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At least 145 records · Page 8Linked to original sources
PubMed2007

Effects of intrathecal injection of T-type calcium channel blockers in the rat formalin test.

T-type Ca2+ channels have been implicated in the induction of long-term potentiation, a synaptic plasticity involved in the central sensitization that contributes to the generation of inflammatory pain, in spinal sensory neurons. In this study, we examined the effects of intrathecal T-type Ca2+ channel blockers, mibefradil, ethosuximide and NiCl2, in the rat formalin test, an inflammatory pain model. Biphasic characteristic nociceptive behaviors were induced by intraplantar injection of formalin (5% formaldehyde, 50 microl) in Sprague-Dawley rats and monitored at 0-9 min (phase 1) and 10-60 min (phase 2) after formalin injection. Intrathecal pretreatment with mibefradil (50-500 microg) and NiCl2 (1-10 microg) dose-dependently decreased the flinch numbers and biting and licking time in both phases. The ID50s of mibefradil in inhibiting the phases 1 and 2 flinch responses were 74.3+/-4.6 and 100.9+/-8.7 microg, respectively, and those of NiCl2 were 2.7+/-1.1 and 3.3+/-0.1 microg, respectively. Ethosuximide, at the doses up to 1200 microg, however, did not affect the nociceptive responses in both phases. It is suggested that spinal T-type Ca2+ channels may play a role in formalin-induced inflammatory pain. The ineffectiveness of ethosuximide is discussed.

Animals↗
PubMed2006

Efficacy of MEM 1003, a novel calcium channel blocker, in delay and trace eyeblink conditioning in older rabbits.

Eyeblink conditioning is a relatively simple form of associative learning that shows neurobiological and behavioral parallels across several species, including humans. Aged subjects acquire eyeblink conditioning more slowly than young ones. In addition, eyeblink conditioning effectively discriminates patients with Alzheimer's disease from healthy older adults. The present study evaluated the effect of a novel L-type Ca2+ channel antagonist, MEM 1003, on delay and trace eyeblink conditioning in older (mean 33.4 months old) female New Zealand white rabbits. In the delay conditioning paradigm, an 850 ms tone conditioning stimulus (CS) was followed 750 ms after its onset by a 100 ms corneal air puff. Several trace conditioning paradigms were evaluated, with a silent period of 300, 400 or 500 ms between the end of the tone CS and the delivery of the air puff. Learning was more difficult in the longer trace paradigms than in the delay paradigm. MEM 1003, at a dose of 2.0 mg/kg, s.c., given daily 30 min prior to training on each of the 15 training days, enhanced learning compared to vehicle injections in both delay and trace paradigms. However, higher or lower doses were ineffective. These results support previous work demonstrating that modulation of Ca2+ channel activity can reduce age-related cognitive impairments.

Age Factors↗
PubMed2005

The antihyperalgesic effects of the T-type calcium channel blockers ethosuximide, trimethadione, and mibefradil.

The purpose of the present study was to explore the analgesic effects of the low voltage-activated T-type Ca2+ channel blockers ethosuximide, trimethadione, and mibefradil in persistent and acute nociceptive tests. The anticonvulsant effects of the compounds were also determined in the intravenous pentylenetetrazol seizure model. Following intraperitoneal administration, ethosuximide and trimethadione dose-dependently reversed capsaicin-induced mechanical hyperalgesia. Similarly, the highest dose of mibefradil tested (30 microg, intracisternal) reversed capsaicin-induced mechanical hyperalgesia. Ethosuximide and mibefradil produced statistically significant analgesic effects in both early and late phase formalin-induced behaviors and trimethadione reduced late phase behaviors. Additionally, ethosuximide and trimethadione produced antinociceptive effects in the rat-tail flick reflex test. In contrast, following intracisternal administration, mibefradil had no effect in the tail flick reflex test. In addition, the anticonvulsants ethosuximide and trimethadione increased the doses of pentylenetetrazol required to produce both first twitch and clonic seizures. In contrast however, mibefradil had no anticonvulsant effect. The present results demonstrate that the clinically used anticonvulsants ethosuximide and trimethadione provide analgesic effects at doses, which are anticonvulsant. Furthermore, the data further supports the idea that T-type Ca2+ channels may be important targets for treating persistent pain syndromes.

Animals↗
PubMed1988

Voltage-dependent binding of dihydropyridine calcium channel blockers to guinea pig ventricular myocytes.

The voltage dependence of the binding of dihydropyridine Ca channel blockers (+)-[3H]PN200-110 and [3H]nitrendipine to enzymatically isolated guinea pig ventricular myocytes was examined. The equilibrium saturation binding of (+)-[3H]PN200-110 could be well described by a simple 1:1 binding scheme under all conditions tested. The results demonstrated that the effect of depolarization induced by high extracellular K+ (50 mM) compared to normal K+ (4.8 mM) was an increase in the observed number of binding sites (Bmax) with no change in the measured affinity of binding (Kd). Similarly, depolarization induced by a combination of Na channel toxins in the presence of normal extracellular K+ caused an increase in the observed binding of (+)-[3H]PN200-110 comparable to that observed with high K+. [3H]Nitrendipine binding was likewise increased by depolarization in the presence of 50 mM K+ compared to 4.8 mM K+. Percoll density gradient centrifugation was found to enrich the cell preparation with viable myocytes and increased the measured voltage-dependent change in binding. In agreement with the predictions from previous studies (Kamp and Miller, 1987a), the magnitude of the observed change in Bmax was directly related to the fraction of cells which were viable in a given experiment. These results are discussed in comparison to the modulated receptor hypothesis proposed from electrophysiological studies.

Animals↗
PubMed2004

L-type calcium channel blockers enhance 5-HTP-induced antinociception in mice.

AIM: To investigate the involvement of L-type Ca(2+) channels in antinociceptive action induced by the 5-HT precursor, 5-hydroxytryptophan (5-HTP). METHODS: Female Kunming mice were treated with either 5-HTP (20-80 mg/kg, ip) alone, or the combination of 5-HTP and fluoxetine (2-8 mg/kg, ip), pargyline (15-60 mg/kg, ip), nimodipine (2.5-10 mg/kg, ip), nifedipine (2.5-10 mg/kg, ip), verapamil (2.5-10 mg/kg, ip), CaCl(2) (5-20 mmol/L, icv), or EGTA (0.5-3 mmol/L, icv) prior to the hot-plate test (55 degree, hind-paw licking latency). In addition, locomotor activity in mice treated with 5-HTP alone was measured using an ambulometer with five activity boxes. RESULTS: Ip injection of 5-HTP alone had no influence on the spontaneous locomotor activity, whereas dose-dependently increased the latency to licking hind-paw in the hot-plate test in mice. The inhibitory effects of 5-HTP on nociceptive response were significantly enhanced by fluoxetine in the mouse hot-plate test. At a sub-effective dose, pargyline could cause a leftward shift in the dose-response curve of 5-HTP-induced antinociception. Co-administration with 5-HTP and nimodipine, nifedipine, or verapamil obviously potentiated the antinociceptive effects elicited by 5-HTP. Interestingly, 5-HTP-induced antinociception was antagonized by CaCl(2) and enhanced by EGTA injected icv in the mouse hot-plate test. CONCLUSION: These findings suggest that systemic administration of 5-HTP may yield the antinociceptive effects, which are related to Ca(2+) influx from extracellular fluid through L-type Ca(2+) channels.

5-Hydroxytryptophan↗
PubMed1992

Effect of calcium channel blockers on platelet GPIIb-IIIa as a calcium channel in liposomes: comparison with effects on the intact platelet.

The platelet membrane glycoprotein IIb-IIIa complex is essential for platelet aggregation and functions as a fibrinogen receptor on the activated platelet. When incorporated into phospholipid vesicles, this glycoprotein complex can function as an apparent calcium channel which facilitates the transit of calcium across a phospholipid barrier. In order to further evaluate this calcium channel, the effect of calcium channel blockers of the dihydropyridine (nifedipine and nicardipine), arylalkylamine (verapamil) and benzothiazepine (diltiazem) classes were evaluated on GPIIb-IIIa liposomes with encapsulated fura-2 (a fluorescent calcium indicator). Nicardipine, verapamil, and nifedipine significantly inhibited calcium influx into GPIIb-IIIa liposomes; however, this required 190 microM, 400 microM, and 140 microM drug, respectively. These concentrations are 10-1,000 fold greater than those clinically obtainable. In contrast, diltiazem at concentrations greater than 220 microM and amiloride at concentrations greater than 800 microM showed no inhibitory effects. When aspirinized platelets were activated with 30 micrograms/ml bovine fibrillar collagen, both nicardipine and diltiazem produced a decrease in both the initial rise and maximum cytoplasmic calcium concentration. Parallel experiments were performed to assess the effects of verapamil, nicardipine, and diltiazem on platelet aggregation in platelet rich plasma. Nicardipine, 190-380 microM, induced a prolongation of the lag phase, but no effect on the final degree of platelet aggregation to collagen. Similar inhibition of platelet aggregation was seen with diltiazem and verapamil although the effect of diltiazem was less pronounced particularly at higher concentrations of collagen. No effect was seen on aggregation with 32 microM ADP which is release independent, or on the primary wave of low dose ADP induced platelet aggregation.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport, Active↗
PubMed1987

Calmodulin-stimulated plasma membrane (Ca2+ + Mg2+)-ATPase: inhibition by calcium channel entry blockers.

Calcium channel entry blockers representing different structural classes were studied for their effects on human erythrocyte basal and calmodulin-stimulated (Ca2+ + Mg2+)-ATPase. Effects on the activity of (Mg2+)-ATPase and (Na+ + K+)-ATPase were also assessed. Of the four Ca2+ entry blockers tested, only verapamil and diltiazem specifically inhibited the calmodulin-stimulated (Ca2+ + Mg2+)-ATPase activity, the basal enzyme activity being unaltered by these drugs. Other membrane-associated ATPases were not affected. Calmodulin concentration effect curves showed the inhibition by verapamil (10(-3) M) and diltiazem (10(-3) M) to be non-competitive. This concentration inhibited the calmodulin-dependent increment (5.1 nM calmodulin) of the ATPase activity by 35 and 36% respectively. Similarly, both drugs inhibited the Ca2+-activation process of calmodulin-stimulated activity in a non-competitive manner, decreasing Vmax by 23 and 17% respectively. Basal (Ca2+ + Mg2+)-ATPase activity was not affected by verapamil or diltiazem at any calcium concentration. In contrast, cinnarizine non-specifically inhibited all four membrane ATPases including calmodulin-stimulated (Ca2+ + Mg2+)-ATPase activity at concentrations above 3 X 10(-6) M. Nifedipine was without effect on any of the four membrane ATPases. From this we conclude that certain calcium channel entry blockers can inhibit calmodulin-regulated plasma membrane Ca2+-pump ATPase. Therefore, this identifies an additional functional low affinity receptor in the plasma membrane for some of the calcium channel entry blockers.

Ca(2+) Mg(2+)-ATPase↗
PubMed1987

Calcium channel blockers: correlation among receptor binding, calcium uptake and contractility in vitro.

Ten known calcium channel blockers were studied for inhibition of K+-induced 45Ca++ uptake into rabbit aortic smooth muscle cells in culture, and for displacement of [3H]nitrendipine [2,6-dimethyl-3-carbomethoxy-5-carbomethoxy-4-(3-nitro)phenyl-1, 4-dihydroxypyridine] binding to rat ventricular membrane preparations, in order to relate their effects on receptor binding with their inhibitory activities on 45Ca++ uptake and on contractile responses of vascular smooth muscle. Steady-state 45Ca++ uptake increased with K+ concentration in a dose-dependent manner. With 25 to 50 mM K+, Ca++ uptake was 0.6 nmol of Ca++ per one million cells. All calcium channel blockers inhibited K+-induced 45Ca++ uptake and [3H]nitrendipine binding in a dose-dependent fashion. The enatiomeric dihydropyridines 202-791 [isopropyl-4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-2, 6-dimethyl-5-nitro-3-pyridinecarboxylate] exhibited marked stereoselectivity in both studies, the agonist (+)-202-791 significantly enhancing 45Ca++ uptake at 15 to 50 mM K+. The similarity between the order of potency in inhibiting 45Ca++ uptake and displacing [3H]nitrendipine resulted in a highly significant linear (1:1) correlation. An equally significant correlation was also established for the 10 blockers between their inhibitory potencies on 45Ca++ uptake and the contractile response of rabbit aortic strips as cited in the literature. These findings support the hypothesis that calcium channel blockers block contraction of vascular muscle by inhibiting cellular calcium uptake through voltage-dependent calcium channels as a result of binding to receptors associated with these channels. The aortic cells possess channels that are functionally similar to those found in intact vascular tissue.

Animals↗
PubMed2006

Treatment with beta-blockers, ACE inhibitors, and calcium-channel blockers is associated with a reduced fracture risk: a nationwide case-control study.

BACKGROUND: Cardiovascular diseases are associated with disturbances in calcium metabolism, including increased urinary calcium, vitamin D insufficiency, and decreased bone mineral density. Antihypertensive drugs may increase the risk of falling. However, risk of fracture in patients treated with non-diuretic cardiovascular drugs is largely unknown. AIM: We investigated associations between fracture risk and treatment with commonly used cardiovascular drugs: beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium-channel blockers. DESIGN: A population-based pharmaco-epidemiological case-control study with fracture in year 2000 as outcome and drug use during the previous 5 years as exposure. We used nationwide computerized registers to assess individual use of drugs and related these data to individual fracture records and information on socio-economic and health-related confounders. RESULTS: We included 124,655 cases that sustained a fracture and 373,962 age and gender-matched controls. After adjustment for potential confounders, risk of any fracture was reduced by 9% [odds ratio (OR) 0.91; 95% confidence interval (CI), 0.88-0.93] in users of beta-blockers, by 6% (OR, 0.94; 95%CI, 0.91-0.96) in users of calcium-channel blockers, and by 7% (OR, 0.93; 95%CI, 0.90-0.96) in users of ACE inhibitors. Moreover, risk of hip fractures was reduced significantly by 7-14% in users of the three groups of drugs. No major differences were found between men and women or in subjects younger or older than 70 years of age. Sub-analyses indicated differences between groups of calcium-channel blockers, as use of non-dihydropyridine drugs was associated with a larger risk reduction than use of dihydropyridine drugs. CONCLUSION: Treatment with beta-blockers, ACE inhibitors, and calcium-channel blockers is associated with a small but significantly reduced risk of fracture.

Adolescent↗
PubMed1990

Calcium channel blockers and atherosclerosis.

There is evidence that calcium antagonists (calcium channel blockers) may suppress atheroma formation in animals fed high-fat diets. Studies on the antiatherosclerotic effects of calcium blockers have suggested a variety of possible mechanisms: (a) lowering of arterial pressure, (b) decrease in atherogenic plasma lipoproteins, (c) suppression of accumulation of intracellular lipids, (d) suppression of atherogenic platelet dysfunction, (e) prevention of dyslipidemic endothelial injury, (f) inhibition of chemotaxis and cell migration, (g) inhibition of cell proliferation, (h) inhibition of deposition of matrix proteins, (i) suppression of tissue mineralization, and (j) retardation of cell necrosis. Although it is tempting to ascribe the antiatherosclerotic effects of calcium blockers to a blockade of calcium channels, other possible common mechanisms of action involving low-affinity drug-binding sites must be considered. Recently, two randomized, prospective clinical trials designed to determine the effects of calcium channel blockers on the progression of coronary artery disease have been completed. Results of the trials suggest that calcium channel blockers suppressed the progression of coronary atherosclerosis. The utility of calcium channel blockers for the treatment of atherosclerosis will require further evaluation.

Arteriosclerosis↗
PubMed2000

Treatment of arterial hypertension with diuretics, beta- and calcium channel blockers in old patients.

Hypertension increases in prevalence with age. Population based studies suggest that more than 50% of people over the age of 65 years may have chronic hypertension. Hypertension, especially systolic hypertension, is the single most common, powerful, however, treatable risk factor for cardiovascular morbidity and mortality in the elderly. In order to assess the effectiveness of antihypertensive drug therapy among the elderly, with diuretics, beta-blockers and calcium channel blockers, a literature search was performed at the Cochrane Library, Medline and Excerpta medica. The Cochrane Hypertension Group identified 14 randomised controlled trials of at least one year duration with 21,785 elderly subjects where diuretics, beta-blockers or calcium channel blockers were used in the treatment group as first line drugs. In their meta-analysis (including one small trial with a central acting antiadrenergic drug) there was a decrease in total mortality (111 vs 129 deaths) and cardiovascular morbidity and mortality (126 vs 177 events) within the treatment group. The three trials restricted to persons with isolated systolic hypertension indicated beneficial effects in the treatment group with regard to cardiovascular morbidity and mortality (104 vs 157 events). Trial data on adverse effects is limited. In three studies, where adverse effects were reported, no substantial differences between treatment and control groups in measures of physical, cognitive and emotional function were found. Cardiovascular benefits of treatment with low dose diuretics or beta-blockers are cleared for elderly subjects with either diastolic or isolated systolic hypertension. Treatment with a long-acting dihydropyridine calcium channel blocker shows beneficial effects in reducing cardiovascular morbidity and mortality for elderly people with isolated systolic hypertension. Due to inconsistent findings in a subgroup meta-analysis of antihypertensive drug treatment in very old people, the efficacy of antihypertensive treatment in these subjects still remains unclear.

Adrenergic beta-Antagonists↗
PubMed1996

Role of calcium channel blockers in reducing acute ischaemia and preventing restenosis in PTCA.

Calcium channel blockers (calcium antagonists) are widely used before, during and after percutaneous transluminal coronary angioplasty (PTCA). When administered during PTCA, calcium channel blockers may be beneficial in decreasing regional ischaemia in patients with proven or suspected variant angina, as a result of their cardioprotective effects, their ability to enhance collateral flow, and their antispastic effects at the epicardial level. More recently, the agents have also proven to be effective in patients who have developed "no-reflow' phenomenon during PTCA. Preliminary findings suggest that calcium channel blockers may also have potential benefits when administered after angioplasty. The combined results of 5 studies, evaluating a total of 919 patients, showed a trend towards angiographic reduction in restenosis. These observations are of interest but may be due to reporting bias. In conclusion, calcium channel blockers are effective in reducing ischaemia induced by PTCA. These agents may, thus, be appropriate in high risk patients. Further large studies examining the effects of calcium channel blockers on restenosis are required to confirm the observations available to date.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

Calcium channel blockers inhibit cellular uptake of thymidine, uridine and leucine: the incorporation of these molecules into DNA, RNA and protein in the presence of calcium channel blockers is not a valid measure of lymphocyte activation.

An important role of transmembrane flux of calcium in lymphocyte activation has been previously demonstrated. Herein, we demonstrate that the calcium channel blockers verapamil and isradipine are able to inhibit in a concentration-dependent manner 3H-thymidine incorporation into DNA in phytohemagglutinin (PHA)-stimulated human peripheral blood mononuclear cells (PBMC). However, verapamil and isradipine diminish PHA-stimulated thymidine incorporation into DNA to the same extent whether they are added at the beginning of culture or 4 h prior to completion of a 72-h culture. Thus, 3H-thymidine incorporation into DNA in the presence of verapamil or isradipine is not a valid measure of mitogen-induced lymphocyte proliferation. Similarly, verapamil and isradipine also inhibit PHA-stimulated incorporation of 3H-leucine into protein and 3H-uridine into RNA whether the drugs are added at the beginning of culture or 4 h prior to completion of 24-h cultures. There is no intracellular accumulation of 3H-thymidine, 3H-leucine, or 3H-uridine into 10% trichloroacetic acid-soluble molecules during inhibition with verapamil or isradipine, suggesting that these drugs impair the cellular uptake of these substances rather than directly inhibiting their incorporation into DNA, protein, or RNA, respectively. Since previous reports documenting the inhibitory effects of calcium channel blockers on lymphocyte proliferation have utilized 3H-thymidine incorporation into DNA to measure proliferation, we have re-examined the antiproliferative effects of these drugs by determining their effect on PHA-stimulated cell cycle progression, employing cytofluorometric analysis of propidium iodide-stained cells. When added at the initiation of culture, both verapamil and isradipine inhibited in a concentration-dependent manner PHA-stimulated cell cycle progression.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed1994

Do calcium channel blockers have renal protective effects?

Calcium channel blockers are used in the treatment of hypertension because of their ability to decrease peripheral vascular resistance. Recent research has suggested that these drugs also preserve or improve renal function in patients with essential hypertensive renal disease or diabetic renal disease, and in renal transplant recipients with or without cyclosporin therapy. In general, studies in animal models of hypertension and in hypertensive humans have demonstrated reduction in renal vascular resistance, and preservation or enhancement of renal plasma flow and glomerular filtration rate. In addition, calcium channel blockers appear to have a positive effect on renal addition, calcium channel blockers appear to have a positive effect on renal haemodynamic function in the setting of diabetes mellitus; prospective trials have also demonstrated reductions in urinary protein excretion in these patients. Current evidence suggests that calcium channel blockers are well-suited for the treatment of patients with hypertensive disease even in the presence of renal impairment, a clinical scenario common in the elderly population.

Aging↗
PubMed1996

How do calcium channel blockers prevent cardiovascular events. Are they all alike?

The calcium channel blockers (calcium antagonists) have vasodilatory and cardiodepressant effects. These pharmacological properties explain, to a large extent, the antihypertensive, antianginal, and antiarrhythmic effects of these agents. Pharmacological differences between members of this class, e.g. differences in vascular selectivity, are well documented and can be exploited clinically. The efficacy of calcium channel blockers in the prevention of cardiovascular events may depend on factors other than their vasodilatory and cardiodepressive effects. Much interest, for example, has been shown in their possible antiatherosclerotic effects. It is, however, at present not possible to ascertain how important these and other ancillary effects (such as plaque stabilisation) are for the putative cardioprotective effects of calcium channel blockers. There are, moreover, few in vitro or in vivo (animal or clinical) studies allowing valid comparison of the different calcium channel blockers with regard to these ancillary properties.

Animals↗
PubMed1988

Granulocyte activation during haemodialysis in the absence of complement activation: inhibition by calcium channel blockers.

The effect of the calcium channel blockers nifedipine (9 and 18 micrograms kg-1 h-1), diltiazem (100 and 200 micrograms kg-1 h-1) and verapamil (19 micrograms kg-1 h-1) continuously infused during haemodialysis on granulocyte and complement activation was investigated. Plasma levels of lactoferrin, elastase in complex with alpha 1-proteinase inhibitor (E-alpha 1PI) and C3a were measured in patients dialysed with dialysers made of cuprophane, polymethylmethacrylate (PMMA) and polyacrylonitrile (PAN). Calcium channel blockers caused no change of blood pressure during haemodialysis in all patients. There was no effect of nifedipine, diltiazem or verapamil on plasma lactoferrin, E-alpha 1PI or C3a levels in patients dialysed with cuprophane. However, plasma lactoferrin and E-alpha 1PI values were significantly reduced by all calcium channel blockers in patients dialysed with PMMA, and also by nifedipine and verapamil in patients dialysed with PAN. Our data indicate that calcium channel blockers inhibit granulocyte activation occurring in dialysers with very little anaphylatoxin formation. These drugs, however, are ineffective in patients dialysed with cuprophane where complement activation takes place. Therefore, granulocyte activation during haemodialysis in the absence of complement activation seems to be mediated by calcium ions.

Aged↗
PubMedDate not supplied

The antagonistic effects of ouabain and calcium channel blockers on the contractility of the isolated rat heart.

The simultaneous prescription of a calcium channel blocker and a cardiac glycoside is a frequently used therapeutic combination in cardiology, although its consequences on inotropism have not been really evaluated. This association is studied on isolated rat heart perfused at constant coronary pressure, paced at a constant frequency and working against a left intraventricular balloon. Since the inotropic effects are dependent on the basic level of myocardium contractility, controls were made hypocontractile by lowering external calcium level to 0.25 mM. For the same initial systolic pressure (45 mm Hg) and + dP/dTmax (150 mm Hg X s-1) the inotropic effect of 10(-5) M ouabain was significantly less pronounced in the presence of 10(-6) M verapamil or 10(-7) M nifedipine at 2.5 mM CaCl2 than at the low external calcium concentration of 0.25 mM (increasing the + dP/dtmax by 35% +/- 4, 29% +/- 6 and 110% +/- 18 respectively). Since we know that the inotropic properties of digitalis are probably due to an increase of the slow calcium inward current, we conclude that the observed effect would be due to a blockade of these channels by calcium blockers.

Animals↗
PubMed2006

Pharmacotherapy review: calcium channel blockers.

As a drug class, calcium channel blockers encompass a heterogeneous group of compounds with distinctive structures and pharmacologic characteristics. These agents are widely used in the treatment of hypertension, chronic coronary ischemia, and/or supraventricular arrhythmias. Much of the early debate alluding to increased cardiovascular risk associated with calcium channel blocker use has been silenced by an array of outcomes trials that show these drugs to be both safe and effective in reducing hard cardiovascular end points. The most common side effects associated with calcium channel blockers are vasodilatory in nature and include a non-volume-dependent form of peripheral edema, flushing, and headache. Despite the sometimes discomforting side effects seen with calcium channel blocker therapy, their robust blood pressure-lowering effect makes them an important component of most multidrug regimens used for blood pressure control.

Calcium Channel Blockers↗