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PubMed1990

Effects of calcium channel blockers on renal function.

Calcium channel or entry blockers (CEBs) exert important vascular and tubular effects on the kidney. These renal effects include an enhancement of glomerular filtration rate (GFR), renal blood flow (RBF), and electrolyte excretion. Experimental studies in animals and humans indicate the potential therapeutic use of CEBs in several important clinical situations, for example attenuating the course of acute renal failure and slowing the progression of chronic renal failure. The latter effect appears to involve both the agent's antihypertensive effect and an additional cytoprotective effect. That CEBs help preserve renal function in renal transplantation has been shown in both animals and humans. In this setting, the effects of cyclosporine (CsA) and CEB on the immune system and on CsA hepatic metabolism are areas of importance for future research.

Acute Kidney Injury↗
PubMed1991

Direct measurement of intracellular free calcium in cultured human puerperal myometrial cells stimulated by oxytocin: effects of extracellular calcium and calcium channel blockers.

The changes in intracellular free calcium concentration ([Ca2+]i) induced by oxytocin in single cells of cultured human puerperal myometrium were measured with the calcium-sensitive fluorescent dye fura 2 in a digital imaging fluorescence microscopic system. Oxytocin at concentrations of 30-300 nmol/L induced a dose-dependent increase in [Ca2+]i with a peak at 20 seconds. This increase depended mainly on extracellular calcium ([Ca2+]ex) at concentrations of 0.6-4.8 mmol/L. In the absence of [Ca2+]ex, the increase was only 16% of that in its presence. The voltage-sensitive calcium channel blockers nicardipine, nifedipine, and nitrendipine had similar effects, causing significant suppression of the increase in [Ca2+]i induced by oxytocin. Diltiazem also suppressed the increase in [Ca2+]i, though less than the other calcium channel blockers. These data indicate that the increase in [Ca2+]i induced by oxytocin is predominantly dependent upon [Ca2+]ex. Furthermore, the data explain why calcium channel blockers are effective for weakening uterine muscle contractions and indicate which type of blocker is most effective.

Calcium↗
PubMed2005

Antioxidant effects and the therapeutic mode of action of calcium channel blockers in hypertension and atherosclerosis.

Drugs 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.

Animals↗
PubMed2005

[Analgesic effect of huwentoxin-I, a new N-type voltage-sensitive calcium channel blocker, on acute visceral pain in rats].

OBJECTIVE: To study the antinociceptive effect of intrathecally administered huwentoxin-I (HWTX-I or HWAP-I) on visceral pain in rats with acute colon inflammation. METHODS: Nociceptive behaviors was induced by formalin injected into the submucosa of the sigmoid colon in rats and the typical behavioral patterns induced served as the indexes for visceral nociception scoring. HWAP-I (0.1-1.0 microg/kg x b x w.), SNX-111 (0.2, 0.5 and 0.75 microg/kg.b.w.) and morphine hydrochloride (0.05, 0.1 and 0.2 microg/kg x b x w.) were administered subarachnoidally 30 min before formalin injection. RESULTS: Similar to SNX-111 and hydrochloride morphine, HWAP-I administered subarachnoidally significantly reduced nociceptive responses in a dose-dependent manner in the rat model of visceral pain (P<0.05). Both HWAP-I and SNX-111 produced pain suppression effect at the dosage of 0.2 microg/kg x b x w., and in spite of the stronger antinociceptive effect of SNX-111 than HWAP-I at the same doses, SNX-111 caused obvious motor dysfunction in the rats at the doses higher than 0.5 microg/kg x b x w., which was not observed with HWAP-1 at such doses. The antinociceptive effect of morphine hydrochloride was initiated faster but lasted for a shorter period of time than the effects of HWAP-I and SNX-111. CONCLUSION: As a potent blocker of neuronal N-type voltage-sensitive calcium channel, HWAP-I induces remarkably dose-dependent inhibitory effect similar to SNX-111 and morphine on visceral pain induced by sigmoid colon submucosal injection of formalin in conscious rats.

Analgesics, Non-Narcotic↗
PubMedDate not supplied

Prenatal toxicity studies in rats and rabbits with the calcium channel blocker diproteverine.

In prenatal toxicity studies, diproteverine, a calcium channel blocker with demonstrated antianginal properties, produced an unusual pattern of digital, heart, tail, and vertebral defects in rat fetuses from mothers treated during the major period of organogenesis, but only a very low incidence of heart abnormalities was seen in the rabbit. Heart changes were rarely seen in association with digital defects. The findings were consistent with those seen with other calcium channel blockers and add weight to the suggestion of Danielsson and colleagues (5) that digital malformations are a class effect for this type of compound, the effects being related to reduced uteroplacental blood flow. In addition, it is proposed that cardiovascular malformations are also a class response with calcium channel blockers. The distribution of fetal death and hemorrhages and the varying association between cardiovascular, digital, and tail abnormalities seen in the rat with increasing doses of diproteverine fits the pattern of changes reported following hypoxia in the chick embryo. Reduced uteroplacental blood flow with resultant embryonic hypoxia secondary to pharmacologic action is considered a probable mechanism of action for the induction of abnormalities produced by calcium channel blockers.

Abnormalities, Multiple↗
PubMed1986

Calcium-channel blockers for combined angina pectoris and systemic hypertension.

Calcium-channel blockers have been successfully used in the treatment of angina of effort and systemic hypertension. Many patients present with concomitant angina pectoris and hypertension. Controlled clinical trials demonstrate that the calcium-channel blockers are safe and effective as monotherapy in the treatment of these patients, and that their use compares favorably with that of propranolol. The effectiveness of these agents in hypertension appears to be primarily due to their ability to induce systemic vasodilation. Calcium-channel blockers have several therapeutic effects in angina pectoris. Beneficial actions on the major determinants of oxygen consumption, i.e. heart rate, blood pressure and contractility, are generally seen. The potent coronary vasodilating actions of these agents allow for increased coronary blood flow. Improvements in ventricular compliance, regression of left ventricular hypertrophy and cardioprotection appear to be additional effects of the calcium-channel blockers; their contribution to the drugs' overall therapeutic efficacy is presently being evaluated. Calcium-channel blockers are a welcome addition to drug regimens available for the management of patients with coexisting angina pectoris and hypertension.

Adult↗
PubMed1996

Anti-ischaemic therapy during the follow-up phase of acute coronary syndromes. Is there a role for calcium channel blockers?

Various pharmacological strategies are currently being sought to enhance the efficacy of thrombolysis after an acute myocardial infarction (AMI). Apart from the use of new thrombolytic agents, novel anticoagulants and antiplatelet drugs, attention has recently been focused on agents such as the calcium channel blockers (calcium antagonists) traditionally used (prior to the thrombolytic era) for secondary prevention after an AMI. In this context, although calcium channel blockers have not been definitively proven to have any benefit with regard to all-cause mortality or subsequent infarctions, diltiazem has been shown to reduce cardiac mortality, recurrent nonfatal infarction and myocardial ischaemia after non-Q-wave AMI. These benefits have been linked to the drug's effect of lowering heart rate. Since both non-Q-wave AMI and the AMI treated with thrombolytic therapy result in early reperfusion and clinical manifestations of 'incomplete infarction', and are characterised by a similar high incidence of ischaemic complications, it is plausible to hypothesise that prophylactic calcium channel blocker administration to AMI patients post-thrombolysis might decrease the cumulative occurrence of reinfarction and refractory ischaemia during long term follow-up. With this in mind, the Incomplete INfarction Trial of European Research Collaborators Evaluating Prognosis Post-Thrombolysis with Tildiem was initiated in September 1994. This represents the first prospective study to investigate the efficacy of a calcium channel blocker (long-acting diltiazem 300 mg/day) administered as adjunctive therapy with aspirin 160 mg/day in up to 920 patients with an uncomplicated first AMI receiving early thrombolytic therapy. The primary trial objective is to assess the efficacy of blinded therapy on the 6-month cumulative occurrence of a combined clinical end-point (cardiac death, recurrent non-fatal infarction, medically refractory ischaemia)-an end-point identical to that utilised in the assessment of diltiazem in non-Q-wave AMI.

Adrenergic beta-Antagonists↗
PubMed2000

Motor and electrographic response of refractory experimental status epilepticus in rats and effect of calcium channel blockers.

Effects of various calcium channel inhibitors have been studied in lithium-pilocarpine model of status epilepticus. Status epilepticus was induced by administration of lithium chloride (3 meq/kg) followed 21 hr later by pilocarpine (30 mg/kg). Diltiazem (5 and 10 mg/kg) was not effective in delaying onset of convulsions. Verapamil (20 mg/kg) showed protection against lithium-pilocarpine-induced convulsions. The dihydropyridine nifidepine (2.5 and 5 mg/kg) did not show any protection in this model. Amlodipine (5 and 10 mg/kg) as partially protective. Flunarizine (10 and 20 mg/kg) delayed the onset of forelimb clonus and rearing and only 60% of the rats underwent status in the 20 mg/kg group. Pre-treatment of MK-801 led to a potentiation of the antiseizure activity of calcium channel inhibitors. The percent increase in amplitude at various time points with amlodipine pretreatment was significant only at the 30th min recording, and at the rest of the time frames was practically similar as the controls. It can be concluded that the anticonvulsant action of MK-801 can be enhanced by centrally acting calcium channel inhibitors.

Animals↗
PubMed1998

[Views on the use of calcium channel blockers in the treatment of heart ischemia and hypertension].

Calcium-channel blockers differ in their molecular structure, their sites and modes of action. Based on rapport's about short acting calcium-channel blockers, several recent publications have questioned the safety of agents in this class, particularly nifedypine. It has been well documented that nifedypine can cause a precipitation uncontrollable drop in arterial blood pressure, which can be dangerous in the presence of ischemic heart disease, hypertension and other hemodynamically unstable situation. The cardiovascular risk for patients prescribed short-acting calcium channel blockers was eight times than for those taking, long-acting ones. Sustained-release preparations are the preferred form of therapy, as they appear, to be safer than short-acting agents. Most calcium-channel blockers, including verapamil, diltiazem, amlodypine, felodipine, nitrendipine and nicardipine have been shown to be effective in reducing symptoms of myocardial ischemia, and all have been used successfully for lowering blood pressure in hypertensive patients. Data from trials of nondihydropyridines have not demonstrated increased mortality or myocardial infarction rates in patients with myocardial ischemia and good left ventricular function. In patients with coronary artery disease and in hypertensive patients with poor left ventricular function, amlodypine or felodipine may be relatively safe alternative. Particular attention should be paid to the benefits of werapamil in postinfarct patients. In patients with hypertension, calcium-channel blockers should be reserved for use when diuretics, beta-blockers or angiotensin-converting enzyme inhibitors have been used already or contraindicated or are not tolerated and when further blood pressure reduction is necessary.

Aged↗
PubMed1993

A one-year evaluation of calcium channel blocker overdoses: toxicity and treatment.

STUDY OBJECTIVE: To examine the cardiovascular toxicity of calcium channel blockers and the efficacy of various treatments. DESIGN: Case series collected prospectively over one year. SETTING: Three regional poison control centers. TYPE OF PARTICIPANTS: One hundred thirty-nine hospitalized patients who had ingested a calcium channel blocker. INTERVENTIONS: Calcium, dopamine, atropine, isoproterenol, glucagon, and pacemakers. MAIN RESULTS: Hypotension, sinus node suppression, and dysrhythmias often occur with calcium channel blocker overdoses, but atrioventricular nodal block occurs more often with verapamil (chi 2 test, P < .025). Calcium was administered to 23 patients and was efficacious in reversing depression of cardiac conduction and increasing blood pressure. Dopamine was administered to ten patients and was efficacious in increasing blood pressure. Atropine was administered to eight patients, but only two had a positive response. CONCLUSION: Atrioventricular nodal depression is more common with verapamil overdoses. Calcium and dopamine are useful in treating toxicity from calcium channel blocker overdose, whereas atropine is sometimes useful.

Adolescent↗
PubMed1988

Role of calcium channel blockers in experimental exercise-induced ischemia.

Calcium channel blockers, which induce vasodilation by relaxing vascular smooth muscle cells, have proven effective in the treatment of angina pectoris. To study mechanisms of calcium blockade in ischemic heart disease, conscious chronically instrumented dogs with a single coronary artery ameroid constrictor were studied during steady-state treadmill runs which induced regional myocardial ischemia. During exercise-induced ischemia, regional systolic wall thickening and subendocardial blood flow were both significantly reduced in the ischemic zone. Calcium channel blockade with verapamil, diltiazem, or nifedipine enhanced regional systolic wall thickening. Regional subendocardial blood flow in the ischemic region, measured during diltiazem and nifedipine experiments, improved during exercise. Reduced coronary artery resistance in the native vessels and/or recruitment of collaterals appears to largely explain the increased total myocardial blood supply in the jeopardized area and the increased function. However, after diltiazem, reduced exercise heart rates as well as reduced left ventricular end-diastolic pressure also contributed to the improvement in the oxygen-supply imbalance in the ischemic myocardium. These data provide a basis for understanding the efficacy of calcium channel blocker treatment in patients with coronary artery disease.

Animals↗
PubMed2005

Is postoperative calcium channel blocker therapy needed in patients with radial artery grafts?

BACKGROUND: Chronic calcium channel blocker therapy has traditionally been considered necessary in patients carrying a radial artery graft, even in the absence of objective data to support it. This report was conceived to evaluate the angiographic and clinical effects of calcium channel blocker therapy during the first postoperative year. PATIENTS AND RESULTS: A total of 100 consecutive patients who received a radial artery graft at our institution were randomly assigned to receive (n = 53) or not receive (n = 47) calcium channel blocker therapy with oral diltiazem 120 mg/daily started in the early postoperative period. At 1-year follow-up, all patients were reassessed clinically and by Tl 201 myocardial scintigraphy, and 83 of them underwent control angiography. In 12 cases we also evaluated the response of the radial artery to the endovascular infusion of serotonin. No difference in terms of clinical outcome, scintigraphic results, and patency rate was found between patients who received or did not receive calcium channel blocker therapy. Endovascular serotonin infusion evoked an evident spastic reaction of radial artery grafts, not attenuated by calcium channel blocker therapy. CONCLUSION: Calcium channel blocker therapy started immediately after surgery and continued for the first postoperative year does not affect radial artery graft patency and clinical and scintigraphic outcomes. On the basis of these data, the prophylactic use of calcium channel blocker therapy in patients with radial artery grafts seems unsubstantiated.

Aged↗
PubMed2005

Therapeutic considerations in the African-American patient with hypertension: considerations with calcium channel blocker therapy.

African Americans have a higher prevalence, earlier onset, and more rapid progression of hypertensive end-organ disease, as well as excessive hypertensive mortality compared with other racial/ethnic groups. Most differences in hypertension and pressure-related complications between African Americans and whites appear to be quantitative and not qualitative. Improving the diagnosis, treatment, and control of hypertension in this highly vulnerable population is a major health care goal for the new millennium. In this regard the dietary pattern to be promoted for reduction of hypertension risk in African Americans is one of increased consumption of dairy products, fruit, and vegetables as well as a continued emphasis on decreased Na+ intake. When pharmacologic therapy is considered, multi-drug approaches are generally required, with diuretics, angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers), and calcium channel blocker therapy as oft-selected components of most such treatment regimens.

Adult↗
PubMed2000

Effect of mibefradil, a T-type calcium channel blocker, on morbidity and mortality in moderate to severe congestive heart failure: the MACH-1 study. Mortality Assessment in Congestive Heart Failure Trial.

BACKGROUND: Calcium antagonists have proved disappointing in long-term congestive heart failure (CHF) studies. Mibefradil, a new calcium antagonist that selectively blocks T-type calcium channels, has been shown to be an effective antihypertensive, antianginal, and anti-ischemic agent, and because of its different mechanism of action, it may be beneficial as adjunct therapy in CHF patients. METHODS AND RESULTS: This multicenter, randomized, double-blind study compared mibefradil with placebo as adjunct to usual therapy in 2590 CHF patients (NYHA class II to IV; left ventricular fraction <35%). The initial 50-mg daily dose of mibefradil was uptitrated to 100 mg after 1 month and continued up to 3 years. Patients were monitored at 1 week; 1, 2, and 3 months; and every 3 months thereafter. All-cause mortality, cardiovascular mortality, and cardiovascular morbidity/mortality were analyzed by use of the log-rank test (alpha=0.05). Substudies included exercise tolerance, plasma hormone and cytokines, echocardiography, and quality of life. Total mortality was similar between mibefradil- and placebo-treated patients (P=0.151). The 14% increased risk of mortality with mibefradil in the first 3 months was not statistically significant (P=0.093). Treatment groups had similar cardiovascular mortality (P=0.246), cardiovascular morbidity/mortality (P=0.783), and reasons for death or hospitalization. Patients comedicated with mibefradil and antiarrhythmics (class I or III), including amiodarone, had a significantly increased risk of death. Substudies demonstrated no significant differences between treatments. CONCLUSIONS: When used as adjunct therapy, mibefradil did not affect the usual outcome of CHF. The potential interaction with antiarrhythmic drugs, especially amiodarone, and drugs associated with torsade de pointes may have contributed to poor outcomes early in the study.

Aged↗
PubMed1992

Calcium channels in embryonic chick skeletal muscle cells after cultivation with calcium channel blocker.

The effects of chronic treatment with calcium channel blockers were studied on the expression of voltage-dependent calcium channels (VDCCs) in chick skeletal muscle cells developing in culture. Myotubes were treated after 2 days in culture with either 20 microM D600 or 10 microM nifedipine, and measurements were made of the maximum rate of rise (M.R.R.) of the two components of action potential, operated by T- and L-type VDCCs, respectively. Treatment with either blocker reduced the M.R.R. of the action potential component operated by the L-type VDCC throughout the culture period examined. The M.R.R. of the T-type VDCC component, on the other hand, was unaffected by either treatment. The reduction in the M.R.R. of the L-type component in blocker-treated cells is thought to be due to the down-regulation of the expression of L-type VDCC. Thus, it appears that the expression of L-type VDCC in the chick skeletal muscle cells can be regulated by a function of L-type VDCC, which mediate the entry of Ca2+ into the cells. The physiological significance of the L-type VDCC, which expressed prominently early in the development of skeletal muscle cells, for the differentiation of excitability is discussed.

Action Potentials↗