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PubMed1992

Effects of orally administered beta-adrenergic blockers and calcium-channel blockers on the intraocular pressure of patients with treated hypertension.

Little attention has been paid to the influence of orally administered antihypertensive drugs on intraocular pressure (IOP). Therefore, we evaluated the effects of oral medications on the IOPs and visual fields of 70 patients with systemic hypertension who had no ocular symptoms and had not visited any eye hospital. In patients with systemic hypertension treated with medication, the IOP value (mean, 18.3 +/- 4.2 mmHg; age range, 63.3 +/- 11.6 years) was significantly higher than in a control group with a similar age range who were not receiving oral medication (mean, 13.7 +/- 2.0 mmHg; age range, 62.5 +/- 7.8 years). In the group in which hypertension was controlled by medication, the IOPs were lower when orally administered beta-adrenergic blockers were given than in those patients with uncontrolled hypertension. In the group to whom calcium-channel blockers were administered orally, the IOPs were not lower. Angiotensin-converting enzyme inhibitors made the visual fields worse. This study suggests a modulating influence of orally administered drugs on the IOP and visual fields, which may be affected by whether or not the patient's blood pressure is controlled.

Administration, Oral↗
PubMed1987

Identification of the multidrug resistance-related membrane glycoprotein as an acceptor for calcium channel blockers.

A radioactive photoactive dihydropyridine calcium channel blocker, [3H]azidopine, was used to photoaffinity label plasma membranes of multidrug-resistant Chinese hamster lung cells selected for resistance to vincristine (DC-3F/VCRd-5L) or actinomycin D (DC-3F/ADX). Sodium dodecyl sulfate-polyacrylamide gel electrophoretic fluorograms revealed the presence of an intensely radiolabeled 150-180-kDa doublet in the membranes from drug-resistant but not from the drug-sensitive parental (DC-3F) cells. A similar radiolabeled doublet was barely detected in a drug-sensitive partial revertant (DC-3F/ADX-U) cell line. The 150-180-kDa doublet exhibited a specific half-maximal saturable photolabeling at 1.07 X 10(-7) M [3H]azidopine. The dihydropyridine binding specificity was established by competitive blocking of specific photolabeling with nonradioactive azidopine as well as with nonphotoactive calcium channel blockers nimodipine, nitrendipine, and nifedipine. In addition, [3H]azidopine photolabeling was blocked by verapamil and diltiazem but was stimulated by excess prenylamine and bepridil suggesting a cross-specificity for up to four different classes of calcium channel blockers. The 150-180-kDa calcium channel blocker acceptor co-electrophoresed exactly with the 150-180-kDa surface membrane glycoprotein (gp150-180 or P-glycoprotein) Vinca alkaloid acceptor from multidrug-resistant cells and was immunoprecipitated by polyclonal antibody recognizing gp150-180. [3H]Azidopine photolabeling of the 150-180-kDa component in the presence of excess vinblastine was reduced over 90%, confirming the identity or close relationship of the calcium channel blocker acceptor and the gp150-180 Vinca alkaloid acceptor. The [3H]azidopine photolabeling of gp150-180 also was reduced by excess actinomycin D, adriamycin, or colchicine, demonstrating a broad gp150-180 drug recognition capacity. The ability of gp150-180 to recognize multiple natural product cytotoxic drugs as well as calcium channel blockers suggests a direct function for gp150-180 in the multidrug resistance phenomenon and a role in the circumvention of that resistance by calcium channel blockers.

Animals↗
PubMed1999

Synthesis and biological activity of substituted bis-(4-hydroxyphenyl)methanes as N-type calcium channel blockers.

Voltage activated calcium channel (VACC) blockers have been demonstrated to have utility in the treatment of stroke and pain. A series of aminomethyl substituted phenol derivatives has been identified with good functional activity and selectivity for N-type VACC's over sodium and potassium channels. The methods of synthesis and preliminary pharmacology are discussed herein.

Calcium Channel Blockers↗
PubMed1990

Gingival hyperplasia in rats induced by oxodipine--a calcium channel blocker.

Oxodipine, a new calcium channel blocker, induced gingival hyperplasia in rats. This is the first time that a calcium channel blocker has been documented as resulting in gingival hyperplasia in rats. In contrast to diphenylhydantoin, the hyperplastic changes induced by oxodipine were not precipitated by any prior irritation. The histology consisted of purely fibroblastic proliferation without infiltrate of inflammatory cells.

Animals↗
PubMed1996

Age-related differential susceptibility to calcium channel blocker and low calcium medium in rat detrusor muscle: response to field stimulation.

The influences of aging on the response of urinary bladder detrusor smooth muscle in response to neurogenic stimulation (electric field stimulation) were investigated in rats aged 3-4 months (young) and 18-20 months (old). In addition, age-associated changes in calcium homeostasis were evaluated by comparing the basal intracellular free calcium concentration ([Ca2+]i), the change of [Ca2+]i in response to field stimulation, the contractile response at different extracellular calcium concentrations (Ca2+ = 1.8, 0.6, and 0 mM), and the sensitivity to the L-type calcium channel blocker. In both groups, the frequency-response curve in response to field stimulation (1-32 Hz) was similar. The contractile response to field stimulation was biphasic (phasic and tonic). The phasic/tonic ratio at different frequencies was similar between the two groups. The contractile responses were equally inhibited by atropine (1 microM) and preincubation with alpha, beta-methylene ATP (50 microM). Tetrodotoxin (1 microM) virtually abolished the responses to field stimulation in both groups. The biphasic components showed different sensitivities to diltiazem and low calcium. The tonic component was more readily inhibited by diltiazem, whereas the phasic component was more sensitive to low calcium medium. In general, the response to lower frequency stimulations was more sensitive to both diltiazem and low calcium. The aged group was more sensitive to the inhibitory effects of both low calcium and diltiazem. In Ca2(+)-free medium, the contractile response to higher frequency (e.g., 32 Hz) was temporarily preserved in most of the preparations. This response disappeared after repeated stimulation. The magnitude of this Ca2(+)-free response to 32 Hz stimulation was significantly lower in the aged group than in the young group (18.1 +/- 1.4 vs.29.1 +/- 3.2% of the control response in normal Tyrode medium, P < 0.05). The basal [Ca2+]i levels were similar in the two groups (young: 131 +/- 12 nM, n = 5; old: 118 +/- 10 nM, n = 4, P > 0.05). The magnitude and time course of the [Ca2+]i response to field stimulation were also similar in the two groups. It is concluded that aging seems to have little effect on the neuromuscular activities of rat urinary bladder. However, the calcium homeostasis may be altered as evidenced by the increased sensitivity to diltiazem and low extracellular calcium.

Aging↗
PubMed1990

Effects of calcium channel blockers on the coronary circulation.

Calcium channel blockers are among the most effective antiischemic therapies currently available. These agents afford a reduction in vascular smooth muscle tone by interrupting the excitation-contraction coupling process dependent on calcium transport. The efficacy of calcium channel blockers in patients with myocardial ischemia is probably due in large part to their effects on coronary circulation. In experimental models of coronary occlusion, these agents have been demonstrated to increase coronary vasodilation and coronary blood flow. Recruitment of coronary vasodilator reserve by nifedipine has been demonstrated indirectly via enhancement of left ventricular function in a canine model. Additionally, calcium channel blockers have been shown to modify the reactive hyperemic response usually seen after coronary artery occlusion. These changes in coronary resistance vessels, which normally regulate myocardial blood flow in response to metabolic requirements, have important clinical implications. Larger collateral vessels are also affected by calcium channel blockers, although the results observed in experimental models are not as clear cut. Although techniques for measuring coronary blood flow in humans are more limited, considerable data have accumulated on the effects of calcium channel blockers in humans. Assessments of coronary vasodilation using quantitative angiography have produced variable results. However, improved myocardial perfusion, as measured by thallium-201 scintigraphy after administration of nifedipine, and beneficial effects on coronary blood flow and coronary vascular resistance as assessed using the precordial xenon-133 washout technique before and after sublingual administration of nifedipine have been observed. Overall, such studies have not only shown the clinical usefulness of calcium channel blockers, but have broadened our understanding about the complex interplay of their mechanisms of action.

Animals↗
PubMed1985

Potentiation of pancuronium induced neuromuscular blockade by calcium channel blockers in vitro.

The calcium channel blockers verapamil, methoxyverapamil, diltiazem, and nisoldipine have been tested for interactions with the nondepolarizing muscle relaxant pancuronium bromide by using the indirectly stimulated in vitro preparation of the rat hemidiaphragm. Dose response curves of each calcium channel blocker, pancuronium bromide, and combinations of both were determined. Each of the four calcium channel blocking drugs showed agonistic interaction in potentiating pancuronium induced neuromuscular blockade.

Animals↗
PubMed1988

Targets for calcium channel blockers in mammalian skeletal muscle and their respective functions in excitation-contraction coupling.

The L-type Ca2+ channel is blocked by 1,4-dihydropyridines (DHP), by phenylalkylamines, by diphenylbutylpiperidines or by benzolactams. We first show with mouse muscle cells in culture that all these L-type Ca2+ channel blockers block contraction. However, voltage-clamp analysis associated to contraction measurements also clearly show that Ca2+ influx through L-type Ca2+ channels is not required for contraction. Therefore, there is a need for a voltage-sensor which would be responsible for the excitation-contraction (E-C) coupling. We are showing here that the voltage-sensor involved in E-C coupling and the L-type Ca2+ channel have a similar pharmacology. Some of the blockers used are more active on the voltage sensor, others on the L-type Ca2+ channel.

Action Potentials↗
PubMed2001

[Calcium channel blockers and tissue remodeling in hypertension].

Calcium channel blockers and tissue remodeling in hypertension. Calcium channel blockers (calcium antagonists) are members of various chemical groups. They share the ability to inhibit calcium entry into depolarized smooth muscle cells. This results in reduction of vascular tone and vasodilatation. This action is the rationale for their use in the management of hypertension. The purpose of this paper is to summarize recent experiments aiming to test the hypothesis that the long term effects of calcium channel blockers are not related to reduction of hemodynamic overload.

Blood Pressure↗
PubMed1991

Calcium channel blockers and gingival overgrowth.

Calcium channel blockers are widely used in medical practice for the management of cardiovascular disorders. Of concern to the dental practitioner is the effect of these drugs on the gingival tissues. All classes of calcium channel blockers have been implicated in causing gingival overgrowth. This review considers the prevalence, clinical features, histopathology, pathogenesis and management of this unwanted side-effect.

Calcium Channel Blockers↗
PubMed2006

Synthesis and SAR studies of a novel series of T-type calcium channel blockers.

For the novel, potent, and selective T-type Ca2+ channel blockers, a series of sulfonamido-containing 3,4-dihydroquinazoline derivatives were prepared and evaluated for their blocking actions on T- and N-type Ca2+ channels. Among them, 9c (KYS05064, IC50 = 0.96 +/- 0.22 microM) was found to be as potent as Mibefradil and also showed the highest selectivity for T-type Ca2+ channel with no effect on N-type Ca2+ channel.

Calcium Channel Blockers↗
PubMed1997

Evidence for antiaggressive property of some calcium channel blockers.

The effect of calcium channel blockers on foot shock induced (aggression (FSA) were studied in mice. Verapamil, (10, 20 and 40 mg kg-1 i.p.) diltiazem (20 and 40 mg kg-1 i.p.) and nifedipine (25 and 50 mg kg-1 i.p.) significantly reduced fighting episodes. Diltiazem and nifedipine blocked the amphetamine induced facilitation of FSA, while verapamil blocked both amphetamine as well as physostigmine induced facilitation of FSA. These findings suggest that calcium channel blockers possess antiaggressive activity, which may be attributed to decrease in central dopaminergic and/or cholinergic mechanism.

Aggression↗
PubMed1997

The voltage-dependent non-selective cation channel sensitive to the L-type calcium channel blocker efonidipine regulates Ca2+ influx in brain vascular smooth muscle cells.

The present study investigated the ion channel responsible Ca2+ influx in cultured smooth muscle cells from bovine brain arteries by monitoring Ba2+ currents. Voltage pulses at a range between -100 and +100 mV from a holding potential of 0 mV induced currents and the current/voltage (I/V) relations were linear with a reversal potential of +/- 0 mV. The currents were increased by elevating extracellular Ba2+ concentrations, suggesting that the voltage-sensitive non-selective cation channel, which favors Ca2+ influx, is expressed in brain vascular smooth muscle cells. In contrast, when voltage pulses at a range between -50 to +50 mV from a holding potential of -80 mV were applied to carotid smooth muscle cells, inward currents were evoked by depolarization to > or = -10 mV and the I/V relations were bell-shaped, typical for the L-type calcium channels. The dihydropyridine derivatives, efonidipine and nicardipine, inhibited the L-type Ca2+ channel-operated currents in carotid smooth muscles, and further efonidipine had an inhibitory effect also on non-selective cation currents in brain vascular smooth muscle cells. These results suggest that the voltage-dependent non-selective cation channel expressed in brain vascular smooth muscle cells is sensitive to a kind of the dihydropyridine derivatives and regulates Ca2+ influx.

Animals↗
PubMed1993

Lactotrope subtypes are differentially responsive to calcium channel blockers.

Pituitary cultures from adult rats contain two subtypes of prolactin (PRL) cells, small-plaque (SP) and large-plaque (LP) lactotropes, which exhibit distinct rates of basal secretion and thereby form PRL plaques of different sizes in reverse hemolytic plaque assay experiments. In the present study, we have used plaque assays to examine the effects of omega-conotoxin (omega-CgTx) and nifedipine, which block Ca2+ entry through high voltage-activated (HVA) channels in the plasma membrane, on basal PRL secretion from single male rat lactotropes. We found that omega-CgTx, like nifedipine, is a potent inhibitor of PRL secretion. In addition, we observed that both drugs decrease the number of cells forming large PRL plaques, while promoting a comparable increase in the abundance of small plaque formers. The results indicate that blocking the HVA Ca channels preferentially suppresses PRL release from LP lactotropes, and suggest that the inhibited PRL secretors tend to behave functionally as SP lactotropes.

Animals↗
PubMed2004

[Effects of calcium channel blockers in atherosclerosis and cardiovascular event and oxidative vascular damage].

Ca antagonists are relevant therapeutic tool for patients with hypertension. The effects of Ca antagonists against oxidative vascular damage and followed atherosclerosis were elucidated in various experimental model accompanied with the vasodilatative effects of Ca antagonists by blocking the L-type Ca channel. The beneficial effects of Ca antagonists in cardiovascular disease have been demonstrated in several clinical trials, as we demonstrated the beneficial effect of Ca antagonist in the incidence of cardiovascular event in Japanese patients with coronary disease. In patient with diabetes mellitus, the cardiovascular disease was also caused by the mechanism involved with the increase in oxidative stress in blood vessels and related factors such as advanced glycation endproducts, protein kinase C and insulin resistance. The beneficial effects of Ca antagonists in cardiovascular disease in patients with diabetes mellitus have been demonstrated in several clinical trials, may be dependent on the effect of Ca antagonist against the oxidative stress in the setting of hyperglycemia.

Animals↗
PubMed1992

Depression of calcium channel blocker binding to rat brain membranes by halothane.

The present study evaluates the action of volatile anesthetics on the voltage-dependent Ca2+ channels in isolated rat brain membranes, measured as changes in binding of the Ca2+ channel blocker [3H]isradipine to these membranes. Equilibrium binding studies with increasing concentrations of [3H]isradipine (0.01-1 nM) in the presence of halothane (1.9%), isoflurane (2.3%), and enflurane (4.8%) at 25 degrees C were performed. Only halothane produced a significant depression in the specific binding of isradipine to the brain membranes at 0.5 and 1.0 nM [3H]isradipine (P = 0.028 and 0.018, respectively). Isoflurane and enflurane had such inconsistent effects that the data were inconclusive. Halothane produced a significant dose-dependent inhibition of binding, the maximum inhibition being 44% (P less than 0.005). Nonlinear regression analysis fit of the binding data indicates halothane produced a 48% decrease (P less than 0.05) in the maximal number of binding sites (Bmax) with no effect on the dissociation constant (Kd). As voltage-dependent Ca2+ channels are important in mediating neurotransmission, the marked decrease in channel number (Bmax) associated with halothane exposure suggests that this phenomenon might be related to the mechanism of general anesthesia.

Animals↗