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PubMed2003

Effect of an educational program on the prevalence of use of antiplatelet drugs, beta blockers, angiotensin-converting enzyme inhibitors, lipid-lowering drugs, and calcium channel blockers prescribed during hospitalization and at hospital discharge in patients with coronary artery disease.

BACKGROUND: There is a marked underutilization of antiplatelet drugs, beta blockers, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), and lipid-lowering drugs, and an overutilization of calcium channel blockers in elderly patients with coronary artery disease (CAD). METHODS: An ongoing educational program is being given by Dr. Wilbert Aronow on the appropriate utilization of cardiovascular drugs in patients with CAD during hospitalization and at hospital discharge. In a prospective study, charts of 200 unselected patients hospitalized for CAD at least 6 months after the onset of the educational program were analyzed by a medical resident to investigate the appropriate utilization of cardiovascular drugs. The 200 patients included 115 men and 85 women, mean age 70 years, with documented CAD. Of the 200 patients, 127 (64%) had the diagnosis of prior CAD. The use of cardiovascular medications in these 127 patients prior to hospitalization served as a control group. RESULTS: After the educational program, aspirin, clopidogrel, or warfarin was given to 93% of patients compared with 67% in the control group; beta blockers were given to 81% of patients compared with 56% in the control group; ACE inhibitors or ARBs were given to 70% of patients compared with 42% in the control group. Lipid-lowering drugs if dyslipidemia were given to 88% of patients compared with 52% in the control group; calcium channel blockers were given to 18% of patients compared with 24% in the control group. CONCLUSIONS: In patients with CAD, the educational program increased the use of antiplatelet drugs by 26%, beta blockers by 25%, ACE inhibitors or ARBs by 28%, and lipid-lowering drugs by 36%, and decreased the use of calcium channel blockers by 6%.

Adrenergic beta-Antagonists↗
PubMed1986

Effects of calcium channel blockers on urinary tract smooth muscle.

Influx of calcium from the extracellular medium seems to be important for spontaneous as well as agonist-induced contractile activity in urinary tract smooth muscle. To a various extent this calcium influx occurs through pathways which can be blocked by calcium channel blockers. These drugs effectively suppress spontaneous ureteral activity in vitro. Whether they affect ureteral motility in vivo or whether they can counteract ureteral spasm associated with ureteral stones have not been established. Calcium channel blockers partially block electrically as well as agonist-induced detrusor contractions. Some of these drugs abolish even atropine-resistant contractile responses induced by electrical stimulation in detrusor muscle. Drugs with combined antimuscarinic and calcium channel blocking effect therefore have an attractive effect profile. Experiences with calcium channel blockers in the treatment of patients with 'unstable bladder' are limited, but results obtained with terodiline seem promising. Even if calcium channel blockers reduce agonist-induced contraction in isolated urethral muscle, their clinical effect on urethral function seems to be small. The effects of calcium blockers on urinary tract smooth muscle may be clinically useful and deserve further study.

Animals↗
PubMed2004

Reduction of human neocortical and guinea pig CA1-neuron A-type currents by organic calcium channel blockers.

In epilepsy models, organic calcium antagonists regularly induce a transient activity increase before suppression of epileptiform discharges. This action was speculated to be mediated by a modulation of potassium currents. Since A-type currents potently regulate neuronal excitability, their modulation by calcium channel blockers was investigated in acutely isolated human neocortical temporal lobe neurons and CA1 neurons of guinea pigs using the whole-cell voltage-clamp technique. In human neurons, 40 microM nifedipine caused an amplitude reduction by 28% at a command potential of -6 mV and produced a biexponential, markedly accelerated current inactivation with time constants of 8.4 +/- 1.1 ms (n = 6) and 62.9 +/- 6.4 ms (n = 5). The time constant under control conditions was 50.1 +/- 8.5 ms (n = 6). Verapamil (40 microM) did not affect the current amplitude, but accelerated the monoexponential current inactivation from 40.2 +/- 7.1 ms to 13.3 +/- 0.8 ms (n = 9). Accordingly, verapamil accelerated the inactivation from 42.3 +/- 5.9 ms to 15.0 +/- 1.3 ms (n = 11) in guinea pig CA1 neurons, without affecting the current amplitude. In this preparation, it was shown that the two enantiomers of verapamil do not differ in their actions. The results show that the A-type current in human neocortical and in guinea pig hippocampal neurons is reduced by organic calcium channel blockers.

Adolescent↗
PubMed2005

[Large scale clinical trials of calcium channel blockers on the prevention of cardiovascular diseases].

In the effects of calcium channel blockers on the cardiovascular diseases, the recent large scale clinical trials indicated that calcium channel blockers are considered to be superior for preventing the cardiovascular diseases. These results are different from that of former meta-analysis (BDLT, etc). This difference may be due to the characteristics of the calcium channel blocker.

Antihypertensive Agents↗
PubMed1993

RWJ-22108--a novel airway tissue--selective calcium channel blocker.

RWJ-22108 is a novel calcium entry blocker that has potential therapeutic use as an antiasthmatic agent. Although displaying typical potent inhibition of 45Ca uptake into aortic rings (IC50 = 7.1 nM) and displacement of [3H]nitrendipine from cardiac membranes (IC50 = 137 nM), RWJ-22108 demonstrates tissue selectivity in the inhibition of KCl-induced contractions. RWJ-22108 inhibits the calcium-dependent contraction of canine bronchiolar smooth muscle with an IC50 of 5.7 nM. The IC50 femoral artery/IC50 bronchiolar ratios are 2.85, 8.02, 1.47 and 1.96 for nifedipine, RWJ-22108, verapamil, and gallopamil, respectively. Furthermore, this selectivity ratio (range 2.8-5.5) of RWJ-22108 is also observed when inhibition of other pulmonary and cardiovascular smooth muscles are compared. Using canine tracheal muscle and rabbit aortae, the IC50 aorta/IC50 trachea ratio is 1.75 for RWJ-22108 compared to approximately 0.5 for several calcium blocker standards. These results indicate that in vitro RWJ-22108 is a bronchoselective calcium channel blocker.

Animals↗
PubMed1999

Structure-activity relationship of N-methyl-N-aralkyl-peptidylamines as novel N-type calcium channel blockers.

Selective N-type voltage sensitive calcium channel (VSCC) blockers have shown efficacy in several animal models of stroke and pain. In the process of searching for small molecule N-type calcium channel blockers, we have identified a series of N-methyl-N-aralkyl-peptidylamines with potent functional activity at N-type VSCCs. The most active compound discovered in this series is PD 173212 (11, IC50 = 36 nM in the IMR-32 assays). SAR and pharmacological evaluation of this series are described.

Animals↗
PubMedDate not supplied

Primary structure of the receptor for calcium channel blockers from skeletal muscle.

The complete amino-acid sequence of the receptor for dihydropyridine calcium channel blockers from rabbit skeletal muscle is predicted by cloning and sequence analysis of DNA complementary to its messenger RNA. Structural and sequence similarities to the voltage-dependent sodium channel suggest that in the transverse tubule membrane of skeletal muscle the dihydropyridine receptor may act both as voltage sensor in excitation-contraction coupling and as a calcium channel.

Amino Acid Sequence↗
PubMed1999

Chemosensory response to high pCO is blocked by cadmium, a voltage-sensitive calcium channel blocker.

In the dark, during normocapnic (pCO2=35 Torr, pHo=7.4) normoxia (pO2=100 Torr), high pCO (>300 Torr) causes Ca2+-dependent photolabile excitation of chemosensors in the carotid body (CB). We previously proposed that the source of this Ca2+ was the [Ca2+]i stores because CO would react only intracellularly. However, influx of extracellular Ca2+ was not excluded. Now, using perfused rat CB (n=6) in the presence of normal extracellular [Ca2+] we show that chemosensory response to CO (pCO approximately 550 Torr) in normoxic (pO2 approximately 100 Torr) normocapnia (pCO2 approximately 30 Torr, pH approximately 7.4) is completely but reversibly inhibited by Cd2+ (200 microM), a voltage-gated Ca2+ channel blocker. Thus, extracellular Ca2+ is necessary for excitatory chemosensory response to high pCO. Cd2+ block occurs in spite of an enhanced [Ca2+]i rise. This shows that Ca2+ rise alone is unable to release neurotransmitter and to elicit a chemosensory response. Therefore, as a corollary, we conclude that Cd2+ blocks the Ca2+ flux that is needed for vesicle-membrane fusion for neurotransmitter release and neural discharge.

Animals↗
PubMed2001

[Tocolysis with calcium-channel-blockers].

OBJECTIVE: To evaluate the use of calcium-channel-blockers (CCBs) for tocolysis. METHODS: We reviewed the literature retrieved from the Medline database from 1967 to 200 dealing with fetal toxicity and efficacy of CCBs compared with beta-adrenergic agonists. RESULTS: Data on fetal toxicity in animals were inconsistent. A teratologic effect has been observed during early pregnancy at supratherapeutic dosage. At usual therapeutic dosage, no fetal abnormalities have been observed. The efficacy of CBs for tocolysis is superior to that of beta-adrenergic drugs and allows a reduction of neonatal morbidity. Calcium channel blockers are better tolerated than beta-adrenergic agonists. CONCLUSION: Published data suggest that CCBs could be used a first line tocolytic agents. Although use of CCBs is extremely simple, they should not be prescribed in low-risk outpatients.

Adrenergic beta-Agonists↗
PubMed1983

Comparative effects of FR 34235, a new slow channel calcium blocker, and nifedipine on hemodynamics and myocardial oxygen consumption in the anesthetized dog.

Five doses of two dihydropyridine calcium antagonists, FR 34235 and nifedipine, were given intravenously to anesthetized dogs to determine effects on hemodynamics and myocardial oxygen balance. Both agents produced dose-related decreases in mean arterial blood pressure and tension time index with little effect on heart rate, dP/dt or myocardial contractile force except at high doses where small decreases were observed. Coronary blood flow increased markedly in the presence of both agents with a maximum increase observed at doses of 10 and 30 micrograms/kg for FR 34235 and nifedipine, respectively. Both compounds decreased myocardial oxygen extraction at all doses and reduced myocardial oxygen consumption at higher doses. These results indicate that FR 34235, a new slow channel calcium blocker, is a potent coronary vasodilator. In addition, this compound possesses oxygen-sparing activity at higher doses.

Anesthesia↗
PubMed1996

Calcium channel blockers modify jejunal uptake of D-galactose in rabbits.

Calcium channel blockers modify the intestinal uptake of lipids. This study was undertaken to test the hypothesis that two different types of calcium channel blockers influence the uptake of D-galactose, a sugar absorbed by the sodium-dependent glucose transporter (SGLT1) in the intestinal brush border membrane. Nisoldipine (1 mg/kg/day) or verapamil (4 mg/kg/day) were given by mouth to New Zealand white rabbits for three weeks, and then the rates of uptake of varying concentrations (2-64 mM) of galactose were examined in an in vitro preparation of jejunum using the incorporation of 14C-labeled substrate into intact tissue segments. The maximal transport capacities (Vmax) for D-galactose were increased in animals given nisoldipine or verapamil, as compared to controls. The value of the apparent Michaelis constant Km* for D-galactose was higher with nisoldipine group and lower with verapamil, than in controls. The apparent passive permeability (Pd*) of D-galactose was estimated from the uptake of L-glucose: Pd* was lower with nisoldipine and higher with verapamil, as compared to controls. The effect of these drugs on sugar uptake is not due to differences in the animals' food intake, body weight gain, or mucosal surface area. Thus, the two different classes of calcium channel blockers, the dihydropyridine nisoldipine and the phenylalkylamine verapamil, have different effects on the K(m)* and Pd*, but not on the Vmax of D-galactose uptake.

Animals↗
PubMed1998

A calcium agonist, Bay k 8644, suppresses the embryotoxic effects induced by dihydropyridines calcium channel blockers in cultured rat embryos.

Day 9 rat embryos were exposed to 1,4-dihydropyridine calcium channel blockers; nifedipine (NIF), nicardipine (NIC) or nitrendipine (NIT), for 48 hr in the whole embryo culture system. There were dose-dependent growth retardation and abnormalities, predominantly in cardiovascular system. The three compounds exhibited very similar pattern of dysmorphogenic effects, but the potency of these compounds were quantitatively different. The incidences of embryos with the abnormalities were 100%, 100% and 85% following either exposure of NIF, NIC or NIT at concentration of 300, 8 and 15 microM, respectively. This study was to investigate whether these blocker-induced embryotoxicity was due to calcium channel blocking properties themselves in the embryos. Day 9 rat embryos were co-exposed to 1,4-dihydropyridine calcium channel agonist, Bay k 8644 (BAY) and each calcium channel blocker under the same culture condition. The retarded embryonic growth induced by 200 or 300 microM of NIF, 8 microM of NIC and 15 microM of NIT nearly of completely ameliorated when embryos were co-exposed with BAY at one-third or half concentration of each calcium channel blocker. Supplementation of BAY reduced the incidence of abnormalities by NIF-, NIC- and NIT-alone. These results suggested that one of mechanisms for embryotoxicity induced by calcium channel blocker was directly related to channel blocking property of the chemicals.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2003

Diethylstilbestrol and tetrahydrochrysenes are calcium channel blockers in human platelets: relationship to the stilbene pharmacophore.

The effects of compounds with the stilbene pharmacophore [diethylstilbestrol (DES), DES derivatives, tetrahydrochrysene (THC), and THC derivatives] were examined for their ability to inhibit thrombin-induced Ca(2+) influx in human platelets. DES derivatives (DES dimethyl ether, DES dipropionate, dienestrol, and hexestrol) had lower inhibitory activity than DES. Esterification of DES with the bulky monobenzyl group eliminated inhibitory activity. Unsubstituted THC diol had the lowest inhibitory activity in the series of the THC derivatives bearing substituents in the 5,11 positions. These derivatives, either diethyl or dipropyl, cis or trans, were potent inhibitors of thrombin-induced [Ca(2+)](i) elevation (near 100% inhibition at 10 microM). Therefore, stilbene pharmacophore having bulk out of the plane of the double bond (from the twisting of the two aromatic rings or from addition of all substituents) seems to be requirement for the inhibitory activity. Free hydroxyl groups are also required for inhibitory activity, most likely for hydrogen bonding, since trans-diethyl tetrahydrochrysene dimethyl ether was inactive. Compounds bearing ethyl substituents (DES and THC derivatives) inhibited thrombin-induced release of calcium from the endoplasmic reticulum. These compounds also inhibited thapsigargin-induced Ca(2+) influx. This result implies that these compounds also block store-operated Ca(2+) influx directly, as well as internal Ca(2+) release. Compounds without ethyl substituents (trans-resveratrol, genistein, daidzein, and THC diol) only inhibited calcium influx into platelets.

Adult↗
PubMed1988

Regulation of relaxin release from monodispersed porcine luteal cells: effect of calcium ionophore A23187 and calcium channel blockers.

The role of calcium ion mobilization in modulation of secretion of the ovarian protein hormone relaxin by porcine luteal cells was examined by use of a reverse hemolytic plaque assay. In this assay, luteal cells were cocultured in monolayers with protein-A-coupled ovine erythrocytes. In the presence of porcine relaxin antiserum and complement, a zone of hemolysis, a plaque, developed around relaxin-releasing luteal cells. The rate of development of plaques in time-course experiments was used in this study as an index of the rate of relaxin release. Exposure of luteal cell-containing monolayers to the calcium-mobilizing agent A23187 (40 nM to 5 microM) resulted in a dose-related increase in the rate of relaxin-plaque formation. This effect [and the influence of a stimulatory secretagogue, prostaglandin E2 (PGE2; 1 microM)] was suppressed by coculture with Co2+ (5 mM), a calcium channel blocker. These results are consistent with the view that calcium ion redistribution within porcine luteal cells forms a pathway that subserves, at least in part, the rates of basal and stimulated relaxin release in vitro. However, A23187 was equally effective in enhancing the rate of plaque formation when the monolayers were bathed in a low calcium medium (mean +/- SEM, 6.61 +/- 0.92 microM Ca2+), rather than a calcium-replete medium (1.56 +/- 0.09 mM Ca2+). Likewise, neither basal nor PGE2-stimulated (1 microM) relaxin secretion was abrogated by culture of monolayers in low calcium medium. These data suggest that the stimulatory effect of A23187 (and perhaps PGE2) arose predominantly through redistribution of calcium stored within intracellular sites in luteal cells, rather than entrance of calcium into the cell from the extracellular medium. Yet, incompatible with this interpretation, we observed that TMB-8 [8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride; a putative inhibitor of intracellular calcium redistribution] enhanced rather than blocked A23187- or PGE2-stimulated relaxin release. This result is consistent with the possibility that TMB-8 mobilized (rather than blocked) calcium in this cell system or that it acted via calcium-independent mechanisms. We conclude that calcium mobilization has the potential to act as a molecular pathway that transduces secretion of an ovarian peptide hormone, relaxin. However, the exact nature and physiological role(s) of the Ca2+ pathway in the control of relaxin secretion and the interrelationships of this mechanism with other intracellular messengers that may also modulate ovarian peptide secretion remain to be more clearly defined.

Animals↗
PubMed1993

Are calcium-channel blockers effective in the treatment of tardive dyskinesia?

OBJECTIVE: To review the data describing the use of calcium-channel blockers in the treatment of tardive dyskinesia (TD). DATA SOURCES: A MEDLINE search of the English-language literature and a bibliographic review of pertinent articles examining the use of calcium-channel blockers in the treatment of TD were performed. Medical Subject Headings (MESH) terms used were calcium-channel blockers, tardive dyskinesia, nifedipine, verapamil, and diltiazem. STUDY SELECTION AND DATA EXTRACTION: Relevant case reports, open trials, and controlled studies reporting on the efficacy of calcium-channel blockers for treating TD are reviewed. Appropriate conclusions are drawn from the data and guidelines are suggested for the practitioner. DATA SYNTHESIS: Studies addressing the efficacy of calcium-channel blockers in the palliative treatment of TD have yielded mixed results. Positive findings have been reported for nifedipine, verapamil, and diltiazem; nifedipine may be the most efficacious treatment and diltiazem the least. It appears that patients with TD who can tolerate higher doses of calcium-channel blockers may respond more favorably to treatment. Patient characteristics that may help determine a better response to treatment with calcium-channel blockers include advanced age and more-severe TD. CONCLUSIONS: To determine the efficacy of calcium-channel blockers in the treatment of TD, additional data are needed from double-blind, placebo-controlled studies with larger sample sizes and longer durations of treatment. Until these data are available, calcium-channel blockers should be considered potentially useful therapy for the heretofore unresponsive TD.

Aged↗
PubMed1987

Comparative studies of calcium-channel blockers and beta-blockers in essential hypertension: clinical implications.

The use of calcium-channel blockers to treat essential hypertension is increasing, and in the United States several new drug applications for this indication are under consideration by the Food and Drug Administration. Although the ability of the calcium-channel blockers to lower blood pressure has been established, their efficacy and safety in relation to current therapy require further clarification. This article reviews studies in which calcium-channel blockers and beta-blockers have been compared, including seven with verapamil, four with nifedipine and nitrendipine and two with diltiazem. These studies indicate that the two classes of agents produce similar antihypertensive effects and are associated with a comparable incidence of adverse reactions. In addition, the preliminary findings of a multicenter trial in which 50 subjects with mild or moderate hypertension were treated with diltiazem (60 to 180 mg bid) or propranolol (80 to 240 mg bid) for 4 to 6 months are presented. Both medications significantly lowered blood pressure (from 148 +/- 17/101 +/- 5 to 133 +/- 25/88 +/- 9 mm Hg on diltiazem and from 154 +/- 22/104 +/- 6 to 146 +/- 23/91 +/- 11 mm Hg on propranolol). Fifty-nine percent of the patients on diltiazem and 40% of those on propranolol achieved the treatment goal of a supine diastolic blood pressure under 90 mm Hg together with minimum 10 mm Hg reduction. In a similar study, exercise blood pressure and exercise capacity were also examined, with the most important finding being a reduction in maximal oxygen consumption and exercise duration on propranolol without a significant change on diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1983

Effects of the calcium-channel blockers cobalt, verapamil, and D600 on Leydig cell steroidogenesis.

The effects of various calcium-channel blockers on androgen production by collagenase-dispersed mouse testicular interstitial cells were investigated. Cobalt caused a dose-dependent inhibition of the maximum rate of luteinizing hormone (LH)-stimulated androgen production without altering the concentration of LH required for half maximum stimulation (EC50). Nickel and manganese also inhibited LH-stimulated steroidogenesis but were less potent than cobalt. The major site at which cobalt treatment inhibited steroidogenesis was beyond cAMP formation and before 3 beta-hydroxysteroid dehydrogenase. This conclusion was based on the observation that cobalt inhibited dibutyryl cAMP-stimulated androgen production but did not affect protein synthesis and pregnenolone-supported androgen production. Androgen production was unaffected by the organic calcium-channel blockers verapamil and the (+) and (-) enantiomers of D600 at concentrations less than 0.1 mM. At a concentration of 0.1 mM the organic calcium-channel blockers inhibited LH- and dibutyryl cAMP-stimulated androgen production. Unlike cobalt, the organic calcium-channel blockers also inhibited pregnenolone-supported androgen production and reduced the rate of protein synthesis. Similarities between the effects of cobalt in the present study and previous reports of the effects of reduced extracellular calcium concentrations on androgen production suggest that cobalt inhibits androgen production as a result of its ability to block calcium influx. The calcium channels involved in the steroidogenic process appear, however, to be relatively insensitive to the organic calcium-channel blockers.

Androgens↗
PubMed1985

A comparison of the efficacy of an alpha-I-adrenergic blocker in the slow calcium channel blocker in the control of autonomic dysreflexia.

Cystometry, using a portable CO2 cystometer, is a convenient method for detecting autonomic dysreflexia (A.D.) in response to bladder distention. Serial tracings on successive days were found to be consistent. This method was used to compare the effect of the antihypertensive drugs, phenoxybenzamine and nifedipine, in modifying the blood pressure responses of 12 tetraplegic patients. Given as regular medication twice daily, neither drug was effective in preventing A.D. responses to bladder filling, and a significant number of patients developed troublesome hypotension. Nifedipine by mouth was found to be a valuable drug for the treatment of attacks which developed, and capable of preventing an anticipated attack if given shortly before the stimulus. The condition of 'status dysreflexicus' and its appropriate management is described.

Adrenergic alpha-Antagonists↗