are widely used for the treatment of cardiovascular disease. In spite of their widespread use, little data about the frequency and spectrum of cutaneous reactions associated with these agents have been published. Based on reports provided to the FDA's Division of Epidemiology and Drug Surveillance, and the American Academy of Dermatology's Adverse Drug Reaction Reporting System, it appears that the frequency of adverse cutaneous events associated with these drugs is low, but that occasionally severe reactions are associated with the use of these drugs. Among the more serious reactions associated with the calcium channel blockers are toxic epidermal necrolysis with diltiazem, Stevens-Johnson syndrome and erythema multiforme, which have been associated with all three drugs in this class, and exfoliative dermatitis, which has also been reported with all three agents. Most serious reactions associated with these agents occur within two weeks of initiating drug therapy. These findings suggest that calcium channel blockers are occasional causes of a wide spectrum of cutaneous reactions and should be considered as possible causative factors in patients who develop adverse cutaneous reactions while using these drugs.

Adult↗
PubMed1990

Calcium-calmodulin binding in ischemic rat neurons after calcium channel blocker therapy.

Calcium channel blockers such as nicardipine improve outcome after global cerebral ischemia and may attenuate ischemic neuronal injury by preventing calcium influx and binding to calmodulin. We followed the temporal and regional sequence of neuronal calcium-calmodulin binding in normal rats (n = 6), untreated ischemic rats (n = 15), and ischemic rats treated with 0.05 mg/kg/hr s.c. nicardipine (n = 13). After 30 minutes of four-vessel occlusion, 40-microns brain sections were incubated in an anti-calmodulin antibody specific for calmodulin not bound to calcium and brain protein. Light-microscopic sections were examined immediately after ischemia and after 2 and 24 hours of reperfusion. Extensive staining of unbound calmodulin was seen in all hippocampal regions and in the cortex in normal rats. In untreated ischemic control rats, staining was lost, indicating calcium-calmodulin binding immediately after ischemia in all regions. However, after 24 hours, staining returned to normal in the cortex and dentate, and minimal staining returned in CA1 and CA3. Nicardipine-treated animals had significantly less calcium-calmodulin binding in CA1 and in the dentate after 2 hours of reperfusion. This study demonstrates that in clinically relevant doses nicardipine has a limited effect on calcium-calmodulin binding in selectively vulnerable regions after severe ischemia.

Animals↗
PubMed1988

Monotherapy of hypertension with darodipine: a new calcium-channel blocker.

Calcium-channel blockers are increasingly used as single agents for the treatment of essential hypertension. Following three weeks of single-blind placebo therapy, 43 patients with essential hypertension were randomized into four groups. Group 1 (10 patients) received placebo twice a day, Group 2 (13 patients) received darodipine (PY 108-068) 50 mg twice a day, Group 3 (9 patients) received darodipine 100 mg twice a day, and Group 4 (11 patients) received darodipine 150 mg twice a day. Patients were seen in the clinic weekly for 4 weeks. Clinical and laboratory evaluations were done on each patient. Darodipine caused a sustained decrease in the supine and standing systolic and diastolic blood pressure (p less than .001) and there were no significant pressure differences between the three drug dosages. The effects of the drug on heart rate were not consistent. Placebo had no effect on either blood pressure or heart rate. Side effects were few, mild, and consisted of headaches and peripheral edema, and did not necessitate discontinuation of the drug. No metabolic abnormalities were seen with either low or high doses of the drug. We conclude that: (1) darodipine is effective, safe, and well tolerated; (2) its antihypertensive effectiveness is similar at high and low doses, although the higher doses seemed to have a slightly greater effect on the diastolic arterial pressure; (3) the low dose may be preferable since side effects were dose related.

Calcium Channel Blockers↗
PubMed1990

Pharmacologic management of ischemic heart disease with beta-blockers and calcium channel blockers.

In myocardial ischemia beta-blockers reduce myocardial oxygen demand, improve flow toward ischemic regions, and have mild antiplatelet and antiarrhythmic effects. These agents are effective in chronic stable angina and unstable angina. In chronic myocardial ischemia, the beta-blockers timolol, metoprolol, atenolol, and propranolol have cardioprotective effects, reducing overall mortality and the incidence of recurrent myocardial infarction. Calcium channel blockers, which reduce myocardial oxygen demand and improve oxygen supply, are effective in the treatment of chronic stable angina, vasospastic angina, and unstable angina. Although calcium channel blockers generally have no effect or adverse effects when used as primary therapy for acute myocardial infarction, diltiazem (when used concomitantly with nitrates or beta-blockers) has been shown to reduce the incidence of reinfarction in patients after non-Q wave myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1992

Effects of calcium channel blockers on calcium uptake in rat aortic valve allografts.

BACKGROUND: The life span of human aortic valve allografts is finite, and many fail because of cusp rupture or calcification. Subcellular changes occurring in aortic valves in response to transplantation include the uptake of calcium. This study uses a heterotropic rat aortic valve transplant model to determine whether the calcium channel blockers diltiazem and verapamil might attenuate leaflet calcification. METHODS AND RESULTS: The 60 rats studied were divided into the following groups: 1) control: valves from normal, unoperated F1 generation of Lewis and Brown Norway cross (LBNF1) rats; 2) control: valves from syngeneic transplant combinations (Lewis/Lewis); 3) control: valves from allogeneic transplant combinations (LBNF1/Lewis, donor/recipient); 4) experimental: valves from allogeneic strain combinations treated with 30 mg/kg per day diltiazem; 5) experimental: valves from allogeneic strain combinations treated with 30 mg/kg per day verapamil. Drugs or saline (controls) were administered with osmotic pumps placed subcutaneously 2 days before transplantation. Animals were killed 3 weeks later, and the valves were harvested and prepared for calcium analysis. Energy-dispersive x-ray microanalysis was used to measure the calcium in a section of one leaflet from each valve studied. Paired t tests showed that allograft valves treated with diltiazem or verapamil contained significantly less calcium than allograft controls treated with saline (p < 0.001). When all five groups were subjected to one-way ANOVA, the valves in the allograft control group contained significantly more calcium than all other groups. All other groups were not different from each other. CONCLUSIONS: The calcium channel blockers verapamil and diltiazem were effective in preventing early calcification that occurs in aortic valves after transplantation. Thus, these agents might play a role in prolonging the life of human aortic valve allografts.

Analysis of Variance↗
PubMed1987

Effect of the calcium-channel blockers on calcium accumulation in sarcoplasmic reticulum of skeletal muscle.

Vesicular fragments of sarcoplasmic reticulum isolated from rabbit skeletal muscle were actively loaded with Ca2+ in the presence of ATP and an ATP-regenerating system using Arsenazo III as metallochromic indicator to monitor Ca2+ movements across the membrane. Once the Ca2+ release is triggered by the presence of tetraphenylboron in the reaction medium, the addition of verapamil or diltiazem gives rise to a net Ca2+ entry inside the vesicles. Preincubation in the presence of verapamil does not abolish the tetraphenylboron-induced Ca2+ release, the verapamil-induced Ca2+ accumulation being still observed. There appears to be a high-affinity site for verapamil titrated in the micromolar concentration range, whereas diltiazem demonstrates more complex behavior when its concentration is raised. This study suggests the existence of a Ca2+ pathway (putative channels) which is blocked by the drugs tested allowing Ca2+ accumulation inside the vesicles owing to the Ca2+-dependent ATPase activity.

Adenosine Triphosphate↗
PubMedDate not supplied

Effects of a calcium channel blocker and calcium chelating agents on cochlear electrical activity in the guinea pig.

Endocochlear potential (EP) in the guinea pig was investigated under the influence of nifedipine and calcium chelating agents. The area from the scala tympani to the scala vestibuli was perfused with control and test solutions. EP decreased gradually after perfusion with the nifedipine solution, when the concentration was higher than 100 ng/ml. At a concentration of 200 ng/ml, EP decreased from +70 mV to +14 mV. At 1000 ng/ml, it decreased from +70 mV to +54 mV and stayed at this level during perfusion. It began to return to the initial level when perfusion with the control solution was recommenced. Cochlear microphonics (CM) also decreased with 200 ng/ml of nifedipine, but less markedly than EP. EGTA (10 mM) decreased EP from +80 mV to +67 mV. This change, however, was only transient and EP returned to the control level. EDTA (4 mM) had no significant effect on EP. These results suggest that Ca ions play a role in maintaining EP in a manner similar to that by which Ca modulates Na-K pump activity of the marginal cells in stria vascularis.

Animals↗