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At least 1,063 records · Page 59Linked to original sources
PubMed2001

Effect of the calcium channel blockers nifedipine and diltiazem on pentylenetetrazole kindling-provoked amnesia in rats.

A large body of research supports the view that memory disturbance is an integral part of epilepsy. Deficit in various behaviour tasks has been found in rats subjected to experimental epilepsy-pentylenetetrazole (PTZ) kindling. In the present study we examined the effect of post-training administered calcium channel blockers nifedipine (10 and 40 mg/kg) and diltiazem (10 and 30 mg/kg) on amnesia induced by PTZ kindling in shuttle-box- and step-down-trained rats. Retention in nifedipine- or diltiazem-treated kindled animals was significantly improved compared to the kindled controls. The mechanisms of action of calcium antagonists studied is considered. Taken together with the data about calcium channel blocker anticonvulsive activity, the results of this study further suggest that nifedipine and diltiazem might be useful in the treatment of cognitive disorders in epileptic patients.

Amnesia↗
PubMed2006

The calcium-channel blocker, azelnidipine, enhances the inhibitory action of AT1 receptor blockade on ischemic brain damage.

OBJECTIVE: The combined effects of a calcium-channel blocker (CCB) with an angiotensin (Ang) II type 1 (AT1) receptor blocker were investigated in focal brain ischemia induced by middle cerebral artery (MCA) occlusion. METHODS AND RESULTS: In male C57BL/6J mice, permanent occlusion of the MCA-induced focal cerebral ischemia and neurological deficit after 24 h, accompanied by a reduction of cerebral blood flow and an increase in superoxide production in the ischemic area. Administration of azelnidipine, a CCB, at 1.0 mg/kg per day for 10 days significantly suppressed these changes after MCA without affecting systolic blood pressure. Such inhibitory effects of azelnidipine on brain ischemia could be observed in AT1a receptor-deficient mice. In addition, olmesartan, an AT1 receptor blocker, at 3.0 mg/kg per day also diminished the ischemic brain area and neurological score, as well as superoxide production and the reduction of cerebral surface blood flow in C57BL/6 mice. The combination of lower doses of azelnidipine (0.1 mg/kg per day) and olmesartan (0.5 mg/kg per day) significantly attenuated the ischemic brain area, neurological score, superoxide production and the reduction of cerebral surface blood flow after MCA occlusion in C57BL/6 mice, whereas either of these agents alone at these doses did not affect brain ischemia. CONCLUSION: These results indicate that azelnidipine inhibited ischemic brain damage induced by MCA occlusion, at least in part, through suppression of blood flow change and oxidative stress via a signaling mechanism independent of AT1 receptor stimulation. Moreover, azelnidipine synergistically enhanced the inhibitory action of olmesartan on brain ischemia, suggesting beneficial combined effects of a CCB with an AT1 receptor blocker on ischemic brain damage.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1987

Confirmation of the interaction between cyclosporine and the calcium channel blocker nicardipine in renal transplant patients.

We report seven cases out of eight reversible raises (350% of mean increase) of cyclosporine (CsA) plasma levels in patients receiving the new calcium channel blocker nicardipine (Loxen-Sandoz) and CsA after renal transplantation. Nicardipine was introduced 3 to 36 weeks post transplantation in 7 cases of hypertension and 1 case of angina pectoris. CsA plasma levels raised considerably 1 to 30 days after nicardipine introduction and returned to pretreatment levels 1 to 7 days after withdrawal. Serum creatinine increased in 1/8 patients. These data suggest that nicardipine interferes with CsA metabolism and this interaction is reversible after nicardipine discontinuation. These findings point out the fact that at least some calcium channel blockers need to be cautiously used in patients receiving CsA.

Adult↗
PubMed1986

Effects of calcium channel blockers on gastric emptying and acid secretion of the rat in vivo.

Experiments were designed to evaluate the effects of three calcium channel blockers (verapamil, diltiazem and cinnarizine) on gastric emptying and secretion in the rat. Pretreatment with the calcium blockers delayed gastric emptying of phenol red in a dose-dependent manner. Verapamil was the most effective of the agents tested. Verapamil and diltiazem inhibited gastric acid secretion in the pylorus-ligated rat without affecting pepsin output. Cinnarizine was ineffective in this model. When the perfused lumen of the anaesthetized rat was used, verapamil was found to inhibit responses to carbachol or histamine more than those to pentagastrin. Further, we found a greater sensitivity to verapamil for basal compared with vagal-stimulated (2-deoxy-D-glucose) acid secretion. Neither diltiazem nor cinnarizine modified gastric acid secretion in this experimental model. These findings are discussed in relation to the role of extracellular calcium in gastric motility and secretion, and the existence of a regional and functional selectivity for calcium blockers is proposed.

Anesthesia↗
PubMed2006

Synthesis and biological evaluation of novel T-type calcium channel blockers.

3,4-Dihydroquinazoline analogues substituted by N-methyl-N-(5-pyrrolidinopentyl)amine at the 2-position were synthesized and their blocking effects were evaluated for T- and N-type calcium channels. Compound 11b (KYS05080), compared to mibefradil (IC50=1.34+/-0.49 microM), was about 5-fold potent (IC50=0.26+/-0.01 microM) for T-type calcium channel (alpha1G) blocking and its selectivity of T/N-type was also improved (7.5 versus 1.4 of mibefradil).

Animals↗
PubMedDate not supplied

Risk of myocardial infarction with combination antihypertensive regimens including a dihydropyridine calcium channel blocker in hypertensive diabetics.

OBJECTIVE: The primary objective of this study was to determine if there was an increased risk of myocardial infarction (MI) in a high-risk hypertensive diabetic managed care population receiving combination antihypertensive therapy including a dihydropyridine (DHP) calcium channel blocker (CCB). METHODS: A retrospective, population-based, case-control study design was used to determine the risk of MI versus the prescribed antihypertensive drug regimen. During 1997-1999, 6,096 diabetics with hypertension were identified. After exclusions, there were 131.high-risk. study patients who suffered an MI during the study period. These were compared to an equally matched sample. High-risk patients were defined as those with a medical history of previous MI, angina pectoris or ischemic heart disease, or those who had undergone a coronary artery bypass graft and/or angioplasty procedure. Patients were then assigned to Group I cases and controls (DHP use) and Group II cases and controls (no DHP use). Odds ratios (OR) and 95% confidence intervals (CI) were determined for the independent variables and antihypertensive drug regimens. Logistical regression analysis was used to model age, ethnicity, and potential risk factors to identify any differences among calcium channel blockers. RESULTS: After adjusting for age and gender, the OR for an MI in patients on a combination DHP regimen was 0.75 (95% CI, 0.44, 1.29). The OR for other regimens ranged from 0.52 to 1.16, with no significant difference between antihypertensive drug classes. In comparison to nondihydropyridines (NDHPs), the OR for DHPs was 1.38 (95% CI, 0.54, 3.54), but it was determined to not be statistically different ( P=0.5065). CONCLUSION: No increase in risk of MI could be determined with the use of a combination antihypertensive regimen including a DHP CCB when compared to other antihypertensive drugs in a matched high-risk population of patients with hypertension and diabetes. Choice of antihypertensive drug regimen may be less important than strategies that focus on achieving optimal disease outcomes to reduce the incidence of MI and hospitalization and lower health care costs in this high-risk population in managed care.

Antihypertensive Agents↗
PubMed1992

Effects of potassium channel openers and calcium channel blockers on the force responses of the electrically driven rat right ventricle strip.

1. The effects of potassium channel openers (cromakalim and pinacidil) and of calcium channel blockers (verapamil, diltiazem and flunarizine) on the contractile responses of the rat right ventricle have been determined. 2. On the electrically driven rat right ventricle cromakalim at 3 x 10(-7), 10(-6), 3 x 10(-6) M and 10(-5) M, and pinacidil at 10(-6), 10(-5) and 3 x 10(-5) M had no effect on the force responses to cardiac stimulation or to isoprenaline. 3. Pinacidil at 10(-4) M in a vehicle of 0.7% ethanol reduced the force responses to cardiac stimulation. This inhibitory effect was solely due to the ethanol. Pinacidil in 5 x 10(-4) M HCl (which had no effect alone) potentiated some of the responses to isoprenaline. 4. Verapamil, greater than or equal to 10(-6) M, diltiazem, greater than or equal to 10(-5) M, and flunarizine, greater than or equal to 10(-6) M, reduced the force responses to cardiac stimulation and to isoprenaline. 5. The present study has shown that calcium channel blockers, but not potassium channel openers, have inhibitory effects on the rat right ventricle.

Animals↗
PubMed2003

Ultrastructure of the gingiva in cardiac patients treated with or without calcium channel blockers.

OBJECTIVES: In the last few years, several studies have suggested that periodontal diseases are related to the development of atherosclerosis and its complications. Our objective was to study the ultrastructural morphology of the gingiva from cardiac patients, some of whom were treated and some not with calcium channel blockers compared to a control group. MATERIAL AND METHODS: Fifty-five patients were studied and grouped in the following way: (a) healthy group (HG) (n=12) healthy patients with at least two pockets between 3 and 5 mm; (b) cardiac group (CG) (n=12) patients with cardiac disease untreated with calcium channel blockers; (c) diltiazem group (DG) (n=13) cardiac patients treated with diltiazem; (d) nifedipine group (NG) (n=18) cardiac patients treated with nifedipine. RESULTS: Ultrastructural studies in the CG showed inflammatory cells, collagen fibers disruption and a more extended morphologically compromised fibroblast mitochondria. Morphometric studies in CG showed mitochondria that were impaired in number but increased in volume, suggesting metabolic cell suffering. In DG and NG, morphometric data were similar to HG. The presence of myofibroblasts and collagen neosynthesis was detected in DG and NG. CONCLUSIONS: Our data showed differences in the ultrastructure of the gingival fibroblasts between the studied groups; the DG and NG showed features that could be interpreted as an attempt to restore the cellular metabolic function.

Calcium Channel Blockers↗
PubMed1991

Differential effects of L-type calcium channel blockers and stimulants on naloxone-precipitated withdrawal in mice acutely dependent on morphine.

The effects of L-type calcium channel blockers and stimulants on naloxone-precipitated withdrawal in mice acutely dependent on morphine were evaluated. Verapamil (10-80 mg/kg), diltiazem (20-120 mg/kg) and nicardipine (20-160 mg/kg), when administered subcutaneously, produced a dose-dependent reduction in forepaw tremor and weight loss during the abstinence reaction; jumping was also reduced by all three drugs, although the effect was not statistically significant in the case of nicardipine. By contrast, the calcium agonist Bay K 8644 (0.5-2 mg/kg, SC) increased forepaw tremor and weight loss, although this latter effect did not reach statistical significance. The effects of the calcium channel active drugs on the rotarod test were also explored, no correlation appearing with the results observed in abstinence (except for the jumping response), which suggests that the withdrawal results are not influenced by motor incoordination or unspecific CNS depression. These findings suggest that L-type calcium channels probably play an important role in withdrawal after acute morphine dependence. Taken together with other observations in chronic models, these results show that calcium channels are similarly involved in morphine abstinence after acute and chronic dependence, in contrast to the differences in the content and uptake of neuronal calcium induced by morphine under both conditions.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Interactions between calcium channel blockers and the anticonvulsants carbamazepine and phenytoin.

We describe a retrospective analysis of the frequency of adverse interactions between calcium channel blockers and anticonvulsant drugs (phenytoin and carbamazepine) in a series of 43 patients. Ten patients receiving carbamazepine and three patients receiving phenytoin exhibited symptoms or signs of toxicity. Toxicity occurred with both diltiazem and verapamil, but not with nifedipine. These results emphasize the need for careful clinical and laboratory monitoring of patients receiving both classes of medication.

Aged↗
PubMed1988

Flordipine, a calcium channel blocker, which does not influence lipidemia or atherosclerosis in cholesterol-fed rabbits.

Data relating to the effects of calcium channel blockers on experimental atherosclerosis in rabbits are inconsistent with most studies finding no effect on either serum lipids or atherosclerosis. We have administered flordipine (5, 15 or 45 mg/kg/day) for 10 weeks to rabbits fed 1% cholesterol and 4% corn oil. At no level of treatment was there an effect on serum or liver lipids or on aortic sudanophilia.

Animals↗
PubMed1993

The calcium channel blocker nifedipine fails to inhibit leucocyte elastase release during cardiopulmonary bypass.

Circulating concentrations of leucocyte elastase were measured in 16 adult patients undergoing cardiopulmonary bypass (CPB) with a flat-sheet membrane oxygenator. Eight patients (Group I) received the calcium channel blocker nifedipine (9 micrograms.kg-1 x h-1) during CPB. Eight patients (Group II) did not receive any calcium channel blocker during surgery and served as the control group. Elastase concentrations were measured at 7 time points: 2 before, 2 during, and 3 after CPB. The bypass procedure was associated with elevation in elastase concentrations (P < 0.001). Comparing to baseline values elastase concentrations were significantly elevated (P < 0.05) 60 min after the start of CPB and on all measurements done after CPB. Elastase concentrations correlated with the duration of CPB (rs = 0.76, P < 0.001), and were not influenced by nifedipine infusion as revealed by comparing the two groups. This study demonstrates moderate elastase release during CPB with a flat-sheet membrane oxygenator and fails to confirm inhibition of elastase release by nifedipine infusion during CPB.

Aged↗
PubMed2001

Calcium channel blockers in hypertension: reappraisal after new trials and major meta-analyses.

This review evaluates the current position of calcium channel blockers (CCB) in antihypertensive treatment in the light of three major comparative studies and two extensive meta-analyses. The latter both show that CCB are equivalent to conventional (initial beta-blocker or diuretic therapy) when total and cardiovascular mortality are the end points. Divergent points between the meta-analyses include stroke and myocardial infarction (MI). One meta-analysis compared CCB with conventional therapy, to find a small 13% reduction in stroke and a small, nonsignificant 12% increase in MI. The other meta-analysis found a 26% increase in MI when CCB were compared with all other therapies including the angiotensin converting enzyme (ACE) inhibitors. This increase was most robust (P < .001) when comparing CCB with ACE inhibitors, consonant with proposed protective effects of ACE inhibitors on cardiovascular risk. At present, only the comparison of CCB with conventional therapy, and not that with ACE inhibitors, rests on secure comparative data. When cost is compelling, conventional therapy is less expensive. For the individual patient, issues of quality of life (for example, impotence with diuretics and beta-blockers) might be decisive. Nonetheless, beta-blockers are preferred in postinfarct patients or in those with heart failure or unstable angina (a contraindication to dihydropyridines in the absence of beta-blockade). In others, the benefits of only a borderline stroke reduction with CCB versus an equally borderline increase in MI should be evaluated for each individual patient, taking into account the age group and the patient's preferences. In conclusion, overall CCB are neither better nor worse than conventional therapy, allowing for possible small differences in stroke and MI. The ACE inhibitors may protect better, although data are incomplete.

Adrenergic beta-Antagonists↗
PubMed1997

Reduction of post-prandial motility by pinaverium bromide a calcium channel blocker acting selectively on the gastrointestinal tract in patients with irritable bowel syndrome.

BACKGROUND: Growing evidence points to irritable bowel syndrome physiologically as a disease of the enteric nervous system characterised by hypermotility. The aim of this study was to investigate the action of pinaverium bromide a calcium channel blocker acting selectively on the gastrointestinal tract on basal and post-prandial recto-anal motility of 40 irritable bowel syndrome patients in a random, double blind and placebo controlled trial. METHODS: Pinaverium bromide (50 mg) or placebo was taken orally t.i.d. with food. Myoelectrical and mechanical activities of the rectum and the internal anal sphincter were recorded before treatment for 2 h in the fasting state and for an additional 2 h post-prandial. RESULTS: Post-prandial rectal spike amplitude and frequency as well as the spontaneous recto-anal inhibitory reflex frequency decreased after pinaverium bromide (P < 0.01) but not after placebo. CONCLUSIONS: These results suggest that the calcium channel blockers acting selectively on the gastrointestinal tract may have a therapeutic role in patients with irritable bowel syndrome.

Adolescent↗