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PubMed2003

The effect of an L-type calcium channel blocker on the hemodynamics of orbital arteries in dogs.

PURPOSE: (1) To determine the effect of the l-type calcium channel blocker amlodipine on color Doppler ultrasound-determined vascular resistance and blood flow velocities in the distal retrobulbar arteries of dogs; (2) to determine any effect of blood pressure and PCO2 rate on such color Doppler-determined circulatory measurements. METHODS: Color Doppler imaging measurements of the short posterior ciliary artery, long posterior ciliary artery, and ophthalmic artery of normal eyes of 10 dogs were obtained under isofluorane anesthesia before and 1 week after oral amlodipine administration. Mean systemic arterial blood pressure and PCO2 were monitored. RESULTS: The mean resistive index decreased significantly in the short posterior ciliary artery (P = 0.0347), in the long posterior ciliary artery (P = 0.0092), and ophthalmic artery (P = 0.0004) following systemic amlodipine administration. The end diastolic velocity increased significantly in the long posterior ciliary artery (P = 0.0368) and ophthalmic artery (P < 0.0001). The peak systolic velocity increased significantly in the ophthalmic artery (P = 0.0256). Mean systemic arterial blood pressure was significantly negatively associated with resistive index (P < 0.0001) and significantly associated with the log of the end diastolic velocity (P < 0.0001). CONCLUSIONS: Systemically administered amlodipine increases color Doppler imaging-determined blood flow velocity and decreases vascular resistive index in the ophthalmic artery, short posterior ciliary artery and long posterior ciliary artery of normal dogs. Changes in systemic arterial blood pressure can significantly affect the measurement of color Doppler imaging parameters.

Administration, Oral↗
PubMed1984

Calcium channel blockers in emergency medicine.

Diltiazem, nifedipine, and verapamil inhibit calcium entry into cells via different mechanisms with different pharmacologies. They display different relative effects on different cardiovascular functions, a complex interplay of direct actions and adrenergic reflexes. Peripheral arterial vasorelaxation causes adrenergic reflex activity which opposes their direct negative chronotropic, dromotropic, inotropic, and hypotensive actions. Verapamil's most potent activity is electrophysiologic, and nifedipine's effects are hemodynamic; diltiazem acts like a less-potent combination of verapamil and nifedipine. All three drugs are efficacious in angina. These three drugs may not be interchangeable in all patients, but individualization of therapy is possible. Future indications for calcium channel blocker therapy may include hypertrophic cardiomyopathy, cerebral vasospasm, migraine headaches, pulmonary hypertension, asthma, esophageal spasm, intestinal ischemia, Raynaud's phenomenon, dysmenorrhea, and premature labor.

Action Potentials↗
PubMed1997

A calcium-channel blocker, amlodipine, attenuates insulin antinatriuresis but does not modulate insulin-mediated attenuation of cardiovascular reactivity in healthy man.

BACKGROUND: Insulin exerts an antinatriuretic effect when administered acutely in vivo. Interestingly, insulin fails to reduce sodium excretion in rats receiving verapamil. The present study was undertaken in order to investigate whether the calcium-channel blocker amlodipine attenuates the antinatriuretic effect of insulin in humans. METHODS: Eight healthy lean men (32 +/- 2 years) were investigated on three different occasions; i.e. time-control, insulin infusion alone, and insulin infusion following pretreatment with amlodipine (5 mg x 1 during 10 days). During the experiments renal haemodynamics (insulin and PAH clearances) and segmental tubular sodium handling (sodium and lithium clearances) were investigated. The cardiovascular reactivity was also assessed by a graded noradrenaline infusion at the end of each experiment. RESULTS: Insulin infusion alone was accompanied by a significant 50% reduction in urinary sodium excretion. Following amlodipine pretreatment, euglycaemic insulin infusion was associated with an attenuated antinatriuretic response and the cumulative sodium excretion following 135 min of insulin infusion was significantly higher (24 +/- 4 vs 18 +/- 3 mmol; P < 0.05) as compared to insulin infusion alone. No significant differences in the proximal and distal tubular sodium handling respectively, were seen following CCB pretreatment. The results also show that the doses of noradrenaline required to increase the basal mean arterial blood pressure by 10 mmHg (262 +/- 38 vs 150 +/- 25 ng/kg/min; P < 0.05) and by 20 mmHg (431 +/- 36 vs 250 +/- 38 ng/kg/ min; P < 0.05) respectively, were significantly higher during the insulin infusion than during the time-control experiment. Pretreatment with amlodipine did not further modulate the cardiovascular reactivity. CONCLUSION: Pretreatment with a calcium-channel blocker, amlodipine, attenuates the antinatriuretic effects of insulin leading to a significantly higher cumulative sodium excretion at the end of insulin infusion, which may be of clinical importance. Moreover, insulin attenuates the cardiovascular reactivity to a graded noradrenaline infusion, suggesting that insulin causes vasodilatation in healthy man.

Adult↗
PubMed1993

Calcium channel blockers impair the pituitary-adrenocortical responses to central adrenergic receptors stimulation.

The role of calcium channels in the hypothalamic-pituitary-adrenal (HPA) activity, stimulated by adrenergic receptor agonists was investigated indirectly through corticosterone secretion in conscious rats. The drugs were given intracerebroventricularly (icv) or intraperitoneally, calcium channel blockers 15 min before adrenergic receptor agonists. Verapamil and nifedipine considerably diminished the increase in serum corticosterone level induced by icv phenylephrine, an alpha 1-adrenergic receptor agonists. Verapamil almost completely suppressed the corticosterone response to icv clonidine, and alpha 2-adrenergic receptor agonist, and abolished the corticosterone response to the centrally administered isoproterenol, a beta-adrenergic agonist. The results demonstrate a significant role of calcium channels and calcium ions in the HPA activity, stimulated centrally by adrenergic receptor agonists. They also indicate that verapamil and nifedipine interfere predominantly with calcium channels on the hypothalamic CRH secreting neurons and anterior pituitary corticotrops when inhibiting pituitary-adrenocortical activity stimulated by adrenergic receptor agonists.

Adrenergic alpha-Agonists↗
PubMed1986

Calcium channel blockers and pulmonary hypertension.

In vascular smooth muscle from the pulmonary circulation, potassium evoked contractions are abolished in calcium-free medium and by calcium channel blockers (CCB). Noradrenaline, histamine, and serotonin induced contractions are partly resistant. Pulmonary arterial hypertension may occur both as a primary disorder and secondary to cardiac and pulmonary diseases; in both types there may be a component of pulmonary arterial vasoconstriction. In animal models, hypoxic pulmonary hypertension is counteracted by CCBs, nifedipine being particular effective. In patients with this disorder, CCBs also seem able to lower pulmonary arterial pressure and vascular resistance, but no controlled trials documenting their clinical efficacy have been performed. This is valid also for primary pulmonary hypertension, where some of the CCBs may have clinical value.

Animals↗
PubMed2001

Epidemiologic review of the calcium channel blocker drugs. An up-to-date perspective on the proposed hazards.

In the setting of soaring popularity, postmarketing studies of calcium channel blockers came to suggest an increase in a variety of major adverse end points. The evidence, however, was largely observational, and large-scale trials capable of addressing the concerns were wanting. Clinical trials now support the safety and efficacy of the long-acting dihydropyridines for patients with both uncomplicated and diabetic hypertension, although conventional therapies and, in the latter case, angiotensin-converting enzyme inhibitors have superior proof of benefit. By contrast, short-acting dihydropyridines should be avoided. In the acute coronary syndromes, beta-blockers remain the treatment of choice; the evidence for nondihydropyridines remains inconclusive. Stable angina calls for beta-blockers as first-line therapy and nondihydropyridines as second-line therapy, whereas in ventricular dysfunction, safety data for nondihydropyridines are lacking. Initial reports of cancer, bleeding, and suicide have been contradicted by subsequent data, making the associations uncertain or unlikely. Remaining questions await completion of ongoing trials to better define the indications for these agents.

Bias↗
PubMed2006

Synthesis of 4-aryl-3,4-dihydropyrimidin-2(1H)-thione derivatives as potential calcium channel blockers.

Biginelli reaction which involves condensation of methyl 3-oxopentanoate, aromatic aldehydes and thiourea with a catalytic amount of HCl at reflux temperature has been used for the synthesis of 4-aryl-6-ethyl-5-(methoxycarbonyl)-3,4-dihydropyrimidin-2(1H)-thiones (1-16). In addition, Lewis acids such as FeCl(3).6H(2)O and/or H(3)BO(3) were also used as catalysts for one-pot synthesis of the products. Compared to the classical Biginelli reaction conditions, the usage of Lewis acids has the advantage of good yields and short reaction times. The calcium channel blocker activities of 1-16 were screened by the tests performed on isolated rat ileum and thoracic aorta. Although product 11, 2-nitrophenyl-derivative, has potent antispasmodic activity on BaCl(2)-stimulated rat ileum, it does not have vasodilator activity on KCl-stimulated rat thoracic aorta. Product 15, 2-ethoxyphenyl-derivative, exhibited significant antispasmodic and vasodilator activities in both screening paradigms.

Animals↗
PubMed1990

Effect of calcium channel blockers on serotonin uptake.

We previously demonstrated that verapamil inhibits serotonin uptake by bovine pulmonary arterial endothelial cells by a mechanism not involving alterations in calcium fluxes. In this study, we determine whether verapamil inhibition of serotonin uptake occurs in other pulmonary cell types (bovine pulmonary artery smooth muscle cells), in cells from other organs and species (rat epididymal endothelial cells), and in intact organs (isolated rat lungs). We also compare the effects of verapamil with those of nifedipine and diltiazem. At concentrations of 10(-6) M or greater, verapamil is an inhibitor of serotonin uptake by cultured cells and isolated lungs. Nifedipine and diltiazem are weak inhibitors of serotonin uptake by cultured bovine cells only at suprapharmacologic doses and have no effect on serotonin uptake by isolated lungs. Surprisingly, nifedipine stimulates serotonin uptake by rat epididymal endothelial cells. We conclude that inhibition of serotonin uptake by verapamil is a generalized phenomenon, occurring in a variety of cell types, in intact organs, and in different species that does not occur consistently with other calcium channel blockers.

Animals↗
PubMed1996

Interaction of calcium channel blockers (CCBs) with histamine and 5-hydroxytryptamine in aorta from normal and diseased rats.

The present study attempts to investigate the interaction of calcium channel blockers (CCBs) with histamine (H) and 5-hydroxytryptamine (5-HT) in rat isolated aortic strip preparations. In preparations obtained from rats chronically treated with various CCBs the contractile responses to H were completely blocked suggesting that this may be due to inhibition of the voltage-dependent channels and inositol 1,4,5-triphosphate induced release of calcium from intracellular stores. The decreased contractions of the aortic strip preparations with 5-HT obtained from rats chronically treated with various CCBs implies a decrease in 5-HT receptor density. DOCA-saline hypertensive rats chronically treated with various CCBs showed variable responses to H and 5-HT suggesting that these changes may be due to different isoforms of L-type calcium channels. In L-thyroxine-treated preparations or those simultaneously treated with L-thyroxine and CCBs the responses to H were abolished and those to 5-HT were partially blocked with decrease in maxima which could be secondary to the primary effect on the heart and to generalised reduced senstivity of the rat aorta.

Animals↗
PubMed1997

Discovery and main pharmacological properties of mibefradil (Ro 40-5967), the first selective T-type calcium channel blocker.

UNLABELLED: PROPERTIES OF MIBEFRADIL: Mibefradil is a novel calcium channel antagonist with structural and pharmacological characteristics clearly distinct from those of classical calcium antagonists. It is a potent vasodilator with a high selectivity for the coronary vasculature over the peripheral vasculature and the myocardium. Most importantly, this compound can relax vascular muscle and slow the heart rate without reducing cardiac contractility. In addition, it does not stimulate neurohormonal reflexes and it exhibits a good pharmacological profile characterized by a long duration of action. MECHANISM OF ACTION: The mechanism of action of mibefradil is characterized by the selective blockade of transient, low-voltage-activated (T-type) calcium channels over long-lasting, high-voltage-activated (L-type) calcium channels, which is probably responsible for many of its unique properties. CLINICAL USE OF MIBEFRADIL: Although calcium antagonists are mainly used for the treatment of hypertension and angina pectoris, there is strong preclinical evidence that mibefradil may also be beneficial in the treatment of congestive heart failure.

Animals↗
PubMed2003

Treatment of sporadic hemiplegic migraine with calcium-channel blocker verapamil.

Gene mutations within the P/Q type neuronal calcium channel in familial hemiplegic migraine (FHM) suggest a therapeutic role for calcium-channel blockade. The authors have previously reported abortive therapy of FHM with IV verapamil. Here the authors describe four cases of sporadic hemiplegic migraine (SHM) responsive to verapamil, administered either orally or IV. The findings indicate that verapamil is effective therapy for both SHM and FHM.

Acetazolamide↗
PubMed1992

Isradipine--another calcium-channel blocker for the treatment of hypertension and angina.

OBJECTIVE: To review the pharmacology, pharmacokinetic disposition, dose recommendations, adverse effects, drug interactions, and efficacy of isradipine in patients with hypertension or ischemic heart disease. DATA SOURCES: Data from scientific literature were extracted, evaluated, and summarized for presentation. A MEDLINE search was conducted using the following indexing terms: isradipine, calcium-channel blockers, hypertension, and angina pectoris. Experiences from studies evaluating isradipine reported in the form of articles, abstracts, or proceedings involving patients or healthy subjects were considered for inclusion. STUDY SELECTION: Special consideration was given to clinical studies that had been designed in a blind, randomized fashion. Studies that compared the effectiveness and safety of isradipine with another antihypertensive or antianginal agent or placebo were included. DATA EXTRACTION: Data from human studies published in the English language were evaluated. Trials were evaluated according to sample size, design, and adequacy of description of therapeutic response. DATA SYNTHESIS: Isradipine is a new dihydropyridine calcium-channel blocker that appears to exert less negative inotropic activity than nifedipine and to selectively inhibit sinoatrial conduction. Pharmacokinetic parameters are quite variable and considerably more work is needed to better describe the kinetic disposition of isradipine. Antihypertensive efficacy has been demonstrated extensively in a number of short-term trials. Antianginal efficacy also has been observed in a few short-term trials and is comparable to that of isosorbide dinitrate and nifedipine. Extensive experience with isradipine is minimal and no clear-cut advantages over existing compounds have been noted thus far. CONCLUSIONS: The place of isradipine in the therapy of hypertension and myocardial ischemia is unclear and its routine use cannot yet be recommended based solely on clinical grounds.

Angina Pectoris↗
PubMed1988

Additive effects of diuretics or sodium restriction with calcium channel blockers in the treatment of hypertension.

The role of dietary sodium intake and diuretic administration on the blood pressure response to calcium channel blockers (CCB) is reviewed. CCB has been shown to have a natriuretic effect irrespective of sodium balance state. Sodium-sensitive hypertensives often have lower blood pressure levels after dietary sodium restriction or diuretic therapy, making the additive benefit of CCB on blood pressure more difficult to discern. The majority of studies including appropriate controls suggest that CCBs of the dihydropyridine class (nifedipine and nitrendipine) and also verapamil have an antihypertensive effect that can be augmented by diuretic administration.

Calcium Channel Blockers↗
PubMedDate not supplied

Antiatherosclerotic effects of calcium channel blockers.

Over the past 30 years, a considerable body of experimental and clinical evidence has accumulated to support the suggestion that calcium channel blockers (CCBs) have significant antiatherosclerotic effects that are independent of their hypotensive effects. Early research using animal models of atherosclerosis and CCBs in concentrations that exceeded the normal therapeutic dose range showed definite antiatherosclerotic effects, especially in the development of new lesions. Investigations of these effects in humans have used quantitative coronary angiography and B-mode ultrasonography and have demonstrated some antiatherosclerotic effects. This article reviews the currently available evidence of antiatherosclerotic effects of CCBs in animal models and in clinical trials.

Calcium Channel Blockers↗
PubMed1996

Protective effects of the calcium channel blocker verapamil on hepatic function following warm ischemia.

The purpose of this study was to investigate the protective effects of the calcium channel blocker verapamil on warm ischemia-reperfusion injury to the liver using a rat model. Ischemia of the left and median lobes was created by total inflow occlusion for 60 min followed by 24 hr of reperfusion. Hepatocell injury was assessed by the release of liver enzymes [alanine aminotransferase (ALT) and lactic dehydrogenase (LDH)], reduced (GSH) and oxygenated (GSSG) plasma glutathione and total biliary glutathione. Hepatocyte function was quantitated by measuring bile flow. Rats were randomized to one of two groups: pretreatment with iv verapamil (0.3 mg/kg) or iv normal saline (controls). Verapamil significantly increased bile flow and GSH efflux while decreasing plasma ALT and LDH compared to those in controls 24 hr after liver ischemia-reperfusion (LIR). A significant correlation existed between bile flow and biliary GSH efflux at 1 but not 24 hr after LIR, suggesting that early LIR injury is mediated predominantly by generation of oxygen free radicals. Liver enzyme elevation and bile flow were inversely correlated at 24 but not 1 hr after injury. We conclude that verapamil significantly protects the liver against warm LIR injury. The minimal protective effect of verapamil on early liver ischemia-reperfusion demonstrates that verapamil does not prevent the early generation of oxygen radicals upon reperfusion. However, the significant restoration of biliary GSH efflux and hepatocyte protection at 24 hr suggests involvement of calcium ions in late hepatocyte injury. Verapamil's protective effects may be related to attenuating pathophysiologic events occurring beyond 1 hr of reperfusion. Future studies investigating the protective effects of verapamil on warm LIR injury should be carried out for at least 24 hr postreperfusion.

Alanine Transaminase↗
PubMed1997

Membrane currents elicited by the organic calcium channel blocker verapamil in native and rat brain RNA-injected oocytes of Xenopus laevis.

For further analysis of the action of the diphenylalkylamine verapamil (CAS 152-11-4), the ability of verapamil to elicit membrane currents by itself was investigated in native and rat brain. RNA-injected oocytes of Xenopus laevis. Administration of verapamil elicited inward currents which remained constant or increased slightly during ongoing application. In native and RNA-injected oocytes the current responses were similar in shape, but larger in size in RNA-injected oocytes. The currents increased up to the maximal tested concentration of 1 mmol/l verapamil; the threshold concentration was below 80 mumol/l. After removal of follicular tissues the verapamil response was nearly doubled. During verapamil administration the input resistance was increased up to 1.7 of the initial value. The current response to verapamil can be subdivided into an early and late component. The equilibrium potential of the early component ranged between -80 and -110 mV; the late component which increased slightly during verapamil application, had an equilibrium potential between 0 and -20 mV. Under the influence of potassium channel blockers (tetraethylammonium and cesium chloride) or chloride channel blockers (anthracene-9-carbonic acid and the indanyloxy-acetic acid derivative IAA-94) the verapamil induced currents were reduced. Thus, the results indicate that beside the calcium channel-blocking effect, verapamil can induce currents by itself, presumably by acting on the potassium and chloride leakage.

Animals↗
PubMed2003

Treatment of calcium channel blocker intoxication with insulin infusion: case report and literature review.

We present a case report of successful treatment of shock induced by the calcium channel blocker (CCB) diltiazem. A 75-year-old woman took a combination of tablets, including diltiazem. Soon after arrival, she developed haemodynamic shock which persisted despite treatment with fluids, dopamine, dobutamine, norepinephrine (noradrenaline), calcium gluconate and glucagon. Haemodynamic stability was not achieved until an insulin infusion and glucose administration was started. We review the literature and the updated guidelines for the treatment of CCB intoxication, with particular emphasis on situations where insulin and glucose infusions can be live saving.

Aged↗
PubMed1990

Calcium channel blocker nisoldipine in chronic renal failure.

Patients with a stable progression of chronic renal failure with a creatinine clearance of 15-45 mL/min were randomly assigned to two groups of antihypertensive therapy: 1--nisoldipine as the only antihypertensive agent and 2--antihypertensive drugs without calcium channel blockers and a placebo tablet instead of nisoldipine. The patients were already on a low-protein diet and some form of antihypertensive therapy but without calcium channel blockers. There were 18 patients in the placebo group and 20 patients in the nisoldipine group. The follow-up period averaged 23.7 +/- 10.6 (SD) months in the placebo group and 23 +/- 11.3 months in the nisoldipine group. The slopes of the reciprocal of serum creatinine were calculated for the period prior to and following our intervention. The number of patients whose slopes improved following intervention was 6/18 in the placebo group and 15/20 in the nisoldipine group (p less than .02). The patients whose slopes improved had a significant fall in systolic and diastolic BP, as well as in the MAP. Those whose slopes did not improve had a significant decrease in systolic BP, but no change in diastolic BP and no significant difference in the MAP. When all 38 patients are analyzed together, regardless of their grouping, the correlation between the difference percent in the slope, and the difference percent in the MAP, was significant. Furthermore, punch biopsies of the skin showed a markedly different calcium content in the two groups, which was significantly less in the nisoldipine-treated patients as compared with the patients not receiving calcium blockers.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗