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PubMed1987

Effects of some calcium channel blockers on isolated human penile erectile tissues.

The effects of the calcium channel blockers (CCBs) verapamil, nifedipine and diltiazem on contractile activation of isolated human penile erectile tissues were investigated. Specimens of the corpus spongiosum (CS) and corpora cavernosa (CC) were obtained from men with a history of normal penile erection undergoing cystourethrectomy because of bladder malignancy. Preparations were mounted in organ baths and isometric tension was recorded. Deprivation of extracellular calcium abolished electrically induced contractions in both CS and CC preparations within 15 min.; norepinephrine (NE)-induced contractions were reduced by 90% (CS) and 83% (CC) after 30 min. All the CCBs reduced electrically induced contractions concentration-dependently, nifedipine being the most potent agent. Contractions induced by exogenous NE were depressed by about 50%, whereas high K+ (124 mM) induced responses were abolished. It is concluded that contraction in penile erectile tissues is mediated mainly by neuronally released NE stimulating postjunctional alpha-adrenoceptors. The contraction is highly dependent on extracellular calcium and can partly be inhibited by CCBs. It cannot be excluded that some CCBs injected intracavernosally may be useful for diagnosis and even treatment of erectile dysfunction. However, calcium channel blockade may not be as effective as a therapeutic principle as blockade of alpha-adrenoceptors.

Aged↗
PubMed2003

Parkinsonian syndrome and calcium channel blockers.

(1) Parkinsonian syndromes have occasionally been attributed to diltiazem, a calcium channel blocker, sometimes with a positive rechallenge. (2) Verapamil and amlodipine have also been implicated. (3) Prescribers should be aware of the possible role of these drugs in patients presenting with a parkinsonian syndrome.

Amlodipine↗
PubMed2005

The effect of calcium channel blockers on outcome following the surgical treatment of phaeochromocytomas and paragangliomas.

The peri-operative management of patients undergoing surgery for phaeochromocytoma or paraganglioma with calcium channel blockers (CCB) and their impact on postoperative morbidity and mortality were studied. The medical records of 105 patients undergoing surgery between 1991 and 2002 were analysed retrospectively. In all patients, the calcium channel blocker nicardipine was used for the peri-operative management of haemodynamic changes. Sixty-five patients (61.9%) showed transient intra-operative hypertension. Systolic blood pressure (SBP) > 220 mmHg and SBP > 180 mmHg for > 10 consecutive minutes was observed in 14 (13%) and four patients (2.8%), respectively. SBP < 80 mmHg for > 10 consecutive minutes occurred in 13 patients (12.3%). Eleven patients (10.4%) developed postoperative complications and three patients died (2.8%). The median (range) ICU and hospital length of stay were, respectively, 1 (0-7) day and 10 (2-35) days. The sole use of calcium channel blockers for the peri-operative management of phaeochromocytoma and paraganglioma resection does not prevent all haemodynamic changes; however, its use was associated with a low morbidity and mortality.

Adolescent↗
PubMed1990

Suppression of epileptiform burst discharges in CA3 neurons of rat hippocampal slices by the organic calcium channel blocker, verapamil.

We studied the effects of the organic calcium channel blocker, verapamil, on spontaneous and bicuculine-induced epileptiform burst discharges in CA3 pyramidal cells of hippocampal slices. A transient increase of burst discharge rate was observed in most cells within 30 min after the addition of verapamil (100 microM) to the perfusing medium. Prolonged verapamil perfusions gradually reduced the rate and duration of burst discharges, then abolished them in all tested slices (over periods of 50-150 min) without blocking synaptic transmission. Responses to intracellular injections of current pulses were also gradually affected by verapamil: Action potential amplitude was decreased, action potential duration increased, frequency adaptation increased, amplitude of the fast hyperpolarization following a single action potential decreased, and amplitude and duration of the slow afterhyperpolarization markedly reduced. The amplitude of calcium spikes elicited in slices perfused with tetrodotoxin-containing medium was not affected by verapamil, but the mean velocity of depolarization near the peak of the calcium spike was decreased. Membrane resting potential and input resistance were not affected by verapamil. These results confirm that verapamil is able to suppress epileptiform activity, but suggest that this effect is rather non-specific, due to inhibition of both postsynaptic sodium and calcium conductances.

Action Potentials↗
PubMedDate not supplied

Application of calcium channel blockers in the treatment of cardiovascular diseases.

In this review the calcium channel blockers (CCB) were divided into three generations. The advantages and shortcomings of these drugs were described. The application of CCB in the treatment of hypertensive disease, ischaemic heart disease, congestive heart failure and heart arrhythmias was discussed. Actually, the optimal drugs from this group are representatives of the third generation: amlodipine and lacidipine. It seems that search for new CCB should be directed to find the substances similar to or better than the chemical entities of this third generation. The calcium sensitizing agents as a new positive inotropic drugs are signalled. The possibility that in the future the new CCB could have an application as psychotropic drugs is mentioned.

Antihypertensive Agents↗
PubMedDate not supplied

Renal cortical remodelling by NO-synthesis blockers in rats is prevented by angiotensin-converting enzyme inhibitor and calcium channel blocker.

The cortical remodelling was studied when chronically nitric oxide synthesis (NOs) blockade (L-NAME-induced) hypertensive rats are simultaneously treated, or not, with angiotensin-converting enzyme inhibitor or calcium channel blocker. Four groups of eight rats each were studied as follows: Control (C), L-NAME (L), L-NAME+Enalapril (L+E) and L-NAME+Verapamil (L+V). The systolic blood pressure (SBP) was weekly recorded. The cortex of the left kidneys was analysed according to the vertical section design. The volume-weighted mean glomerular volume (VWGV) was made through the "point-sampled intercepts" method. Enalapril and verapamil were efficient in reducing the SBP in rats submitted to NOs blockade. Glomeruli had considerable alterations in L group rats (glomerular hypertrophy or sclerosis) and tubular atrophy. The VWGV was 100% greater in L group rats than in the C group rats, while it was 30% smaller in L+E and L+V groups than in L group. The tubular volume was 30-50% greater, while the tubular length was 20-30% smaller in the L group than in the other groups. The renal cortical region showed glomerular sclerosis/hypertrophy and tubular remodelling in rats with NOs blockade that was efficiently prevented with the simultaneous treatment with enalapril or verapamil.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

[The effects of calcium channel blockers on the frequency and amplitude of the spontaneous contractions and the responses to acetylcholine on isolated rat duodenum].

The effects of calcium channel blockers on the frequency, amplitude of the spontaneous contractions and responses to acetylcholine are investigated in isolated duodenum of rat. Verapamil, diltiazem and nifedipine were used as calcium channel blockers. All the blockers decreased the frequency significantly. When the effects of verapamil, diltiazem and nifedipine were compared with each other, significant difference was not found. Nifedipine, diltiazem and verapamil significantly reduced the amplitude of spontaneous contraction by blocking the influx of calcium ions. On the other hand, they reduced the responses to acetylcholine significantly, comparing with control groups.

Acetylcholine↗
PubMed1997

The influence of three L-type calcium channel blockers on morphine effects in healthy volunteers.

UNLABELLED: Numerous animal studies and several clinical studies have shown that calcium channel blockers (CCBs) augment opioid analgesia. We sought to determine whether three CCBs from three L-type subgroups (i.e., L-CCBs) enhanced morphine analgesic effects in healthy volunteers, and whether other effects of morphine (e.g., mood-altering effects) were altered by the CCB pretreatment. We examined the effects of three L-CCBs--diltiazem (30 mg, per os [P.O.]), nimodipine (60 mg, P.O.), and verapamil (80 mg, P.O.)--on morphine (10 mg/70 kg, intravenously) effects in nine healthy volunteers. Subjects first ingested the oral drug or placebo and 120 min later were injected with morphine or saline. Dependent measures included pain ratings measured during a cold-pressor test and subjective, psychomotor, and physiological effects. The L-CCBs alone had no effect on any of the dependent measures. Morphine alone and in combination with the L-CCBs reduced pain ratings, but there were no statistically significant differences in the pain measures between the morphine alone and the L-CCB/morphine conditions. Pretreatment with the L-CCBs in most cases neither potentiated nor attenuated the other effects of morphine. L-CCBs as well as the N-type CCBs currently under drug development should continue to be investigated to determine their potential as analgesic adjuvants. IMPLICATIONS: This study is important because the results are at odds with numerous animal studies and several clinical studies, which indicate that calcium channel blockers of the L-type increase the amount of analgesia produced by morphine. Using clinically relevant doses of L-type blockers, we could find no potentiation of morphine analgesia.

Adjuvants, Anesthesia↗
PubMed1992

The calcium channel blocker LAS 30538, unlike nifedipine, verapamil, diltiazem or flunarizine, potently inhibits insulin secretion in-vivo in rats and dogs.

The effects of a novel calcium channel blocker, LAS 30538 (1-[2-(2,6-dimethylphenoxy)ethyl]-alpha,alpha-bis-(p-fluorophenyl)-4- piperidine methanol), were studied on glucose tolerance and insulin secretion in rats and dogs in-vitro and in-vivo. Some comparisons were made with nifedipine, verapamil, diltiazem, flunarizine, diazoxide, cromakalim and minoxidil. LAS 30538, like a number of calcium channel blockers, was found to inhibit insulin secretion in-vitro, but was 1000-fold more potent than verapamil or diltiazem in this respect. LAS 30538 differed from the other calcium channel blockers studied in that it also potently inhibited insulin secretion and impaired glucose tolerance in-vivo. The evidence that LAS 30538 is more potent than diazoxide as a hyperglycaemic agent in-vivo suggests that this could be a useful drug for the treatment of hyperinsulinaemia in man.

Administration, Oral↗
PubMed1998

Use of calcium channel blockers and risk of suicide: ecological findings confirmed in population based cohort study.

OBJECTIVE: To investigate possible associations between use of cardiovascular drugs and suicide. DESIGN: Cross sectional ecological study based on rates of use of eight cardiovascular drug groups by outpatients. A population based cohort study including users of drugs to control hypertension. SUBJECTS: The ecological study included 152 of Sweden's 284 municipalities. The cohort study included all inhabitants of one Swedish municipality who during 1988 or 1989 had purchased cardiovascular agents from pharmacies within the municipality. Six hundred and seventeen subjects (18.2%) were classified as users of calcium channel blockers and 2780 (81.8%) as non-users. MAIN OUTCOME MEASURES: Partial correlations (least squares method) between rates of use of cardiovascular drugs and age standardised mortality from suicide in Swedish municipalities. Hazard ratios for risk of suicide with adjustments for difference in age and sex in users of calcium channel blockers compared with users of other hypertensive drugs. RESULTS: Among the Swedish municipalities the use of each cardiovascular drug group except angiotensin converting enzyme inhibitors correlated significantly and positively with suicide rates. After adjustment for the use of other cardiovascular drug groups, as a substitute for the prevalence of cardiovascular morbidity, only the correlation with calcium channel blockers remained significant (r = 0.29, P < 0.001). In the cohort study, five users and four non-users of calcium channel blockers committed suicide during the follow up until the end of 1994. The absolute risk associated with use of calcium channel blockers was 1.1 suicides per 1000 person years. The relative risk, adjusted for differences in age and sex, among users versus non-users was 5.4 (95% confidence interval 1.4 to 20.5). CONCLUSIONS: Use of calcium channel blockers may increase the risk of suicide.

Calcium Channel Blockers↗
PubMed2005

Effects of a new calcium channel blocker, azelnidipine, on systemic hemodynamics and renal sympathetic nerve activity in spontaneously hypertensive rats.

Antihypertensive treatment with dihydropyridine calcium channel blockers elicits sympathetic nerve activation, which may contribute to cardiovascular events. However, recent clinical studies showed that treatment with azelnidipine, a new dihydropyridine calcium channel blocker, significantly reduced blood pressure in hypertensive patients while either maintaining or actually decreasing heart rate (HR). In this study, we examined the effects of azelnidipine and amlodipine on systemic hemodynamics and renal sympathetic nerve activity (RSNA) in anesthetized spontaneously hypertensive rats (SHR). We also examined the effects of these agents on baroreflex functions by infusing phenylephrine (30 microg/kg/min, i.v.) and sodium nitroprusside (10 microg/kg/min, i.v.) into azelnidipine- or amlodipine-treated SHR. Fifty min after administration of azelnidipine (10 microg/kg/min for 10 min, i.v.), mean arterial pressure (MAP) significantly decreased from 153+/-5 to 122+/-5 mmHg; however, HR and integrated RSNA did not change significantly (from 352+/-9 to 353+/-10 beats/ min and 115+/-5% of baseline, respectively). Infusion of amlodipine (50 microg/kg/min for 10 min) elicited similar effects on MAP (from 152+/-5 to 120+/-4 mmHg). However, amlodipine significantly increased HR (from 351+/-9 to 375+/-11 beats/min) and integrated RSNA (165+/-5% of baseline). Analyses of baroreflex function curves revealed that azelnidipine-treated rats showed a smaller baroreflex function than amlodipine-treated rats (p<0.05). These data suggest that azelnidipine possesses sympathoinhibitory effects, which may be one reason why it had less pronounced effects on HR in hypertensive patients.

Amlodipine↗
PubMed1997

N-type calcium channel blockers from a marine bacterium, Cytophaga sp. SANK 71996.

N-(3-Acyloxyacyl)glycines were isolated as N-type calcium channel blockers from a marine bacterium Cytophaga sp. SANK 71996. The identification and fermentation of the producing strain and structure characterization of N-(3-acyloxyacyl)glycines by spectral analyses and chemical syntheses are described together with their antagonistic activities.

Animals↗
PubMed1982

Comparison of cardiovascular, renal, and humoral effects of acute administration of two calcium channel blockers in normotensive and hypertensive subjects.

The acute effects of two calcium channel blockers, nifedipine and verapamil, were compared in eight normotensive subjects and eight patients with essential hypertension. Nifedipine 10 mg and verapamil 160 mg orally had no effect on blood pressure of normal subjects, but reduced systolic and diastolic pressures of hypertensive patients to the same extent. The blood pressure reduction caused by nifedipine was more prompt and of lesser duration than that caused by verapamil. In both normal subjects and hypertensive patients nifedipine caused a transient rise in heart rate and plasma renin activity, and plasma catecholamines showed a tendency to increase; verapamil did not affect these variables. Nifedipine induced a marked increase in urine volume and renal sodium excretion in hypertensive patients, with a much smaller change in normotensives. Verapamil did not influence water and sodium excretion in either direction. Thus, this study shows similarities and differences between the effects induced by acute oral administration of the most-used vasodilating calcium antagonists.

Blood Pressure↗
PubMedDate not supplied

[Effect of the calcium channel blockers on rotation induced by apomorphine and amphetamine in rats lesioned with 6-hydroxydopamine].

We have studied the effects of calcium channel blockers cinarizine, flunarizine, nicardipine, nifedipine, verapamil and diltiazem on the motor anomalies which can be found in rats with unilateral nigrostriated lesion due to 6-OH-DA. All of them reduce rotation induced by apomorphine according to this order: nifedipine greater than nicardipine greater than diltiazem greater than flunarizine greater than verapamil greater than cinarizine. No effects on rotation induced by amphetamine have been observed. Our data suggest that calcium channel blockers cause dopamine receptor blockade but they do not modify the calcium-non-depending releasing of dopamine induced by amphetamine.

Amphetamine↗
PubMedDate not supplied

Calcium ion and pituitary hormones: effect of calcium channel blockers on stimulated secretion of pituitary hormones.

The effects of two calcium channel blockers nifedipine (20 mg sublingual), and verapamil (10 mg i.v.) on growth hormone (GH), thyrotropin (TSH), prolactin (PRL) and gonadotropin (LH and FSH) secretion induced by growth hormone releasing hormone (GHRH), hypoglycemia, thyrotropin releasing hormone (TRH), metoclopramide and gonadotropin releasing hormone (GnRH), were studied in a group of normal volunteers (27 men and 8 women). Neither nifedipine nor verapamil had any effect on PRL, TSH or gonadotropin release. Verapamil did not cause variations in GH secretion following GHRH and insulin-induced hypoglycemia, whereas nifedipine significantly reduced the elevation in GH induced by GHRH; however the GHRH-mediated GH rise still remained within the normal range in all subjects. Our results suggest that neither nifedipine nor verapamil have important effects on stimulated pituitary hormone secretion, at least under conditions of acute administration.

Adolescent↗
PubMed1987

Effects of peripheral and central administration of calcium channel blockers in the naloxone-precipitated abstinence syndrome in morphine-dependent rats.

The effects of two calcium channel blockers (verapamil and flunarizine) were evaluated on the naloxone-precipitated syndrome in morphine-dependent rats. The withdrawal signs in saline-treated rats were mainly diarrhea, body weight loss, jumping and ptosis. On i.p. administration, verapamil and flunarizine prevented diarrhea and body weight loss but not jumping. Verapamil also reduced the incidence of ptosis at the highest dose tested (40 mg/kg). Administered i.c.v., 160 micrograms verapamil reduced the body weight loss and the number of jumps without modifying diarrhea or ptosis. The results show that calcium channel blockers inhibit morphine abstinence syndrome manifestations through both peripheral and central mechanisms.

Animals↗
PubMed1988

Cardiovascular profile of FPL 62129, a novel dihydropyridine calcium channel blocker, in anaesthetised dogs: a comparison with nifedipine.

The cardiovascular effects of FPL 62129, a novel dihydropyridine calcium channel blocker, were studied in chloralose-anaesthetised dogs in comparison with those of nifedipine. FPL 62129 and nifedipine produced dose-related falls in blood pressure and total peripheral resistance and were of similar potency in these respects. While the vasodilator effects of nifedipine were accompanied by reflex tachycardia, FPL 62129 reduced blood pressure without altering heart rate. Both compounds increased cardiac contractility and cardiac output. Nifedipine reduced PR interval duration of the ECG, whereas FPL 62129 produced no change. These differences between FPL 62129 and nifedipine are reflections of their respective cardiac profiles. In studies performed after cardiac autonomic block (to eliminate the contribution from reflexes), FPL 62129 showed marked activity at the sinus node and to a lesser extent at the atrioventricular node. Unlike nifedipine, FPL 62129 demonstrates vasodilator and direct decelerator properties over the same dose range, which accounts for its ability to lower blood pressure without causing reflex tachycardia in this model. The observed profile of FPL 62129 questions attempts to classify calcium channel blockers of the dihydropyridine type as selective vasodilators.

Anesthesia↗
PubMedDate not supplied

Cocaine toxicity and the calcium channel blockers nifedipine and nimodipine in rats.

Two dihydropyridine type calcium channel blockers (CCBs) were studied for any protective or therapeutic effect upon cocaine-induced toxicity and death in rats. To test for the protective effects, rats were pretreated with vehicle (control), nifedipine or nimodipine, intraperitoneally (IP) 30 minutes prior to an LD85 of cocaine, or intravenously (IV) 10 minutes prior to cocaine administration. Animals receiving IP control vehicle developed seizures in 5.6 +/- 1.0 minutes and respiratory arrest in 9.8 +/- 1.4 minutes. Animals pretreated IP with nifedipine or nimodipine developed seizures and respiratory arrest significantly sooner than the controls, although the overall incidences of seizures and respiratory arrest were not significantly different. Pretreatment with IV CCBs resulted in similar findings. To test the therapeutic effect of CCBs given following cocaine overdose, rats were administered cocaine IP and then treated with IV nifedipine or nimodipine once seizures occurred. In these animals, there was no significant difference in the incidence or time to respiratory arrest compared to vehicle controls. This study demonstrates that neither pretreatment nor posttreatment with the CCBs nifedipine or nimodipine reduces cocaine toxicity in this rodent model.

Animals↗