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PubMedDate not supplied

Cutaneous reactions due to diltiazem and cross reactivity with other calcium channel blockers.

BACKGROUND: The spectrum of cutaneous eruptions in association with calcium channel blockers is extensive, varying from exanthemas to severe adverse events. Reactions due to diltiazem occur more frequently than with other calcium channel blockers. Patch testing has been used as confirmatory testing in patients with extensive cutaneous reactions. Cross-reactivity among these drugs have not been established. MATERIAL: We present 3 patients: 1) A 54-year-old man developed a generalized erythema-multiforme-like reaction followed by erythrodermia and exfoliative dermatitis 6-7 days after starting on diltiazem. The drug was stopped and remission was obtained with emollients and systemic corticosteroids and antihistamines within 12 days. 2) A 80-year-old woman experienced a pruritic exanthematous eruption on her trunk which evolved to generalized erythrodermia and superficial desquamation. This reaction appeared 10 days after taking diltiazem, and gradually improved in 10-12 days after discontinuation of this drug. 3) A 79-year-old man presented with erythema and pruritus initially on the back, and then affecting thorax, extremities and face. He had started treatment with diltiazem three days before. Diltiazem was stopped and steroid and antihistamine therapy was given. His skin condition improved, but 3 days later the patient received verapamil with worsening of previous situation. He recovered within 7 days. METHODS AND RESULTS: Two to six months after the reaction, we carried out epicutaneous tests with calcium channel blockers from different groups. Diltiazem proved positive (at 48 and 96 hours) in the three patients; nifedipine was also positive in patient 2, and verapamil in patient 3. Controlled administration of verapamil was well tolerated in patient 2 after the reaction, and the patient 1 has taken nifedipine without problems. CONCLUSIONS: 1) We report 3 cases of cutaneous reactions due to diltiazem. 2) Epicutaneous tests have been useful for diagnosis. 3) As one of patients had positive patch tests to diltiazem and nifedipine, and other one with diltiazem and verapamil, more studies are needed to demonstrate cross reactions among calcium channel blockers.

Aged↗
PubMed1997

Calcium channel blockers. Consensus amid controversy.

Although the calcium channel blockers have been used to treat hypertension for a number of years, they are now under close scrutiny because of disturbing findings regarding their safety. Drs Kochar and Qurashi sort out the controversies surrounding these widely used drugs and make recommendations based on current consensus.

Antihypertensive Agents↗
PubMed2004

The role of existing and newer calcium channel blockers in the treatment of hypertension.

Calcium channel blockers (CCBs), which include both dihydropyridines such as nifedipine and amlodipine and non-dihydropyridines (verapamil and diltiazem), are among the most widely prescribed agents for the management of essential hypertension. Several large outcome risk trials and comprehensive meta-analyses have found that CCBs reduce the cardiovascular morbidity and mortality associated with uncontrolled hypertension, including stroke. CCBs, however, appear less effective than angiotensin-converting enzyme inhibitors and diuretics for preventing heart failure and myocardial infarction. CCBs are among the agents listed as potential first-line therapy, either alone or in combination with other agents in hypertension management guidelines. Furthermore, CCBs are suitable for add-on therapy in combination with diuretics, angiotensin-converting enzyme inhibitors, and angiotensin-II receptor blockers. CCBs may be partially suitable for patients with comorbid Raynaud's syndrome, isolated systolic hypertension (dihydropyridine), or angina pectoris (non-dihydropyridine). The newer inherently long-acting dihydropyridine agents (e.g., lacidipine, lercanidipine), which are not currently available in the United States, appear to have comparable efficacy to older agents of the dihydropyridine class but may have an improved tolerability profile, especially with regard to peripheral edema.

Amlodipine↗
PubMed1991

Calcium channel blockers and excitatory amino acids.

The calcium channel blockers (CCB), diltiazem, verapamil and nifedipine, antagonize in mice both N-methyl-DL-aspartate- (NMDLA) and kainate-induced convulsions, which were not affected by carbamazepine and ethosuximide. The CCB, on the other hand, were ineffective against convulsions induced by bicuculline, pentylenetetrazol and electroshock. The results suggest that the CCB may be efficacious in the treatment of those neurodegenerative diseases putatively caused by the excitatory amino acids.

Amino Acids↗
PubMed1992

The fate of altered hepatocytic foci as a result of treatment with oxodipine, a calcium channel blocker.

The dietary administration of the calcium channel blocker oxodipine to Fischer (F344) rats for 12 and 30 months resulted in increased incidence of altered hepatocytic foci (AHF). As the Environmental Protection Agency (EPA) regards AHF as potentially precancerous it is important to accumulate experimental evidence which may negate this theory. In the case of oxodipine we proved that with dosages close to maximum tolerated dose (MTD) for prolonged periods no hepatic neoplasms were produced. The possible nature of such AHF is discussed.

Alkaline Phosphatase↗
PubMed1992

Thickening of the adrenal zona glomerulosa in dogs induced by oxodipine, a calcium channel blocker.

Subchronic effects of oxodipine, a calcium channel blocker affecting the adrenal gland of the dog, are described. Thirteen wk of treatment at a high dose (24 mg/kg/day) of oxodipine resulted in drug-induced thickening of the zona glomerulosa and increased stimulation of its secretory activity. It is postulated that subchronic administration of oxodipine at this dosage resulted in a decrease in blood pressure, with uninterrupted stimulation of the adrenal zona glomerulosa to release aldosterone, causing an increase in the width of this portion of the gland involving cellular hyperplasia. Support for this indirect effect is found in the increased presence of renin granules in the juxtaglomerular apparatus.

Adrenal Glands↗
PubMed1991

Calcium channel blockers in geriatric hypertension.

Though the calcium channel blockers have been used to treat angina pectoris for almost a decade, the long-acting forms of these agents that have become available in the last few years have made them practical for use as antihypertensive agents as well. They are becoming increasingly popular in this role, especially to treat elderly hypertensive patients. Because they are vasodilators with a mild diuretic action, they are logical treatment choices for the majority of hypertensive patients who have increased peripheral vascular resistance. They offer the advantage of a dual benefit for hypertensive patients with angina, and they have no effect on carbohydrate or lipid metabolism. Disadvantages include cost and a side effect profile that includes headaches, palpitations, ankle edema, and constipation.

Aged↗
PubMed1984

Elevation of intraocular pressure by calcium channel blockers.

Topical administration of three different calcium channel blockers (verapamil hydrochloride, diltiazem hydrochloride, or nifedipine) increased intraocular pressure transiently in rabbits. Outflow facility and episcleral venous pressure were unchanged. Aqueous humor flow seemed to be increased 30 minutes after topical application of verapamil when estimated by the Goldmann equation or by changes in anterior chamber fluorescein-labeled dextran concentration. However, aqueous humor ascorbate concentrations and turnover of radioactive iodide did not differ from that in the untreated eye. Ocular blood volume was found to be increased after topical application of verapamil, which suggested vascular changes as a possible mechanism for the induced increase in IOP. Topical verapamil raised IOP in healthy human volunteers, but the elevation was less than observed in rabbits. Single oral doses of verapamil in rabbits or human beings had no effect on IOP.

Administration, Oral↗
PubMed1983

The calcium channel blockers: pharmacology and clinical applications.

The calcium channel blockers provide an exciting and effective new therapeutic tool in the management of ischaemic cardiac syndromes and may prove popular and effective in the treatment of a variety of other disorders. They have provided a new approach to treatment and have added new insights into the pathogenesis of ischaemic cardiac syndromes. Their introduction into clinical practice has been swift and many of our concepts regarding their pharmacologic activities in man remain based on theoretic considerations. Their expanding clinical use and further comparative studies will undoubtedly provide further information in regard to indications, adverse effects, drug interaction and long-term safety. Particular caution is advised when they are combined with certain antiarrhythmic agents, digitalis and particularly beta adrenergic blocking agents. Little is known about their interaction with various general anaesthetic agents and for this reason particular vigilance is required as more patients receiving these agents are admitted for surgical procedures.

Calcium Channel Blockers↗
PubMed1988

Potentiation of neuromuscular blocking agents by calcium channel blockers in rats.

The effect of calcium channel blockers (Ca-antagonists) on the potency and reversibility of muscle relaxants (MR) was investigated in the in vitro phrenic nerve-hemidiaphragm and in vivo sciatic nerve-tibialis anterior preparation of rats. To increase the relevance of the experimental findings to the clinical situation, the [Ca++] and [Mg++] in vitro were the same as in the plasma of rats and humans and the stimulation parameters used in vitro and in vivo were similar to those that elicit voluntary movements of the muscles used. Both verapamil and nifedipine significantly decreased the I50 and I90 of d-tubocurarine (d-Tc), pancuronium, vecuronium, and atracurium in vitro and those of the first three MR in vivo (P less than 0.001). In vitro, the depression of the force of contraction of the diaphragm (P) caused by all the Ca-antagonist-MR combinations could be reversed only partially by washout, neostigmine, or 4-aminopyridine. In vivo, because of limitations imposed by their cardiovascular depressant effect, the muscles were exposed to lower concentrations of Ca-antagonists for shorter periods. Under these circumstances the decrease of P caused by all Ca-antagonist-MR combinations recovered spontaneously close to control levels. This study indicates that acute administration of verapamil during anesthesia may increase MR potency, but it is unlikely that spontaneous recovery or reversibility of the residual neuromuscular (NM) block at the end of anesthesia will be significantly affected. However, long-term administration of Ca-antagonists may make difficult the reversal of the residual NM block.

Anesthesia↗
PubMed1996

Calcium channel blockers and transmitter release at the normal human neuromuscular junction.

Transmitter release evoked by nerve stimulation is highly dependent on Ca2+ entry through voltage-activated plasma membrane channels. Calcium influx may be modified in some neuromuscular diseases like Lambert-Eaton syndrome and amyotrophic lateral sclerosis. We studied the pharmacologic sensitivity of the transmitter release process to different calcium channel blockers in normal human muscles and found that funnel web toxin and omega-Agatoxin-IVA, both P-type calcium channel blockers, blocked nerve-elicited muscle action potentials and inhibited evoked synaptic transmission. The transmitter release was not affected either by nitrendipine, an L-type channel blocker, or omega-Conotoxin-GVIA, an N-type channel blocker. The pharmacologic profile of neuromuscular transmission observed in normal human muscles indicates that P-like channels mediate transmitter release at the motor nerve terminals.

Action Potentials↗
PubMed1989

The use of ryanodine and calcium channel blockers to characterize intra- and extracellular calcium pools mobilized by noradrenaline in the rat vas deferens.

Ryanodine (0.03-10 microM) abolished the phasic component of the contractile response to noradrenaline in the rat vas deferens but had less effect on the tonic component of this response. In contrast, nifedipine and methoxyverapamil (D600, 0.3-0.8 microM) blocked only the tonic component of the noradrenaline, adrenaline or phenylephrine-induced contractions. These results suggest that the phasic component of the noradrenaline-induced response is related to the release of intracellular calcium whereas the tonic phase of the contraction involves calcium influx via membrane channels sensitive to dihydropyridine and diphenylalkylamine calcium channels blockers.

Alkaloids↗
PubMed1986

Calcium channel blockers enhance extrarenal potassium disposal in the rat.

The effect of calcium channel blockers on the extrarenal disposition of an acute potassium load was examined in acutely nephrectomized rats infused with KCl (0.75 meq X kg-1 X h-1 for 60 min) alone or in combination with either verapamil or nifedipine. The increment in plasma potassium concentration during the potassium infusion (delta PK) with either verapamil or nifedipine was less than control (P less than 0.05 and 0.01, respectively). Studies were repeated in acutely adrenalectomized rats (ADX) to evaluate whether the changes in plasma potassium were consequent to the enhanced activity of epinephrine and other adrenal hormones. delta PK with ADX was higher than control (P less than 0.01). Verapamil or nifedipine with ADX resulted in a lower delta PK than ADX alone (P less than 0.05). Further studies were then conducted with the selective beta 2-adrenergic blocker butoxamine hydrochloride to rule out enhanced peripheral sympathetic activity of the beta 2-adrenergic system in facilitating the potassium disposal. delta PK with butoxamine was greater than control (P less than 0.01) but not significantly different from ADX. Verapamil or nifedipine in conjunction with butoxamine resulted in a lower delta PK than butoxamine alone (P less than 0.01). Changes in arterial pH and plasma bicarbonate were similar in all groups. In conclusion, during potassium infusion the delta PK is lower in the presence of calcium channel blockers. The alteration in potassium transport produced by calcium channel blockers does not appear to be dependent on adrenal function or peripheral sympathetic activity. Impaired calcium entry into cells may alter potassium transport in the intact animal.

Adrenalectomy↗
PubMed1993

Calcium-channel blockers and gastrointestinal motility: basic and clinical aspects.

Several calcium-channel blockers currently in use for the treatment of cardiovascular disorders have recently been tested for their effects on gastrointestinal motility. The rationale for this approach centers on the concept that calcium-channel blockers are at least as potent in inhibiting intestinal smooth muscle as in relaxing vascular smooth muscle. This review will give an outline of the most recent findings on the role of calcium and calcium channels in smooth muscle and neuronal function in the digestive system. It will also consider the mechanisms by which calcium-channel blockers may affect gastrointestinal motility and assess potential clinical applications in gastroenterology. The main goal for researchers in this field will be the development of gut-selective agents, with no cardiovascular side effects.

Animals↗
PubMed1996

Effect of calcium channel blockers on withdrawal syndrome of lorazepam in rats.

Effects of calcium channel blockers were investigated on withdrawal signs in lorazepam dependent rats. Physical dependence was produced by giving lorazepam admixed with the food in the following dose schedule: 10 x 4, 20 x 4, 40 x 4, 80 x 4 and 120 x 7 (mg/kg daily x days). Parameters such as body weight, food intake, spontaneous locomotor activity (SLA), body temperature, reaction time to pain, foot shock-aggression (FSA) and audiogenic seizures were observed during the period of administration of lorazepam and after its withdrawal. Calcium channel blockers viz. verapamil, nifedipine and nimodipine in different doses were administered orally twice daily in separate groups during the withdrawal period. The withdrawal signs observed in control group (without calcium channel blockers) were hyperkinesia, hyperthermia, hyper-aggression and audiogenic seizures. The administration of verapamil (5-20 mg/kg), nifedipine (1.75-7 mg/kg) and nimodipine (5-20 mg/kg) during the withdrawal period of lorazepam showed dose dependent significant blockade of all the withdrawal signs. Audiogenic seizures were completely blocked by 20 mg/kg dose of verapamil and nimodipine while nifedipine was partially effective. It may be concluded that calcium channel blockers exert protective effects on benzodiazepine withdrawal syndrome.

Acoustic Stimulation↗
PubMed1999

Changes in optic nerve head blood flow and retrobular hemodynamics following calcium-channel blocker treatment of normal-tension glaucoma.

BACKGROUND: Because calcium channel blockers reduce vascular resistance, they may have a clinical application in the treatment of normal-tension glaucoma (NTG). This study investigates changes in both the optic disc blood flow and the hemodynamics of retrobulbar vessels in NTG patients after the systemic administration of a calcium channel blocker. METHODS: Twelve eyes of 12 NTG patients (mean age 57.6 +/- 15.3 years) were examined before and after a 4-week treatment with 2 mg b.i.d. oral nilvadipine, an L-typc calcium channel blocker. By scanning laser-Doppler flowmetry (SLDF), we obtained the velocity, flow, and volume from within a 10 x 10 pixel window placed on the temporal rim region of the optic disc perfusion map. By ultrasound color Doppler imaging (CDI), we measured the peak systolic velocity (PSV) and the end diastolic velocity (EDV) of the ophthalmic artery (OA), central retinal artery (CRA), nasal posterior ciliary artery (NPCA), and temporal posterior ciliary artery (TPCA). We then calculated a resistance index (RI) for each vessel. RESULTS: After treatment, the flow and velocity of the optic disc blood flow significantly increased (P < 0.05). Nilvadipine also significantly reduced RIs of the CRA, NPCA, and TPCA (P < 0.05), and increased both the PSV of the NPCA and the EDVs of the CRA, NPCA, and TPCA. The percent change in velocity correlated significantly with the percent changes of the CRA RI and NPCA RI. CONCLUSIONS: Oral nilvadipine appears to reduce orbital vascular resistance, which consequently increases the optic disc blood flow.

Adult↗
PubMed2005

BCRP transports dipyridamole and is inhibited by calcium channel blockers.

PURPOSE: We investigated whether dipyridamole and various calcium channel blockers are inhibitors and/or substrates of breast cancer resistance protein (BCRP). METHODS: The effect of dipyridamole and the calcium channel blockers on mitoxantrone efflux by BCRP-overexpressing human embryonic kidney (HEK) cells was determined by flow cytometry. The ability of some of these compounds to reverse BCRP-mediated mitoxantrone resistance was measured by cytotoxicity assays. Transport studies were performed using radiolabeled compounds. RESULTS: Dipyridamole, nicardipine, nitrendipine, and nimodipine effectively inhibited BCRP-mediated mitoxantrone efflux; however, bepridil, diltiazem, and verapamil had no significant effect. Nifedipine is a much weaker BCRP inhibitor compared with other dihydropyridines tested. Nicardipine and dipyridamole were the most potent BCRP inhibitors among the compounds tested with IC50 values of 4.8 +/- 1.3 and 6.4 +/- 0.9 microM, respectively. Nicardipine and dipyridamole also effectively reversed BCRP-mediated mitoxantrone resistance in HEK cells. [3H]Nitrendipine was found not to be transported by BCRP. However, the transport of [3H]dipyridamole by BCRP was observed in both HEK and Madin-Darby canine kidney cells stably expressing the transporter, and this transport was completely abolished by fumitremorgin C, a known BCRP inhibitor. CONCLUSIONS: Dipyridamole and several dihydropyridines are effective BCRP inhibitors, but bepridil, diltiazem, and verapamil are not. We also identified a new BCRP substrate, dipyridamole.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed1998

Renal function in noninsulin-dependent diabetes mellitus patients treated with angiotensin-converting enzyme inhibitors and calcium channel blockers.

BACKGROUND: Data have not shown consistent effects with calcium channel blockers on the course of renal function in patients with noninsulin-dependent diabetes mellitus (NIDDM) who have hypertension alone or in association with renal damage. The differences between the antiproteinuric effects of subclasses or formulations of calcium channel blockers and the heterogeneity of renal lesions may contribute to the discrepancy in these data. Clinical studies conducted by the authors and other recent data that describe the course of renal dysfunction in hypertensive NIDDM patients treated with antihypertensive agents are reviewed. Renal structural changes were also evaluated. RESULTS: Most available data indicate that angiotensin-converting enzyme inhibitors and dihydropyridine and nondihydropyridine calcium channel blockers produce similar effects on glomerular filtration rate. In one study of patients achieving intensified, strict control of blood pressure (target<140/85 mmHg) with either cilazapril or amlodipine, glomerular filtration rate declined by 2.03+/-0.66 ml/ min/1.73 m2 per year and 2.01+/-0.71 ml/min/1.73 m2 per year, respectively, in the subgroup with normoalbuminuria and by 2.15+/-0.69 ml/min/1.73 m2 per year and 2.33+/-0.83 ml/min/ 1.73 m2 per year, respectively, in the subgroup with microalbuminuria. Renal lesions in NIDDM patients were found to be structurally heterogeneous and glomerular filtration rate appeared to decline only in patients with renal structural changes typical of NIDDM. CONCLUSIONS: The extent of blood pressure control, rather than the method by which this is accomplished, is the most important factor in determining the evolution of incipient nephropathy in hypertensive NIDDM. The kidneys of microalbuminuric NIDDM patients are structurally heterogeneous with less than one-third of patients having 'typical' diabetic nephropathology.

Angiotensin-Converting Enzyme Inhibitors↗