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PubMed1989

Dihydropyridine inhibition of single calcium channels and contraction in rabbit mesenteric artery depends on voltage.

1. The effects of membrane potential and the dihydropyridine calcium channel inhibitor, nisoldipine, on single calcium channels in the presence of Bay K 8644 and contraction in the presence and absence of Bay K 8644 were examined in the rabbit mesenteric artery. 2. Membrane depolarization decreased the peak average single calcium channel current that could be elicited by a test pulse to 0 mV. The steady-state inactivation relationship could be described by the Boltzmann equation, [1 + exp[Vm-V0.5)/k)]-1, with a steepness factor, k, of 7.1 mV. Nisoldipine shifted the steady-state inactivation curve to more negative potentials by increasing the fraction of test pulses without openings. 3. The degree of nisoldipine inhibition of average single calcium channel currents increased with membrane depolarization. Depolarization of the holding potential from -100 to -55 mV decreased the concentration of nisoldipine needed for 50% inhibition (Kapp) from 12.1 to 1.9 nM in the presence of 1 microM-Bay K 8644. 4. Membrane depolarization by external potassium (K+) of the intact artery in the presence of nisoldipine decreased contractions evoked by depolarizing test pulses. The relationship between membrane potential and contraction could be empirically described by the Boltzmann equation, with a steepness factor, k, of 7.1 mV. Increasing the nisoldipine concentration from 0.25 to 2.0 nM shifted the mid-point of this relationship from -20.5 to -33.0 mV, without affecting the steepness factor. 5. Nisoldipine inhibition of contraction increased with membrane depolarization. Membrane depolarization from -68.6 to -30.0 mV decreased the Kapp of nisoldipine for contractions from 3.02 to 0.69 nM. Bay K 8644 (1 microM) elevated Kapp about 9.3-fold at 5 mM-K+. In the presence of Bay K 8644, membrane depolarization from -68.6 to -30.0 mV reduced Kapp from 28.4 to 4.0 nM. 6. In the presence of nisoldipine, the effect of membrane depolarization on the time course of development of inhibition was examined. In 3 nM-nisoldipine, after membrane depolarization with 20 mM-K+, the time course of development of inhibition of force could be described by a single exponential with a time constant of 16.5 min. Membrane depolarization to a more positive potential accelerated the development of inhibition. 7. The results were interpreted by a model in which nisoldipine binds with higher affinity to the inactivated state than to the resting state of calcium channels in the mesenteric artery. The approach presented here can be used to estimate the properties of steady-state calcium channel inactivation and dihydropyridine interactions in smooth muscle cells in the intact artery under physiological conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

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

PubMed1987

Induction of seizures in mice by intracerebroventricular administration of the calcium channel agonist BAY k 8644.

The calcium channel agonist BAY k 8644 was used to investigate the role of the calcium ion (Ca2+) in epileptogenesis. Intracerebroventricular administration of the compound induced murine seizures that were reversed by calcium channel inhibitors (CCIs) but not by anticonvulsants such as carbamazepine, pentobarbital, and diazepam. The seizures were exacerbated by phenytoin and valproic acid. Chronic administration of CCI's, previously shown to produce down-regulation of the binding of the CCI [3H]nitrendipine, resulted in augmentation of BAY k 8644-induced seizures.

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

PubMed2002

Clinical and electrophysiologic effects of calcium channel blockers in patients receiving ibutilide.

BACKGROUND: Ibutilide is indicated for the acute termination of atrial fibrillation and atrial flutter. Recent work concludes that ibutilide activates a late inward sodium current that is blocked by nifedipine. Because calcium channel blockers are commonly used in patients with atrial fibrillation, it is important to exclude an antagonistic effect on ibutilide in the clinical setting. METHODS: We performed a retrospective electrocardiographic (ECG) review of patients enrolled in 3 clinical trials of ibutilide (2 atrial fibrillation conversion protocols and 1 ventricular tachycardia suppression protocol) to determine clinical efficacy and ECG effects of ibutilide in patients receiving and not receiving calcium channel blockers. Calcium channel blockers were administered as clinically indicated. A meta-analysis of the effects of calcium channel blockers on the conversion efficacy of atrial fibrillation and atrial flutter by ibutilide was also performed for studies in the literature. RESULTS: One hundred thirty patients were included in the ECG analysis (106 from atrial fibrillation protocols and 24 from the ventricular tachycardia protocol). Sixty-eight of the 130 patients were taking calcium channel blockers at the time of ibutilide administration. There were no differences in the QT or QTc intervals, conversion rate for atrial fibrillation or atrial flutter, or suppression of ventricular tachycardia between patients taking and not taking calcium channel blockers. In the meta-analysis of 4 studies, there was no difference in the conversion rates between patients taking (52%, n = 221) and not taking (45%, n = 402) calcium channel blockers (P =.09). CONCLUSIONS: In the clinical setting, the concomitant use of calcium channel blockers does not alter the ECG effects or efficacy of ibutilide for the treatment of atrial or ventricular arrhythmias.

Aged↗

PubMed1993

Are calcium-channel blockers effective in the treatment of tardive dyskinesia?

OBJECTIVE: To review the data describing the use of calcium-channel blockers in the treatment of tardive dyskinesia (TD). DATA SOURCES: A MEDLINE search of the English-language literature and a bibliographic review of pertinent articles examining the use of calcium-channel blockers in the treatment of TD were performed. Medical Subject Headings (MESH) terms used were calcium-channel blockers, tardive dyskinesia, nifedipine, verapamil, and diltiazem. STUDY SELECTION AND DATA EXTRACTION: Relevant case reports, open trials, and controlled studies reporting on the efficacy of calcium-channel blockers for treating TD are reviewed. Appropriate conclusions are drawn from the data and guidelines are suggested for the practitioner. DATA SYNTHESIS: Studies addressing the efficacy of calcium-channel blockers in the palliative treatment of TD have yielded mixed results. Positive findings have been reported for nifedipine, verapamil, and diltiazem; nifedipine may be the most efficacious treatment and diltiazem the least. It appears that patients with TD who can tolerate higher doses of calcium-channel blockers may respond more favorably to treatment. Patient characteristics that may help determine a better response to treatment with calcium-channel blockers include advanced age and more-severe TD. CONCLUSIONS: To determine the efficacy of calcium-channel blockers in the treatment of TD, additional data are needed from double-blind, placebo-controlled studies with larger sample sizes and longer durations of treatment. Until these data are available, calcium-channel blockers should be considered potentially useful therapy for the heretofore unresponsive TD.

Aged↗

PubMed1986

[Central cardiovascular effects of a calcium inhibitor, nifedipine, and a calcium channel activator, Bay k 8644, in the anesthetized rat].

The antihypertensive effect of calcium channel inhibitors (CCI) results mainly from their direct action on the vascular smooth muscle. However CCI may pass through the blood-brain barrier and may modulate central mechanisms involving calcium channels. Normotensive (WKY) and spontaneously hypertensive (SHR) (Okamoto) rats weighing 300 g were anaesthetized with pentobarbital (50 mg/kg i.p.) and ventilated. Mean arterial pressure (MAP) was measured from a catheter inserted into the femoral artery. Heart rate (HR) was electronically integrated. Vehicle (ethanol 95%), nifedipine and Bay k 8644 (Bay) were injected under a 1.5 microliter volume into the lateral ventricle of the brain (i.c.v.). Vehicle alone did not change significantly MAP or HR. The calcium-channel inhibitor nifedipine and the calcium-channel activator Bay had opposite effects, when i.c.v. injected: hypotension with bradycardia and hypertension without tachycardia, respectively. These effects are dose-dependent (5-50 micrograms/kg). They are of central origin since they are suppressed by ganglionic blockade by hexamethonium(100 mg/kg i.c.). Bilateral vagotomy suppressed the i.c.v.-nifedipine induced bradycardia. Previously i.c.v. administered nifedipine (5 micrograms/kg) suppressed the pressor response to Bay (5 micrograms/kg i.c.v.). Changes in MAP and HR are significantly more marked in SHR than in WKY. These results indicate that a calcium-channel inhibitor and a calcium-channel activator can modulate in opposite fashion central calcium-dependent mechanisms involved in blood pressure control.

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

PubMed1999

Calcium channel blockers and mortality in elderly patients with myocardial infarction.

BACKGROUND: Although calcium channel blockers are a useful therapy in relieving angina, lowering blood pressure, and slowing conduction of atrial fibrillation, growing evidence has cast doubt on their safety in patients with coronary disease. OBJECTIVE: To examine the association between calcium channel blocker therapy at hospital discharge and mortality in a population-based sample of elderly patients hospitalized with acute myocardial infarction. DESIGN: Retrospective cohort study using data from medical charts and administrative files. SETTING: All acute care hospitals in 46 states. PATIENTS: All Medicare patients with a principal diagnosis of acute myocardial infarction consecutively discharged from the hospital alive during 8-month periods between 1994 and 1995 (N = 141,041). MAIN OUTCOME MEASURE: Mortality at 30 days and 1 year. RESULTS: Calcium channel blockers were widely prescribed at hospital discharge to elderly patients with myocardial infarction between 1994 and 1995 (n = 51,921), the most commonly prescribed being diltiazem (n = 21,175), nifedipine (n = 12,670), amlodipine (n = 11,683), and verapamil (n = 3639). After adjusting for illness severity and concomitant medication use, patients who were prescribed calcium channel blockers at hospital discharge did not have increased risk for 30-day or 1-year mortality, with the exception of the few (n = 116) treated with bepridil. Bepridil differs from other calcium channel blockers because of its tendency to prolong repolarization, and its association with proarrhythmic effects in elderly patients. CONCLUSION: We did not identify a mortality risk in a large consecutive sample of elderly patients with myocardial infarction, which supports the need for additional prospective trials examining calcium channel blocker therapy for ischemic heart disease.

Aged↗

PubMed1999

N-type calcium channels and their regulation by GABAB receptors in axons of neonatal rat optic nerve.

Axons of neonatal rat optic nerves exhibit fast calcium transients in response to brief action potential stimulation. In response to one to four closely spaced action potentials, evoked calcium transients showed a fast-rising phase followed by a decay with a time constant of approximately 2-3 sec. By selective staining of axons or glial cells with calcium dyes, it was shown that the evoked calcium transient originated from axons. The calcium transient was caused by influx because it was eliminated when bath calcium was removed. Pharmacological profile studies with calcium channel subtype-specific peptides suggested that 58% of the evoked calcium influx was accounted for by N-type calcium channels, whereas L- and P/Q-type calcium channels had little, if any, contribution. The identity of the residual calcium influx remains unclear. GABA application caused a dramatic reduction of the amplitude of the action potential and the associated calcium influx. When GABAA receptors were blocked by bicuculline, the inhibitory effect of GABA on the action potential was eliminated, whereas that on the calcium influx was not, indicating involvement of GABAB receptors. Indeed, the calcium influx was inhibited by the GABAB receptor agonist baclofen. This baclofen effect was occluded by a previous block of N-type calcium channels and was unaffected by the broad-spectrum K+ channel blocker 4-AP. We conclude that neonatal rat optic nerve axons express N-type calcium channels, which are subjected to regulation by G-protein-coupled GABAB receptors. We suggest that receptor-mediated inhibition of axonal calcium channels plays a protective role in neonatal anoxic and/or ischemic injury.

Action Potentials↗

PubMedDate not supplied

Expression of c-FOS in the brain after activation of L-type calcium channels.

In rodents, administration of the L-type calcium channel activators, +/-Bay K 8644 and FPL 64176, causes an unusual neurobehavioral syndrome that includes dystonia and self-injurious biting. To determine the regional influence of these drugs in the brain, the induction of c-FOS was mapped after administration of these drugs to mice. In situ hybridization with an antisense riboprobe directed to c-FOS mRNA revealed widespread induction, with the highest levels in the striatum, cortex, hippocampus, locus coeruleus, and cerebellum. The induction of c-FOS mRNA was dose dependent, reached maximal expression approximately 60 min after drug treatment, and could be blocked by pretreatment with the L-type calcium channel antagonist, nifedipine. Immunohistochemical stains with an antibody directed to c-FOS protein revealed a pattern of induction similar to that obtained with in situ hybridization in most brain regions. These results demonstrate a very heterogeneous influence of L-type calcium channel activation in different brain regions, despite the nearly universal expression of these channels implied by more classical anatomical methods.

Age Factors↗

PubMed1993

The effect of polyamines on voltage-activated calcium channels in mouse neuroblastoma cells.

1. Putrescine has been implicated in modulating cytoplasmic calcium concentration and is correlated with selective neuronal vulnerability in cerebral ischaemia. In order to determine whether putrescine modulates voltage-activated calcium channels, whole-cell and single channel patch clamp experiments were performed with N1E-115 mouse neuroblastoma cells. 2. L-type calcium channel currents showed a 34 +/- 21% increase (n = 6 cells) during external application of 1 mM putrescine. There was no change in the kinetics of the current and no shift in the current-voltage relationship along the voltage axis. 3. T-type calcium channel currents were not affected by 1 mM putrescine. 4. The effect of putrescine on single L-type calcium channels was studied using the cell-attached configuration of the patch clamp technique. Putrescine (5 mM) applied to the bathing solution, but not present in the pipette, caused an increase in open time of the single channel current without changing the conductance of the channel. In 345 depolarizing steps compiled from three cells, the number of channel openings longer than 3 ms increased from six to seventy-six, and the number of channel openings longer than 9 ms increased from zero to twenty-seven. This single channel study supports the hypothesis that putrescine acts on the L-type channel from the inside of the cell. 5. External application of 1 mM spermine and 1 mM spermidine had no effect on T- and L-type calcium channels. Thus, the effect of putrescine is probably not mediated by the higher polyamines. 6. In order to test whether the effect of putrescine is mediated by a second messenger, specific protein kinase C and cyclic AMP-dependent protein kinase inhibitors, staurosporine and KT5720, respectively, were applied prior to putrescine. When cells were preconditioned with 200 nM staurosporine, the increase of the L-type calcium current by 1 mM putrescine was inhibited. By contrast, 200 nM KT5720 did not inhibit the putrescine effect. Therefore, the increase of L-type channel currents by putrescine may be mediated by protein kinase C but not the cyclic AMP-dependent protein kinase. 7. The putrescine-induced enhancement of the L-type calcium channel activity may play an important role in calcium-induced neurotoxicity.

Alkaloids↗

PubMed1993

Calcium channel current in cultured rat mesangial cells.

The presence of voltage-dependent calcium channels has been suggested in mesangial cells by using calcium-sensitive fluorescent probes. However, direct electrophysiological evidence for voltage-dependent calcium channels has not yet been presented. In this study voltage-dependent calcium channels were studied in cultured rat mesangial cells. Whole-cell patch-clamp experiments were done with 50 mM Ba2+ as a charge carrier. Step depolarizing pulses from a holding potential of -50 mV produced an inward barium current at potentials more positive than -10 mV, and a peak current (10-45 pA) was obtained at a membrane potential of approximately +30 mV. The inward current was augmented by 100 nM Bay K 8644, attenuated by 1 microM nifedipine, and abolished by 50 microM Cd2+. These results indicate that the inward current is a barium current flowing through L-type calcium channels. This may be the first study that demonstrates the presence of L-type calcium channels in mesangial cells.

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

PubMed1999

Regulation of neuronal voltage-gated calcium channels by ethanol.

Voltage-gated calcium channels are key regulators of neuronal excitability. Several studies indicate that intoxicating concentrations of ethanol inhibit L-type, N-type and possibly T-type channels. The effects of ethanol on other channel subtypes are not yet clear. Chronic exposure to ethanol is associated with increases in functional L-type channels and this may contribute to signs of ethanol withdrawal. Preclinical studies in animals suggest that L-type calcium channel antagonists decrease ethanol consumption and signs of alcohol withdrawal. Although L-type channel antagonists do not appear to alter the performance impairing or psychological effects of acute ethanol administration, clinical trials will be needed to determine if L-type channel antagonists reduce ethanol consumption in humans.

Calcium Channels↗

PubMed1994

Interactions between diltiazem and ethanol: differences from those seen with dihydropyridine calcium channel antagonists.

It has previously been shown that dihydropyridine calcium channel antagonists prevent the ethanol withdrawal syndrome and potentiate the acute effects of ethanol and other central depressant drugs. We now report that, in contrast, the benzothiazepine calcium channel antagonist, diltiazem, gave no protection against the behavioural hyperexcitability seen during ethanol withdrawal, when given either acutely, on withdrawal, or chronically, during the ethanol treatment. A significant increase in convulsive behaviour on handling was seen during the withdrawal period when diltiazem was given on cessation of a mild chronic ethanol treatment schedule. Diltiazem decreased the acute general anaesthetic effects of ethanol, and did not appear to potentiate the ataxic action of ethanol. Centrally administered diltiazem did not enhance the hypothermic action of ethanol, but this effect was significantly increased by diltiazem when the calcium channel antagonist was given peripherally. When given alone by the intraperitoneal route, diltiazem decreased spontaneous locomotor activity and lowered body temperature. When the intracerebral route was used for administration of diltiazem, a significantly decrease in body temperature was seen when this compound was given alone, accompanied by a brief hyperexcitability. The interactions between ethanol and diltiazem therefore appear to differ from those seen with other calcium channel antagonists.

Anesthesia, General↗

PubMed1993

Differential phosphorylation of two size forms of the neuronal class C L-type calcium channel alpha 1 subunit.

L-type calcium channels mediate long-lasting calcium currents which are modulated by protein phosphorylation. Using site-directed anti-peptide antibodies, we show that the alpha 1 subunit of the neuronal class C L-type calcium channel from rat brain exists in two size forms. The longer form, LC2, with an apparent molecular mass of 210-235 kDa was phosphorylated in vitro by cAMP-dependent protein kinase (cA-PK), but the shorter form, LC1, with an apparent molecular mass of 190-195 kDa was not a substrate for cA-PK. In contrast, LC1 and LC2 are both substrates for protein kinase C (PKC), calcium- and calmodulin-dependent protein kinase II, and cGMP-dependent protein kinase (cG-PK). The site-directed anti-peptide antibody CNC2 was produced against the COOH-terminal end of the class C L-type alpha 1 subunit as predicted by molecular cloning and sequencing of cDNA. CNC2 recognized LC2 but not LC1 by immunoblotting and immunoprecipitated only LC2 phosphorylated by either cA-PK or PKC. These results indicate that LC1 is truncated at its COOH-terminal end with respect to LC2 and that cA-PK preferentially phosphorylates sites in the COOH-terminal region of the alpha 1 subunit that are present in LC2 but not LC1. The selectivity of cA-PK for phosphorylation of the COOH-terminal region of LC2 suggests that the channel activities of the two alpha 1 subunit size forms may be differentially regulated by neurotransmitters and hormones which act through cAMP-dependent mechanisms, while both alpha 1 subunit isoforms may be modulated by PKC, cG-PK, and calcium- and calmodulin-dependent protein kinase II.

Amino Acid Sequence↗

PubMed1998

Contact-dependent regulation of N-type calcium channel subunits during synaptogenesis.

The developmental regulation of the N-type calcium channel during synaptogenesis was studied using cultured rat hippocampal neurons to elucidate the roles of extrinsic versus intrinsic cues in the expression and distribution of this channel. Prior to synapse formation, alpha1B and beta3 subunits of the N-type calcium channel were distributed diffusely throughout neurites, growth cones, and somata. As synaptogenesis proceeded, the subunit distributions became punctate and colocalized with the synaptic vesicle protein synaptotagmin. Isolated neurons were also examined to test for the requirement of extrinsic cues that control N-type calcium channel expression and distribution. These neurons expressed N-type calcium channel subunits, but their distributions remained diffuse. Functional omega-conotoxin GVIA-sensitive channels were expressed in isolated neurons, although the distribution of alpha1B subunits was diffuse. The distribution of the alpha1B subunit and synaptotagmin only became punctate when neuron-neuron contact was allowed. Thus, the expression of functional N-type calcium channels is the result of an intrinsic program while extrinsic regulatory cues mediated by neuron-neuron contact are required to control their distribution during synaptogenesis.

Animals↗

PubMed1988

Gating and permeation properties of two types of calcium channels in neuroblastoma cells.

The gating and permeation properties of two types of calcium channels were studied in the neuroblastoma cell line N1E-115. Calcium channel currents as carried by Ba2+ (50 mM) were recorded using the whole-cell variation of the patch electrode voltage-clamp technique. The two types of calcium channels showed similar membrane potential dependence with respect to the steady-state activation and inactivation gating properties. However, the properties of the long-lasting type II channels were shifted approximately 30 mV in the depolarizing direction compared with those of the transient type I channels. Activation of type I channels developed with a sigmoidal time course which was described by m2 kinetics, whereas the activation of type II channels was described by a single exponential function. Tail current upon repolarization followed an exponential decay in either type of calcium channels. In comparison to type I channels, the activation process of type II channels was shifted approximately 30 mV in the positive direction, while the deactivation process showed a 60 mV shift in the positive direction. The rate constants of activation obtained from the activation and deactivation processes indicated that under comparable membrane potential conditions, type II channels close 2.4 times faster than type I channels upon repolarization. When external 50 mM Ba2+ was replaced with Ca2+ or Sr2+ on the equimolar basis, the amplitudes of transient and long-lasting currents were altered without a significant change in their time courses. The ion permeability ratios determined from the maximum amplitude of the inward current were as follows: Ba2+ (1.0) = Sr2+ (1.0) greater than Ca2+ (0.7) for type I channels, and Ba2+ (1.0) greater than Sr2+ (0.7) greater than Ca2+ (0.3) for type II channels. Replacement of Ba2+ with Ca2+ caused a 10-12 mV positive shift in the current-voltage relation for type II channels. However, the shift for type I channels was much less. This suggests that negative surface charges are present around type II channels. After correction for the surface charge effect on the ion permeation, there was no significant difference between the permeability ratios of these cations for the two channel types. It was concluded that the two types of calcium channels have many common properties in their gating and permeation mechanisms despite their differential voltage sensitivity and ion selectivity.

Animals↗

PubMed1994

Differential involvement of voltage-dependent calcium channels in apomorphine-induced hypermotility and stereotypy.

The involvement of the voltage-dependent calcium channel in behavioral effects of apomorphine was tested in naive rats and in animals which were morphine-abstinent or were subjected to chronic electroconvulsive treatment (ECS). In naive rats a calcium channel blocker, nifedipine, which by itself does not affect locomotor activity, inhibited the locomotor stimulation induced by apomorphine, while it facilitated stereotyped behavior. Morphine-abstinent and ECS-treated rats displayed elevated responsiveness to apomorphine, reflected by hypermotility and stereotyped behavior after a dose of 1 mg/kg IP that does not produce overt behavioral effects in naive animals. Nifedipine, 5 mg/kg IP, significantly reduced hypermotility produced by apomorphine in morphine abstinent or ECS-treated rats. The calcium channel blocker did not, however, antagonize enhanced stereotyped behavior. The results indicate that apomorphine hypermotility is controlled by dihydropyridine calcium channels and that enhancement of calcium channel density produced by morphine abstinence and by chronic ECS potentiates the hypermotility response. Calcium channels seem to be differently involved in control of apomorphine-induced hypermotility and stereotypy.

Animals↗

PubMedDate not supplied

Effects of the blockade of high voltage-activated calcium channels on in vitro pineal melatonin synthesis.

The presence of high voltage-activated calcium channels in the rat pineal gland is well known. However, their role in pineal metabolism is not completely understood and is even controversial. Better to understand this matter, we investigated the effects of L-, N- or P/Q-type calcium channel blockers (nifedipine, omega-conotoxin GVIA, omega-agatoxin IVA, respectively) on melatonin content and arylalkylamine-N-acetyltransferase activity of denervated rat pineal glands kept for 48 h in culture and stimulated with norepinephrine. Melatonin was measured by high performance liquid chromatography with electrochemical detection and arylalkylamine-N-acetyltransferase activity was quantified by radiometric assay. Pre-incubation with any of these high voltage-activated calcium channel blockers reduced the melatonin production induced by norepinephrine although arylalkylamine-N-acetyltransferase activity was reduced only by the N-type calcium channel antagonist, omega-conotoxin GVIA. The results indicate that calcium influx through L-, N- or P/Q-type of high voltage-activated calcium channels is necessary for the full expression of the metabolic process leading to melatonin synthesis in the rat pineal glands. However, the mechanisms involved in this process are different for the L- or P/Q- and N-type calcium channels.

Animals↗

PubMed1987

Stimulatory influences of calcium channel antagonists on stress-induced opioid analgesia and locomotor activity.

The effects of the calcium channel antagonists diltiazem, nifedipine and the calcium channel agonist, BAY K 8644, on immobilization-induced opioid analgesia and locomotor activity were examined in CF-1 and C57BL strains of mice, respectively. The calcium channel antagonists enhanced the experimenatlly induced analgesia and activity, whereas the agonist reduced these responses. In addition, the calcium channel antagonists augmented, while the agonist attenuated, the analgesic effects of the specific mu and delta opioid agonists, DAGO and [D-Pen2,D-Pen5]-enkephalin (DPDPE), respectively. These results indicate that calcium channel antagonists have facilitatory and/or modulatory effects on the behavioral and physiological consequences of endogenous mu and delta opioid activity.

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