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At least 163 records · Page 9Linked to original sources
PubMed1997

Effects of aranidipine, a novel calcium channel blocker, on mechanical responses of the isolated rat portal vein: comparison with typical calcium channel blockers and potassium channel openers.

We investigated the effects of aranidipine, a dihydropyridine-type Ca2+ channel blocker, on contractile responses to KCl and spontaneous contractions in isolated rat portal veins in comparison with those of the Ca2+ channel blockers, nifedipine, nicardipine, nitrendipine, diltiazem, and verapamil, and of the K+ channel openers, cromakalim and nicorandil. All the Ca2+ channel blockers concentration-dependently inhibited contractions induced by KCl. Interestingly, aranidipine was more potent against the low K+ (20 mM)-induced contraction than the high K+ (80 mM)-induced contraction, whereas the other Ca2+ channel blockers were equally potent against contractions induced by either concentration of KCl. Cromakalim and nicorandil were effective only on the low K(+)-induced contraction. In addition, all the Ca2+ channel blockers and the K+ channel openers tested inhibited the amplitude of spontaneous contractions of isolated rat portal vein. Tetraethylammonium (TEA), a classic K+ channel blocker, significantly attenuated the effect of aranidipine but not of other Ca2+ channel blockers on the spontaneous contractions. The cromakalim-induced inhibition of spontaneous contractions was antagonized by TEA. Thus aranidipine was found to be different from the typical Ca2+ channel blockers and in part similar to the K+ channel openers in inhibiting mechanical responses of isolated rat portal vein, suggesting that activation of K+ channels may in part in part be involved in the aranidipine-induced vasodilation.

Animals↗
PubMed2004

Different effects of L-type and L+N-type calcium channel blockers on hamster cheek pouch venules.

Dihydropyridine calcium channel blockers are not uniform in terms of their action on calcium channel. L-type calcium channel blockers dilate the resistance arterioles. Cilnidipine is a dihydropyridine calcium channel blocker that also acts on N-type calcium channels, and may dilate venules through its effect on the sympathetic receptor. The influence of an L-type calcium channel blocker (nifedipine) or this L+N type blocker at 10(-7) mol to 10(-4) mol on venular diameter was examined by superfusion of male Syrian hamster cheek pouches. Nifedipine dose dependently dilated the arterioles alone, whereas cilnidipine dilated both arterioles and venules. Application of 10(-7) mol omega conotoxin, an inhibitor of N-type channels, after nifedipine led to significant dilation of venules, while it had no influence when administered after cilnidipine. These findings indicate that the effects of calcium channel blockers on the venules differ according to the action on N-type calcium channels, and that cilnidipine (an L+N type calcium channel blocker) dilates venules through its additional action on N-type channels.

Animals↗
PubMedDate not supplied

Hyperinsulinemic-euglycemic therapy for intoxication with calcium channel blockers.

Conventional therapy for intoxication with calcium channel blockers consists of crystalloid solutions, calcium gluconate, glucagon and vasopressor agents. These therapies often fail to improve hemodynamic function in intoxicated patients. The pathophysologic mechanism proposed for intoxication with these agents, suggest hypoinsulinemia as the determinant factor. We will describe the case of a 77 years old man treated for an overdose of nifedipine and atenolol who arrived at our institution with hypotension and bradycardia. After conventional therapy failed to improve the patient's hemodynamic status, hyperinsulinemia and euglycemia contributed to the improvement of the patient's neurologic and hemodynamic condition. Thus, hyperinsulinemic-euglycemic therapy was of benefit in this patient with hemodynamic compromise secondary to intoxication with calcium channel blocker not responding to conventional therapy. We will review the mechanism of action of calcium channel blocker drugs as well as the clinical presentation and treatment options for calcium channel blocker intoxication.

Aged↗
PubMed1982

Anti-aggregatory actions of calcium channel blockers in cat platelets.

Four calcium channel blockers, verapamil, nifedipine, nisoldipine and nimodipine were studied in terms of their ability to inhibit platelet aggregation in cat platelet rich plasma by optical aggregometry. Only verapamil and nisoldipine significantly inhibited aggregation in cat platelets to ADP (2 microM). None of the calcium channel blockers exerted marked inhibition of aggregation induced by 1mM arachidonic acid. However, verapamil produced a moderate but significant inhibition of aggregation to arachidonic acid. Increasing the calcium ion concentration could reverse this inhibition. Thus, there are significant differences in the anti-aggregatory activity of calcium channel blockers in cat platelet rich plasma.

Adenosine Diphosphate↗
PubMed1994

Pharmacological profile of a novel neuronal calcium channel blocker includes reduced cerebral damage and neurological deficits in rat focal ischemia.

Excessive calcium entry into depolarized neurons contributes significantly to cerebral tissue damage following ischemia. Therefore, blocking voltage-operated calcium channels on nerve cells should provide significant neuroprotection in ischemia. We now report on a novel neuronal calcium channel blocker, NNC 09-0026, in terms of its selective effects on neuronal calcium current and its efficacy in reducing infarct size and neurological deficits in a rat model of focal stroke. In the present studies, the effects of NNC 09-0026 on neuronal calcium influx, calcium channel binding, and cardiovascular parameters were determined. Also, phencyclidine, NNC 09-0026, or vehicle were administered i.v. to rats subjected to permanent middle cerebral and common carotid artery occlusions. Infarct volumes and contralateral forepaw and hindlimb neurological deficits were assessed at 24 and 48 h after onset of stroke. NNC 09-0026 exhibited a pharmacological profile suggesting selectivity at neuronal calcium channels. It inhibited potassium-stimulated calcium uptake into rat synaptosomes with an IC50 of 13 microM. Voltage-operated calcium currents measured from cultured rat dorsal root ganglion cells using the patch clamp technique were blocked by 43% at 10 microM (p < 0.05). The compound showed only weak effects on smooth muscle from the guinea pig taenia coli and was relatively inactive at displacing nitrendipine and omega-conotoxin in receptor-binding studies. Single, bolus injections of NNC 09-0026 as high as 10 mg/kg i.v. produced only 12% reduction in heart rate and a 28% decrease in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Adverse effects of atrial fibrillation and syncope induced by calcium-channel blockers in hypertrophic cardiomyopathy.

Calcium-channel blockers are useful for the treatment of hypertrophic cardiomyopathy (HCM), but, their adverse effects, especially, those of diltiazem, have not been of much concern. Forty patients with HCM were treated with calcium-channel blockers such as nifedipine, diltiazem, and verapamil. Atrial fibrillation was induced by diltiazem in two patients and verapamil induced syncope in one patient. The clinical and hemodynamic characteristics of the patients were as follows. All of them had the obstructive type of HCM (HOCM). One of them had a high pressure gradient of the left ventricular outflow tract and the others had earlier onset. In these patients, the left atrial overload seemed to be severe. The vasodilating action of calcium-channel blockers decreases the systemic pressure and in turn, may increase the pressure gradient and the left ventricular end-diastolic pressure. The elevated left ventricular end-diastolic pressure causes the left atrial overload which could be at risk of atrial fibrillation in patients with HCM. Therefore, calcium-channel blockers should be used carefully in peculiar cases of HOCM.

Adult↗
PubMed1987

Calcium channel blocker drugs and diabetic control.

Calcium channel blockers are now widely used and there have been case reports of hyperglycemia with nifedipine. In a double-blind, randomized, crossover study of the effects of 4 weeks of therapy, each with two dihydropyridine calcium channel blocker drugs, nifedipine and nicardipine, glucose tolerance, plasma insulin levels, and hemoglobin A1 were assessed in 20 patients with non-insulin-dependent diabetes (mean age 59 years). There was no significant difference in glucose tolerance on active therapy (AUC: control, 548.3 +/- 24.8; nifedipine, 559.3 +/- 41.0; and nicardipine, 589.3 +/- 40.3). Similarly, despite producing significant hemodynamic effects, these drugs produced no significant effect on plasma insulin and hemoglobin A1 levels. Calcium channel blocker drugs may be useful alternatives to thiazide diuretics and beta-blockers in the treatment of ischemic heart disease and hypertension, especially in patients with diabetes.

Adult↗
PubMed1987

Reconstitution of the purified receptor for calcium channel blockers.

The purified receptor for calcium channel blockers from rabbit skeletal muscle was reconstituted into phospholipid vesicles. The reconstitution did not alter the stoichiometry of the peptide chains. [3H]PN 200-110 bound to one site with apparent KD and Bmax values of 9.8 nM and 980 pmol/mg protein, respectively. The binding was stereospecific. D-cis-diltiazem and (-) desmethoxyverapamil affected allosterically the binding of dihydropyridines. This demonstrates the coinsertion of specific binding sites for the three calcium channel blocker into phospholipid vesicles.

Allosteric Regulation↗
PubMed2003

[The effect of calcium channel blocker on human sperm].

Calcium ion exists extensively in cells as the second messenger, and calcium channel blocker (CCB) is widely used to treat cardiac, skeletal muscular diseases. With the advances in the investigation of human sperm calcium channel, CCB has been proved to affect not only the shape, activation and acrosome reaction, but also the function of human sperm, which may afford a new approach to male contraception.

Calcium Channel Blockers↗
PubMed1990

Calcium-channel blockers and the elderly.

Calcium-channel blockers may well be the drugs of choice for treating angina, hypertension, and supraventricular arrhythmia in the elderly. They are effective, have no serious side effects, and when wisely matched to the patient, are very well tolerated. Most calcium-channel blockers can be administered once or twice daily. A choice of four is available; only verapamil and diltiazem hydrochloride are useful for supraventricular arrhythmia. All four, however, are effective for the treatment of hypertension and angina. Expanding uses of calcium-channel blockers include peripheral vascular disease and migraine. There may be a theoretical advantage in humans from the point of view of the anti-atherosclerosis demonstrated in animals.

Angina Pectoris↗
PubMedDate not supplied

[The relationship between anticonvulsant and anti-anxiety effects of calcium channel blockers].

The effect of calcium channel blockers on the development of convulsive and anxiogenic actions of corasole and caffeine was studied on mice. Verapamil, nifedipine, cinnarizine, and fendilin attenuated corasole-induced convulsions were attenuated by convulsions. Nifedipine also weakened while fendilin increased the course of convulsions induced by caffeine. All calcium antagonists did not change the effects of corasole and caffeine in the dark-light chamber test and the test in an elevated plus maze (anxiogens shortened the time that the mice stayed in the open sections of the maze). It is concluded that there are no relations between the anticonvulsive and anxiolytic effects of calcium antagonists.

Animals↗
PubMed1985

Calcium-channel blockers and systemic hypertension.

Calcium-channel blockers selectively inhibit transmembrane flux of calcium in excitable tissues. Their ability to block calcium-mediated electromechanical coupling in contractile tissue produces peripheral vasodilation and has led to interest in their use for systemic hypertension. A postulated involvement of calcium in the development of the increased vascular tone of hypertension makes these agents appear particularly attractive for use as vasodilators. Clinical trials suggest a potentially important role for the calcium-channel blockers in the treatment of systemic hypertension.

Acute Disease↗
PubMed1993

Modification of tricyclic antidepressant analgesia by calcium channel blockers.

The influence of calcium channel blockers (CCB) on the analgesic activity of tricyclic antidepressants (TCA) was examined using hot plate (thermal) and writhing (chemical) method. Intraperitoneal injections of TCA, imipramine and amitriptyline or CCB viz: verapamil, nifedipine, nicardipine and cinnarizine per se produced analgesia. The Analgesic effect of TCA was further enhanced by prior treatment with CCB. The increase in TCA analgesia could not be ascribed to unitary mechanism but could possibly be mediated by opioid and/or nonopioid systems. These results clearly provide an evidence that a combination treatment of CCB and TCA may permit reduction of the TCA doses while treating chronic pain of organic origin.

Analgesics↗
PubMed1986

Inhibition of leukotriene actions by the calcium channel blocker, nisoldipine.

Nisoldipine, a calcium channel blocker having a highly potent effect on vascular smooth muscle relative to cardiac muscle, was tested to determine its anti-leukotriene properties. Nisoldipine, at concentrations from 1 to 300 ng/ml, significantly attenuated the vasoconstrictor effects of both LTC4 and LTD4 in isolated perfused cat coronary arteries and in isolated Langendorff perfused cat hearts. In isolated perfused coronary arteries, nisoldipine exerted a greater percentage inhibition of LTC4- and LTD4-induced constriction than of the constriction induced by the thromboxane analog, carbocyclic thromboxane A2 (CTA2). In isolated cat lung fragments, higher concentrations of nisoldipine were required to inhibit leukotriene formation (i.e., 10-200 microM). These concentrations of nisoldipine markedly inhibited the formation of the chemotactic leukotriene (LTB4) as well as the peptide leukotrienes (LTC4 and LTD4) stimulated by A-23187. Both types of leukotrienes were inhibited to a comparable degree. Thus, nisoldipine has significant anti-leukotriene actions. At normally employed concentrations, nisoldipine inhibits leukotriene actions on vascular smooth muscle, and at higher concentrations, it inhibits leukotriene formation.

Animals↗
PubMed2001

Potentiation of analgesia and reversal of tolerance to morphine by calcium channel blockers.

Effect of four calcium channel blockers (CCBs) belonging to different chemical classes, alone and in combination with morphine was investigated on two models of pain sensitivity, i.e. formalin and tail flick tests in mice. All the studied CCBs, i.e. diltiazem, flunarizine, nimodipine and verapamil inhibited formalin-induced pain responses; however, with verapamil, though there was a trend towards a reduction of paw-licking response to formalin, it was not found to be statistically significant. In contrast, none of the CCBs affected the tail flick latency at any of the doses studied. Morphine, a mu-receptor agonist exerted a significant analgesic effect in formalin as well in tail flick tests. Pretreatment with all CCBs significantly enhanced the analgesic effect of morphine in both tests of nociception. Further, concomitant administration of one of the CCBs, diltiazem with morphine prevented the development of tolerance to the latter. However, combination of diltiazem with morphine, like morphine alone was found to be ineffective in morphine tolerant animals. Results, thus, show that CCBs produced an analgesic effect of their own in formalin-induced tonic pain and potentiated the analgesic activity of morphine. They also modulated opioid-induced tolerance.

Analgesia↗
PubMed1997

Cost containment for treating hypertension in African Americans: impact of a combined ACE inhibitor-calcium channel blocker.

The use of calcium channel blockers (CCBs) and angiotensin-converting enzyme (ACE) inhibitors has increased dramatically over the last 10 years and now accounts for 60% to 70% of all new antihypertensive prescriptions. Even though these two classes are efficacious, they are costly. Combined ACE inhibitor/CCB therapy (amlodipine-benazepril) was introduced in 1995. An analysis was done to assess the potential financial impact of substituting this agent for patients being treated with on ACE inhibitor/CCB combination. A pharmaceutical profile review of prescriptions during October 1995 was performed on 219 randomly selected patients enrolled in a Medicaid managed care program. Eighty-four profiles were analyzed; 24% of patients were on a combination ACE inhibitor/CCB regimen with an average monthly cost of $135. If the single agent amlodipine-benazepril with an average monthly cost of $45 (all strengths) was substituted, the savings would be considerable: $1080 per patient per year and $1,080,000 annualized for the calculated number of hypertensives on combination therapy in our network of 15,000 patients. Therapeutic substitution is one method of achieving cost containment in managed care. The cost differential between separately prescribed CCBs and ACE inhibitors and amlodipine-benazepril is significant. Compliance also should be enhanced as the patient would need to take only one pill daily. Once a patient has been maintained on a stable dose of a CCB/ACE inhibitor, substitution with amlodipine-benazepril should be considered.

Amlodipine↗
PubMed1985

Increase in rat spinal cord blood flow with the calcium channel blocker, nimodipine.

Nimodipine, a calcium channel blocker, is known to increase cerebral blood flow. In the present study, the authors investigated the effect of nimodipine on spinal cord blood flow in normal rats. Cardiovascular parameters, including mean systemic arterial blood pressure, cardiac output, and heart rate, were recorded during infusion of nimodipine in a dose-response fashion. The experiment was a randomized blind study in which four groups of five rats received different doses of nimodipine (0.001, 0.01, 0.05, and 0.10 mg/kg) intravenously over 30 minutes, and a control group of five rats received only the diluent. The hydrogen clearance and thermodilution techniques were used to measure spinal cord blood flow and cardiac output, respectively. The 0.05-mg/kg dose of nimodipine caused the largest increase in spinal cord blood flow, with a 40% increase over the preinfusion level, although there was a 25% reduction in mean arterial pressure. The 0.10-mg/kg dose did not increase spinal cord blood flow more than the 0.05-mg/kg dose, most likely due to the concomitant 37% reduction in mean arterial pressure. Cardiac output was significantly increased by the 0.05- and 0.10-mg/kg doses secondary to the drop in total peripheral resistance. The increase in spinal cord blood flow produced by nimodipine lasted approximately 20 minutes after the termination of the infusion. Thus, nimodipine at a dose of 0.05 mg/kg markedly increased blood flow in the normal spinal cord even though there were major changes in mean systemic arterial pressure and cardiac output. Further research is required to determine whether this drug might be beneficial in treating ischemic states of the spinal cord, such as posttraumatic ischemia.

Analysis of Variance↗