Effects of nicardipine and diltiazem on the bispectral index and 95% spectral edge frequency

 significantly decreased arterial pressure.

Impact of calcium antagonists on bleeding time in patients with chronic renal failure

 antagonist-treated patients with prolonged bleeding time, the withdrawal of 

 markedly shortened bleeding time (from 11.3 ± 0.8 to 5.4 ± 0.8 min, P < 0.05, n = 12).

Calcium-channel blocking agents.

 through these channels in smooth and cardiac muscle; the specific agents in this class differ markedly in their inhibitory effects.

Structural Basis for Diltiazem Block of a Voltage-Gated Ca2+ Channel

Our results reveal the chemical details of diltiazem binding in a blocking position in the pore of a model calcium channel and show that binding of another

[Investigation of uterus-relaxing effects of nifedipine in the presence of terbutaline and K(+)-channel blockers].

Use and safety of calcium channel blockers in obstetrics.

), or calcium antagonists, are a heterogeneous group of drugs that produce cardiovascular effects by preventing the influx of 

 through L-type voltage-dependent calcium channels in specialized electrical system and conduction tissue cells, like myocardial and vascular smooth muscle cells.

Channel-mediated calcium current in the heart

There also exists a class of drugs, called

 (or calcium antagonists) that decrease the flow of 

Vascular aspects of calcium antagonists

Schistosomiasis: a new target for calcium channel blockers.

 block voltage-gated calcium channels in a wide variety of animals and thereby inhibit the influx of 

 from the extracellular milieu” says Walter. “

Calcium enhances Acanthamoeba polyphaga binding to extracellular matrix proteins.

, lanthanum and cobalt, suppressed the effect of 

Role of calcium antagonists in progression of arteriosclerosis. Evidence from animal experiments and clinical experience. Part I. Preventive effects of calcium antagonists in animal experiments.

 uptake in all experimental models of arteriosclerosis tested so far.

Protective effects of various calcium antagonists against experimental arteriosclerosis.

 accumulation in the internal elastic membrane of abdominal arteries of NaCl-loaded salt-sensitive Dahl-S rats, and consequently also exerts protective effects against arteriosclerotic lesions, shown particularly in the distal mesenteric artery branches.

Calcium antagonists and left ventricular function.

 into myocytes and inhibit myocardial contraction.

Calcium-channel blockers in postmyocardial infarction patients with special notation to the Danish verapamil infarction trial II.

The term “calcium-channel blocking agent” or 

” is used to describe a group of drugs that share the common pharmacological property of blocking the entrance of 

 into striated cardiac and smooth vascular muscle.

Differentiation Between Calcium‐and Cholesterol‐Dominated Types of Arteriosclerotic Lesions: Antiarteriosclerotic Aspects of Calcium Antagonists

 uptake were found to prevent pathogenic mural calcium accumulation and damage.

Treatment and prevention of ventricular fibrillation: are there better agents?

 into cells, in particular reducing the spontaneous depolarisation of phase 4 in the atrio-

[Toxicity of calcium inhibitors].

 decrease the intracellular concentration of 

The Role of Calcium and Magnesium in the Development of Atherosclerosis

It has been reported that migration of SMCs from arterial media to intima is enhanced by the presence of

, and can be inhibited by the pretreatment of 

Calcium channel blockers in systemic hypertension.

 selectively inhibit transmembrane flux of 

Calcium-channel blockade in the management of severe chronic congestive heart failure: a bridge too far.

Patients with severe left ventricular dysfunction, however, … exquisitely dependent on the transmembrane transport of

 for maintenance of contractile function and show marked attenuation of adrenergic reflexes, which can no longer … a homeostatic support function; hence, such patients are likely to experience notable cardiodepressant effects after 

Differentiation of calcium entry blockers into calcium channel blockers and calcium overload blockers.

 selectively and competitively inhibit the transmembranous slow inward current, which is carried by 

 both in cardiac tissues and in vascular smooth muscle under physiological conditions.

Calcium-channel blockers and systemic hypertension.

Role of calcium and calcium antagonists in airway function.

 may inhibit the ingress of Ca2+ ions from the extracellular environment or may influence the availability of 

 from plasma membrane or subcellular organelles.

Can hypoinsulinemia induced by calcium channel blockers be associated with cardiac events?

 prevent the opening of voltage-gated calcium channels and reduce the entrance of 

 into the cells during the second phase of the action potential.

Identifying the Transcriptome Signatures of Calcium Channel Blockers in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.

Without inducing cell death and damage to myofilament structure,

Calcium channel blockers and the incidence of breast and prostate cancer: A meta‐analysis

 (CCBs) have been thought to increase the risk of cancer by inhibiting 

 signal‐mediated apoptosis, but the evidence for this association remains inconclusive.

Idiopathic Calcinosis Cutis Universalis Treated Successfully with Oral Diltiazem—A Case Report

 are known to work by inhibiting intracellular entry of 

Calcium antagonists as an add-on therapy for drug-resistant epilepsy.

 on brain cells have been investigated for their effect on epileptic seizures.

Can Calcium Antagonists Provide a Neuroprotective Effect in Parkinson’s Disease?

 in neurotoxicity, and specifically in mediating the process of apoptosis, raises the possibility that 

 may have a salutary effect on conditions such as PD in which apoptosis may be the ultimate mode of cell death.

Acute episode of reversible blindness after an overdose of beta blockers and calcium channel antagonist.

 through L-type calcium channels, resulting in arterial smooth muscle relaxation in vessels.

Amlodipine‐induced gingival overgrowth: Considerations in a geriatric patient

Amlodipine is a member of the dihydropyridine class of

 which selectively inhibit the influx of 

Calcium antagonists for Duchenne muscular dystrophy.

Cardiogenic shock secondary to combination of diltiazem and sotalol

 through the calcium channels in both smooth muscle and myocardium.

Genetic variation in the NOS1AP gene is associated with the incidence of diabetes mellitus in users of calcium channel blockers

) bind to a receptor on the voltage-dependent calcium channels and they regulate calcium handling by reducing the influx of 

A Review of Calcium Channel Antagonists in the Treatment of Pediatric Hypertension

 (CCAs) are a class of drugs that exert their antihypertensive effect by inhibiting the influx of 

Myocardial stunning—Are calcium antagonists useful?

When given exactly at the time of reperfusion, the proposal is that the

 via the calcium channel and thereby diminishing pathogenic cytosolic calcium oscillations.

Effects of calcium channel blockers on atherosclerosis: new insights.

 in atherogenesis has created interest in the antiatherogenic potential of 

Calcium has been established to play a major role in seizure occurrence, thus,

 on brain cells have been investigated for effect on epileptic seizures.

Lymphocytic intracellular calcium in a patient with complicated verapamil overdose.

 into the cell, thus lowering intracellular calcium ([Ca2+]i).

Calcium-antagonist drugs.

Drugs classified as calcium antagonists or calcium-channel blockers … treatment of cardiovascular diseases.1 Although the currently available

 through voltage-gated L-type (slowly inactivating) channels.2 These drugs have proved effective … diastolic dysfunction, Raynaud's phenomenon, migraine, preterm labor, esophageal spasm, and bipolar disorders.

Calcium antagonists--pharmacologic considerations.

 from the outside of the cell to the inside of the cell through the voltage-dependent calcium channels.

[Clinical pharmacokinetics of calcium antagonists].

) represent a heterogeneous group of pharmacons, being its mechanism of action the inhibition of the flow of entrance of 

 through type L depending-voltage channels of the membranes of the excitable cells.

[The feasibility and current limits in the prevention of diabetic nephropathy].

It is believed that some classes of anti-hypertensive drugs have a direct pharmacological depressive effect … growth factors that lead to mesangial sclerosis: ACE-inhibitors would thus depress angiotensin II, and the

 of the mesangial cells which … expression of early growth.

Calcium channel blockers for anxiety disorders?

 profoundly influence calcium metabolism and the transport of 

Review: the central role of calcium in the pathogenesis of cardiovascular disease.

 drugs principally act on L-type calcium channels to reduce the influx of 

[Does the diuretic effect of calcium inhibitors play an important role in the hypertensive efficacy?].

, a group of first line drugs in the treatment of hypertension, reduce the intracellular content of 

 in vascular smooth muscle cells, and decrease the peripheral vascular resistance and blood pressure.

[Calcium antagonists and heart failure. Critical review of the literature].

Toxic Effects of Diltiazem in a Patient with Chronic Renal Failure

 during membrane depolarization ….1 Through their 

 blocking effects, they depress the rate of the sinoatrial node, slow the atrioventricular node conduction, and are negative inotropic agents.… in the liver.1 Small percentage of unchanged drugs and some of their metabolites are excreted in the urine.

The effect of nifedipine, a calcium channel blocker, on human spermatozoal functions.

In vitro addition of 0.1-100 microns of a

, Nifedipine, resulted in a significant non-competitive inhibition in the uptake of 

Therapies for perioperative hypertension: pharmacodynamic considerations

 into vascular smooth muscle cells, and others (e.g. nitrovasodilators) that boost the intracellular levels of vasodilating second messengers (e.g. cyclic GMP).

[Diabetic nephropathy and arterial hypertension: the physiopathological aspects and antihypertensive treatment].

This could be explained by the fact that ACE-inhibitors suppress the trophic effects of angiotensin II on the nephron, while

 might interfere with intracellular processes involved in cell hypertrophy that require the interaction of 

EVIDENCE THAT THE ANTIPROLIFERATIVE EFFECT OF VERAPAMIL ON AFFERENT AND EFFERENT IMMUNE RESPONSES IS INDEPENDENT OF CALCIUM CHANNEL INHIBITION

This effect is thought to be related to the ability of the

Calcium channels in the heart.

 by occupying binding sites on the outside of the membrane channel but do not affect the release of calcium from the sarcoplasmic reticulum.

 rise on reperfusion if applied before ischaemia but not when added at the time of reperfusion.

 is to inhibit the ion channel in the cell membrane, which allows the slow influx of 

Calcium current depression in isolated human atrial myocytes after cessation of chronic treatment with calcium antagonists.

The present study investigates the possibility that the

 current of human atrial cardiac cells is modified by chronic treatment (1-24 months) with 

 (nifedipine, nicardipine, or diltiazem) in a manner different from a simple drug-induced blocking effect.

Poisoning Due to Calcium Antagonists

 are a heterogeneous class of drugs which block the inward movement of 

 into cells through ‘slow channels’ from extracellular sites.

Calcium channel blockers in chronic heart failure. The risks of "physiologically rational" therapy.

 can depress contractility in both experimental systems and the clinical setting.

Interactions between gall bladder bile and mucosa; relevance to gall stone formation.

 ions also stimulate mucus glycoprotein secretion by the gall bladder mucosa" and this effect can be blocked by 

[Calcium intestinal absorption in normotensive and essential hypertensive subjects before and after nicardipine].

 would become higher in hypertensive subjects and diminished by 

[Use of calciotropic agents in psychiatry and neurology].

Calcium Antagonists in the Treatment of Prinzmetal's Angina and Unstable Angina Pectoris

 into vascular smooth muscle cells, producing pharmacological vasodilation.

[Calcium inhibitors and anesthesia].

 from entering the cell by inhibiting the slow voltage-dependent calcium channels.

Nitrendipine in patients with end-stage renal disease and hypertension.

Pharmacokinetics of calcium antagonists.

 are a biochemically heterogeneous group of drugs that share the property of blocking the entry of 

 into cells by voltage-operated channels in cardiac and smooth muscle.

Effect of nitrendipine on histamine release from human basophil leukocytes

The histamine release induced by calcium ionophore A23187, f‐met peptide and anti‐IgE was inhibited, in a dose‐dependent fashion, by nitrendipine in the concentration range of 1–100 μM. The activity of this

 seems complex and related to an interference with 

Advances in calcium blocker therapy.

 are drugs that interfere with the entry of 

CALCIUM ANTAGONISM—WITH SPECIAL REFERENCE TO DILTIAZEM

 across cell membranes and hence the concentration of calcium at different sites within the cell.

Calcium dependency in the growth of adult T-cell leukemia cells in vitro.

Furthermore, the expression of interleukin 2 receptors (Tac antigens) on ATL cells was also enhanced by

Calcium-channel blockers and advanced cardiac life support.

 after ischemia and reperfusion, and thereby attenuate cerebral and myocardial injury, although most studies have failed to show benefit of treatment unless the drug is administered before the onset of ischemia.

Cardiovascular pharmacology. III: Atropine, calcium, calcium blockers, and beta-blockers.

 has been advocated to prevent or retard the intracellular accumulation of 

, which may cause irreversible postanoxic tissue damage.

Mechanisms of action and differences in calcium channel blockers.

 into the cell, and thus prevent calcium from gaining access to the high-affinity, intracellular calcium-binding proteins.

Areolar sebaceous hyperplasia.

It is a calcium ion influx inhibitor (slow-channel blocker or

) and inhibits the transmembrane influx of 

Basic cellular mechanisms of action of the calcium-channel blockers.

 (Ca++) into excitable cells, including those of coronary and peripheral arterial smooth muscle and the heart.

Calcium signal and calcium antagonists.

 and its modulations allows a better comprehension of mechanisms of action of 

Calcium-channel blockers in the treatment of migraine.

 selectively inhibit the intracellular influx of 

, investigators have begun evaluating the efficacy of these agents for migraine prophylaxis.

Rebound vasospasm after coronary revascularization in association with calcium antagonist withdrawal.

 at the completion of coronary revascularization may be ill-advised in patients in whom 

[Secondary prevention of myocardial infarct with beta blockers].

Beta-blockers and calcium blockers reduce the myocardial oxygen consumption by a variety of mechanisms: beta-blockers block the beta-adrenergic receptors and

Calcium, vascular smooth muscle, and calcium entry blockers in hypertension.

A heterogeneous group of compounds known as

 inhibit smooth muscle contraction induced by physiologic and pharmacologic stimuli by blocking transmembrane transport of 

The effect of a calcium-channel blocking agent on intraocular pressure.

, used in the management of coronary heart disease, inhibit the entrance of 

 into the smooth muscle cells of the vessel and produce vasodilatation.

The role of calcium and the significance of calciumantagonists in some neurological and neurosurgical diseases

 are a heterogenous group of substances with one property in common, that is they interfere with the transmembrane movement of 

Calcium blocking drugs for angina pectoris.

, sometimes called calcium antagonists or slow channel blockers, have as their primary mechanism of action the ability to reduce intracellular 

 (Ca2+) concentration in cardiac and vascular smooth muscle (6-10).

High sensitivity of chicken's skeletal muscle sarcoplasmatic reticulum to effects of diltiazem or verapamil on calcium uptake and release.

Addition of tris-ATP to the microsomes caused ATP-induced calcium uptake in a concentration dependent manner with half-maximal calcium uptake around … of diltiazem or verapamil followed by added tris-ATP resulted a significant decrease in the fluorescence intensity of chlortetracycline, showing that these

[Regulation of myocardial lysosomal enzyme activity by calcium].

 overloading of cardiomyocytes and limit activation of myocardial lysosomal enzymes under conditions of acute hypoxia, acute total ischemia of myocardium and experimental hyperlipidemia.

Effect of Dietary Calcium Supplements and Amlodipine on Growth, Arterial Blood Pressure, and Cardiac Hypertrophy of Spontaneously Hypertensive Rats

Moreover, it has been suggested that the combination of

 could paradoxically have a synergistic effect in order to decrease arterial blood pressure.

 to control arterial blood pressure seems not to be advisable, and the present data do not prove the usefulness of the mentioned antihypertensive treatments in preventing cardiac hypertrophy.

Calcium‐dependent acetylcholine release from Xenopus oocytes: simultaneous ionic currents and acetylcholine release recordings

 and voltage‐dependent and partially reduced in the presence of several 

The Combined Effects of N-type Calcium Channel Blockers and Morphine on A&dgr; Versus C Fiber Mediated Nociception

, such as &ohgr;-conotoxin GVIA (&ohgr;-CTX), produce analgesia by impeding flux of 

 into A&dgr; and C fiber nociceptor terminals.

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