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PubMed2006

[The effect of calcium channel blocker lercanidipine on lowgrade inflammation parameters in essential hypertension patients].

INTRODUCTION: Oxidative stress (OS), inflammation and insulin resistance are among the mechanisms that have been recently implicated in pathogenesis of essential hypertension (EH). Peripheral polymorphonuclear leukocytes (PMNLs) are primed in EH patients, releasing uncontrolled superoxide anion contributing to OS and chronic low-grade inflammation in these patients. PMNL priming correlates with insulin resistance and with PMNL intracellular calcium ([Ca2+]i). Recent studies have attributed additional anti-oxidative characteristics to the anti-hypertensive drug Lercanidipine (Vasodip), a third generation calcium-channel blocker. AIM: To evaluate possible novel effects of two months of Lercanidipine treatment on systemic and PMNL-related inflammation and on insulin resistance in EH patients. METHODS: Fifteen non-smoking EH patients with untreated mild to moderate high blood pressure (BP) and age- and gender-matched healthy controls (HC) were included in the study. Low-grade inflammation was expressed by PMNL counts and apoptosis, by plasma fibrinogen, CRP and albumin (as a negative acute phase reactant) levels. Fasting serum insulin levels served as a marker of insulin resistance. RESULTS: Inflammation parameters and insulin levels were higher in EH compared to HC. PMNL counts, fibrinogen and insulin levels positively correlated with mean arterial blood pressure values. Two months of Lercanidipine treatment showed a significant decrease in BP, PMNL counts and apoptosis, CRP and serum insulin levels and a significant increase in serum albumin levels. CONCLUSION: The authors imply that the low-grade systemic inflammation and insulin resistance detected in EH patients may be attenuated by the use of Lercanidipine, adding new unknown anti-inflammatory properties to this calcium channel blocker.

Adult↗
PubMed1998

The effect of nilvadipine, a calcium-channel blocker, on the hemodynamics of retrobulbar vessels in normal-tension glaucoma.

PURPOSE: To investigate the effect of nilvadipine, a calcium-channel blocker, on the hemodynamics of retrobulbar vessels in normal-tension glaucoma. METHODS: Twenty-five patients who prospectively met the enrollment criteria underwent color Doppler imaging of the retrobulbar vessels before and after receiving 4 weeks of treatment with 2 mg oral nilvadipine twice daily. RESULTS: Nilvadipine significantly increased the end-diastolic velocity in the central retinal artery and a short posterior ciliary artery. It significantly reduced the resistance index in the central retinal artery and posterior ciliary arteries, but not in the ophthalmic artery. The calculated ocular perfusion pressure was not affected. CONCLUSION: Oral nilvadipine reduces vascular resistance in distal retrobulbar arteries in normal-tension glaucoma without affecting more proximal blood vessels. Therefore, nilvadipine may have a beneficial effect on the hemodynamics of retrobulbar vessels in normal-tension glaucoma.

Administration, Oral↗
PubMed1997

Cardiovascular effects of CPU-23, a novel L-type calcium channel blocker with a unique molecular structure.

1. The cardiovascular effects of CPU-23 (1-[1-[(6-methoxy)-naphth-2-yl]]-ethyl-2-(1-piperidinyl)-acetyl-6, 7-dimethoxy-1,2,3,4-tetrahydroisoquinoline), a cleavage product of tetrandrine, were investigated using the whole cell perforated patch-clamp technique, in vitro tension measurements and in vivo haemodynamic recordings. 2. CPU-23 (1 and 10 microM) dose-dependently reduced concentration-response curves for KCl and phenylephrine (PE) in the rat tail artery; inhibition of KCl-induced contraction was much more potent than for PE. At the same concentrations, CPU-23 inhibited the inward Ba2+ currents in single smooth muscle cells isolated from the rat tail artery, while CPU-23 (10 microM) produced 95% vasorelaxation of the rat middle cerebral artery preconstricted with BayK 8644. 3. CPU-23 (10 and 30 microM) inhibited the noradrenaline-induced phasic contraction of the rat tail artery in the absence of extracellular Ca2+ from 40% of control to 23% and 14%, respectively (P<0.01) and tonic contraction of the artery after addition of Ca2+ (2 mM) from 100% of control to 83% and 75%, respectively (P<0.01). In the presence of extracellular Ca2+ the PE-induced contraction was reduced by CPU-23 (30 and 100 microM) to 27% and 37%, respectively. 4. The haemodynamic profile of CPU-23 in the rat was very similar to diltiazem. At 5 mg kg(-1) CPU-23 induced a rapid onset and long-lasting decrease in left ventricular systolic pressure (LVSP), maximal velocity of pressure increase (dP/dt(max)), systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR). When haemodynamic actions of CPU-23, verapamil, diltiazem and nifedipine were compared at equidepressor doses, the order of potency for reducing LVSP and dP/dt(max) was verapamil > CPU-23 = diltiazem > nifedipine and the order of potency for decreasing HR was verapamil = CPU-23 = diltiazem > nifedipine. 5. These data indicate that CPU-23 is a novel calcium channel blocker with unique molecular structure, which exerts antihypertensive and cardiac depressant effects due primarily to its action on L-type voltage-gated calcium channels.

Adrenergic alpha-Agonists↗
PubMed2000

The calcium-channel blocker lacidipine reduces the development of atherosclerotic lesions in the apoE-deficient mouse.

BACKGROUND: Lacidipine is a widely used calcium-channel blocker, which has both long-lasting antihypertensive activity and also antioxidant properties. Previous studies have demonstrated the ability of lacidipine to reduce the development of atherosclerotic lesions in several animal models. OBJECTIVE: The present study investigated the antiatherosclerotic potential of lacidipine in the apoE-deficient mouse, an experimental model of atherosclerosis showing progressively complex and widespread lesions which closely resemble the inflammatory-fibrous plaques seen in humans. METHODS: Lacidipine was administered daily by gavage for 10 weeks at dose levels of 0 (control), 0.3, 1.0 and 3.0 mg/kg. RESULTS: Lacidipine administration reduces the extension of atherosclerotic lesions in the aorta of the apoE-deficient mouse without affecting plasma lipid levels. We also show that apoE-deficient mice have four-fold higher values of the proatherogenic peptide, endothelin, compared with the wild-type C57BL/6 mouse and that lacidipine administration reduced, in a dose-dependent manner, the concentrations of plasma endothelin. CONCLUSION: Lacidipine has anti-atherogenic effects in the apoE-deficient mouse, and reduces plasma endothelin concentrations.

Animals↗
PubMed1987

Certain calcium channel blockers bind specifically to multidrug-resistant human KB carcinoma membrane vesicles and inhibit drug binding to P-glycoprotein.

The calcium channel blockers verapamil and diltiazem have been shown to reverse multidrug resistance, but the mechanism of action of these agents is still unknown. We measured [3H]verapamil, [3H]desmethoxyverapamil, [3H]diltiazem, and [3H]nitrendipine binding to membrane vesicles made from drug-sensitive (KB-3-1), multidrug-resistant (KB-C4 and KB-V1), and revertant (KB-V1-R2) cells. Membrane vesicles from KB-V1 cells bound 10-20-fold more [3H]verapamil and [3H]diltiazem and about 30-fold more [3H]desmethoxyverapamil than did vesicles from the parental KB-3-1 or revertant KB-V1-R2 cell lines. These drugs reverse the multidrug resistance phenotype by increasing accumulation of drugs in the resistant cells. No difference in binding of [3H]nitrendipine, which did not reverse drug resistance, was observed. The binding of vinblastine, desmethoxyverapamil, and diltiazem to KB-V1 vesicles was specific and saturable and was inhibited by desmethoxyverapamil and quinidine greater than vinblastine and diltiazem much greater than daunomycin. In addition, verapamil and diltiazem inhibited the vinblastine photoaffinity labeling of P170, the protein previously shown to be a marker of multidrug resistance.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Pinaverium acts as L-type calcium channel blocker on smooth muscle of colon.

The effect of pinaverium was electrophysiologically characterized and compared with the established L-type calcium channel blockers diltiazem, D600, and nitrendipine on canine colonic circular smooth muscle. Effects were studied on the electrical activity of the smooth muscle cells, in particular the spontaneously occurring slow wave. In addition, effects were examined on spontaneous contraction patterns and contractile activities generated by stimulation of cholinergic nerves or directly by stimulating muscarinic receptors. Effects were also examined on excitation of NO-releasing intrinsic nerves. Pinaverium bromide affected the slow wave by selectively inhibiting the plateau potential that is associated with generation of contractile activity. Pinaverium, similar to diltiazem and D600, produced reductions in cholinergic responses as well as spontaneous contractions. The IC50 values for inhibition of cholinergic responses for pinaverium, diltiazem, and D600 were 1.0 x 10(-6), 4.1 x 10(-7), and 5.3 x 10(-7) M, respectively. The IC50 values for inhibition of spontaneous contractile activity for pinaverium, diltiazem, and D600 were 3.8 x 10(-6), 9.7 x 10(-7), and 8.0 x 10(-7) M, respectively. Increases in contractility by carbachol were abolished by pretreatment with either pinaverium or D600. In addition, neither pinaverium nor D600 had any effects on the inhibitory NO-mediated relaxations. These data provide a rationale for the use of pinaverium in the treatment of colonic motor disorders where excessive contraction has to be suppressed.

Animals↗
PubMed1992

Improvement of liver preservation by the calcium channel blocker nisoldipine. An experimental study applying intravital microscopy to transplanted rat livers.

It has been shown recently that inclusion of the calcium channel blocker nisoldipine to University of Wisconsin (UW) solution significantly improves survival after rat liver transplantation. To further elucidate the mechanisms involved, rat livers were stored for 1 h in UW solution with or without the addition of 1.4 microM nisoldipine (Miles, West Haven, Conn., USA). The liver grafts were investigated in vivo 90 min after transplantation by intravital fluorescence microscopy. Sinusoidal perfusion was reduced in all sublobular regions of the liver in the UW group (e.g. portal area: 76.7 +/- 2.1%) and in the nisoldipine group (85.8 +/- 1.5%). Diameters of liver sinusoids were comparably reduced in the UW and nisoldipine groups indicating that nisoldipine did not cause vasodilatation. Adhesion of leukocytes, however, rose significantly after liver transplantation particularly in periportal regions (25.8 +/- 2.5%) compared to controls (17.1 +/- 2.8%; P < 0.05). Adhesion of leukocytes was reduced when nisoldipine was included in UW solution (13.3 +/- 1.7%; P < 0.05). Administration of latex particles, which were given in additional experimental groups, demonstrated an impressive increase in phagocytic activity of Kupffer cells after liver transplantation in periportal and pericentral areas (161 +/- 14% and 184 +/- 19% of controls). Phagocytosis was significantly reduced by nisoldipine in the periportal region (101 +/- 10%; P < 0.01). Thus, the beneficial effect of nisoldipine was most pronounced in periportal regions, where the majority of Kupffer cells are located and leukocyte adhesion was at a maximum.

Adenosine↗
PubMed1984

The calcium channel blocker nitrendipine in single- and multiple-agent antihypertensive regimens: preliminary report of a multicenter study.

The antihypertensive efficacy of the calcium channel blocker nitrendipine was evaluated in a 12-center collaborative study during 6 months of treatment. Following an initial placebo period, 318 patients with supine diastolic blood pressures greater than 90 mm Hg were given nitrendipine 5 mg twice daily for 1 week; if goal blood pressure was not reached (supine diastolic blood pressure less than 90 mm Hg with a fall of at least 10 mm Hg), the dose was doubled, and if necessary it was doubled again after an additional week. By the end of titration, goal blood pressure had been achieved in 132 patients (43%). During the subsequent 5 months of study, 155 patients continued to take nitrendipine alone; their post-titration supine diastolic blood pressure was 85 +/- 7 mm Hg, and at the end of the 6-month study it was 84 +/- 7 mm Hg. There were no changes in body weight or in heart rate. In 38 patients with a supine diastolic blood pressure of 95 +/- 9 mm Hg after titration, propranolol was added to the nitrendipine and decreased the supine diastolic blood pressure to 86 +/- 9 mm Hg by the end of the study; and in another 74 patients with a post-titration supine diastolic blood pressure of 93 +/- 7 mm Hg, addition of hydrochlorothiazide decreased the supine diastolic blood pressure to 86 +/- 7 mm Hg by the end of the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Effect of calcium channel blockers, nifedipine and benidipine, on death of cultured mouse mesangi al cells.

We examined the effects of the short-acting calcium channel blocker (CCB) nifedipine and the long-acting CCB benidipine on the death of mouse cultured mesangial cells induced by tumor necrosis factor alpha (TNF-alpha) and/or cycloheximide (CHX). Cell death was evaluated by a morphological study using semithin sections. The dead cells were divided into three types, i.e., apoptotic cells (type 1), necrotic cells (type 3) and other types of dead cells, the so-called 'secondary necrotic cells' or 'postapoptotic necrotic cells' (type 2). In the morphological study with semithin sections, cells in the presence of TNF-alpha or CHX and nifedipine or benidipine showed low percentages of all dead cell types with 24 h incubation. Both nifedipine and benidipine have protective effects against TNF-alpha or CHX. It is postulated that CCB might inhibit the apoptotic or necrotic processes by TNF-alpha or CHX with 24 h incubation. With 36 h incubation, CCB increased the percentages of all types of dead cells except for treatment with 1x10(-5) M benidipine and CHX. It appears that these cell-protective effects might be decreased after treatment with TNF-alpha or CHX and CCB for 36 h. In conclusion, the short-acting CCB nifedipine and the long-acting CCB benidipine have protective effects on mouse cultured mesangial cells against TNF-alpha or CHX. However, nifedipine and benidipine did not inhibit specific types of cell death using semithin sections in this study.

Animals↗
PubMed2000

Calcium channel blockers inhibit proliferation and matrix production in rat mesangial cells: possible mechanism of suppression of AP-1 and CREB activities.

BACKGROUND: Calcium channel blockers (CCBs) are reported to attenuate the loss of renal function in various glomerulonephritides. METHODS: To determine the mechanism of action of these drugs, we investigated the effects of CCBs on cell proliferation and extracellular matrix (ECM) production in cultured rat mesangial cells. RESULTS: While stimulation with 5% fetal calf serum (FCS) increased [(3)H]thymidine and [(3)H]proline incorporation into quiescent mesangial cells, incubation with nifedipine and cilnidipine inhibited the increase in a dose-dependent manner. Northern blot analysis demonstrated that 5% FCS increased the expression of transforming growth factor beta (TGF-beta) and fibronectin (FN) mRNA and that CCBs significantly reduced this induction, indicating that CCBs may reduce ECM production through inhibiting TGF-beta and FN. Since activator protein 1 (AP-1) regulates cell proliferation and TGF-beta expression, we evaluated the AP-1 activity by gel mobility shift analysis. Nuclear extracts of FCS-treated cells showed a strong binding to AP-1-specific oligonucleotides which was suppressed by CCBs, suggesting that these agents may inhibit cell proliferation by suppressing AP-1. CCBs also inhibited the binding activity of cyclic adenosine monophosphate responsive element binding protein which regulates FN gene expression. However, neither CCBs nor FCS affected the NFkappaB activity. CONCLUSION: These results suggest that CCBs may, in part, inhibit the progression of glomerulonephritis through non-hemodynamic actions that include the suppression of mesangial cell proliferation and the production of ECM.

Animals↗
PubMed1999

Effects of mebudipine and dibudipine, two new calcium-channel blockers, on rat left atrium, rat blood pressure and human internal mammary artery.

Mebudipine and dibudipine are two new dihydropyridine calcium-channel blockers that have been synthesized in our laboratory. In a previous study, they showed considerable relaxant effect on vascular and ileal smooth muscle. Here, the pharmacological effects of mebudipine and dibudipine on isolated rat left atrium, rat blood pressure and isolated human internal mammary artery are described. Results are compared with those obtained for nifedipine. Mebudipine and dibudipine reduced contraction force of rat left atrium (pIC30 values: 5.37+/-0.13 and 5.49+/-0.15, respectively) but their negative inotropic effects were significantly weaker than that of nifedipine (pIC30 value: 6.63+/-0.11). Mebudipine and dibudipine lowered rat blood pressure. The hypotensive effect of mebudipine was similar to that of nifedipine while dibudipine was weaker than nifedipine. It was found that the half-life of the hypotensive action of dibudipine (41.91+/-3.77 min, 31.13+/-2.26 min and 28.20+/-4.37 min at 2, 4 and 8 mg kg(-1) orally administered doses, respectively) was longer than that of nifedipine (11.85+/-2.88 min, 16.65+/-2.42 min and 14.03+/-0.10 min at the same doses, respectively). Also, it appeared that mebudipine had a slower rate of absorption compared with nifedipine (the time to reach peak hypotensive action at 2, 4 and 8 mg kg(-1) orally administered doses were, respectively, 24.00+/-6.96 min, 23.75+/-2.39 min and 15.00+/-2.04 min for mebudipine and 7.80+/-0.86 min, 13.75+/-3.15 min and 833+/-0.88 min for nifedipine). The two new compounds, as well as nifedipine, relaxed KCl-treated isolated human internal mammary artery (pEC50 values; 7.87+/-0.12, 7.22+/-0.24 and 7.67+/-0.12 for mebudipine, dibudipine and nifedipine, respectively). The relaxant effects of mebudipine and dibudipine did not show any significant difference compared with that of nifedipine. It is concluded that these new compounds are weak cardiodepressants and, with due attention to its significant vasorelaxant action, mebudipine is a vasoselective compound. In addition, these two compounds have potent blood pressure lowering effects. Also, their vasorelaxant action can be reproduced in human vascular preparations.

Animals↗
PubMed1990

Use of heart rate spectral analysis to study the effects of calcium channel blockers on sympathetic activity after myocardial infarction.

We used spectral analysis of heart rate variability (HRV) to study the effects of the calcium channel blockers diltiazem and nifedipine and the beta-blocker metoprolol on the sympathetic nervous system in patients following myocardial infarction. Energy in the low-frequency range (0.04 to 0.12 Hz) in the standing (tilt) position was used as a quantitative index of sympathetic activity. Twenty-seven male patients, mean age 62 +/- 13 years, were studied 2 to 6 weeks after myocardial infarction. Eight patients received metoprolol, 100 mg twice daily; nine patients received diltiazem, 60 mg three times daily; and 10 patients received nifedipine, 10 mg three times daily. HRV and arterial blood pressure were recorded before and 5 to 7 days after initiation of therapy. None of the drugs had significant effects on the systolic blood pressure, and only nifedipine significantly reduced the diastolic blood pressure. Metoprolol and diltiazem reduced the low-frequency HRV in all patients studied, but nifedipine had no consistent effects. Our results suggest that diltiazem had a depressant effect on sympathetic activity similar to beta-adrenergic blockers. This effect was not observed with nifedipine. The reduction in sympathetic activity by diltiazem may contribute to its therapeutic effects in the post-infarction period.

Adult↗
PubMed1991

The future of calcium channel blocker therapy in diabetes mellitus.

Diabetes mellitus is associated with significant morbidity and mortality caused by the micro- and macro-vascular complications that all too frequently develop during the lifetime of the diabetic patient. In attempts to treat the complications of diabetes, several different treatment strategies have been investigated. The role of tight blood glucose control in the treatment of diabetic vascular complications has recently been challenged, as the existing data in support of this mode of therapy are currently inconclusive. Perhaps more effective in preventing many of the vascular complications is the rigorous treatment of hypertension that frequently accompanies diabetes mellitus. Epidemiological studies have demonstrated that the presence of hypertension significantly contributes to the development and progression of diabetic nephropathy, retinopathy, cardiovascular disease, and possibly neuropathy. Preliminary clinical studies demonstrate that the progression of diabetic renal disease can be slowed by vigorous antihypertensive therapy. Among the various antihypertensive agents used to treat the hypertension associated with diabetes mellitus, calcium channel blockers are emerging as one of the agents of first choice. This is because of their very low side effect profile and their absence of detrimental effects on serum lipid levels and glucose tolerance. Calcium channel blockers may be of additional potential benefit to the diabetic patient by slowing the progression of atherosclerosis, reversing the intracellular calcium defects that may contribute to the pathogenesis of diabetic cardiomyopathy, and protecting against the progression of chronic renal disease.

Calcium Channel Blockers↗
PubMed1991

Preliminary study of the protective effect of the calcium channel blocker, nifedipine, on adriamycin-induced tissue injury.

The effect of nifedipine, an oral calcium-channel blocker, on adriamycin-induced wound healing was studied. Nifedipine was administered to animals prior to treating with adriamycin. The healing strengths of cecal, fascial, and skin anatomoses were measured. Animals treated with adriamycin alone had significant decreases in healing strength compared to controls: for cecum at postoperative days (POD) 7 and 14; for skin at PODs 14, 21, and 28; for fascia at POD 28. Overall, nifedipine reduced the impact of adriamycin injury on the strength of healing incisional anastomoses. Nifedipine also appeared to protect collagen synthesis at anastomotic sites from adriamycin-induced impairment.

Animals↗
PubMed2002

SUNCT syndrome: priming of symptomatic periods and worsening of symptoms by treatment with calcium channel blockers.

We report a SUNCT patient who showed both a precipitation and worsening of symptomatic periods after treatment with L-type calcium channel blockers. This pharmacological response may provide us with important clues for understanding the pathophysiology of SUNCT, and hopefully to find a remedy for the victims of this syndrome. This observation could also support a verapamil trial in SUNCT patients as a precipitating of attacks.

Aged↗
PubMed1996

Action of the calcium channel blocker lacidipine on cardiac hypertrophy and endothelin-1 gene expression in stroke-prone hypertensive rats.

1. The tissue-protective effects of calcium channel blockers in hypertension are not well dissociated from their effect on systolic blood pressure (SBP). We have previously shown that lacidipine, a dihydropyridine-type calcium antagonist, reduced the cardiac hypertrophy and the cardiac endothelin-1 (ET-1) gene overexpression occurring in salt-loaded stroke-prone spontaneously hypertensive rats (SL-SHRSP), an effect occurring without systolic blood pressure (SBP) change. In the present study, we have examined whether this action was dose-related and if it could be associated with ET receptor changes. The action of lacidipine was also examined in control SHRSP and in Wistar Kyoto rats (WKY). 2. The daily dose of 0.3 mg kg-1 lacidipine which did not lower SBP but significantly prevented ventricle hypertrophy and cardiac preproET-1-mRNA expression in SL-SHRSP was inactive in control SHRSP. With the higher dose of lacidipine (1 mg kg-1 day-1), we observed a further reduction of cardiac hypertrophy and of ET-1 gene expression in SL-SHRSP and a significant effect on those parameters in control SHRSP but only a small reduction of SBP in both groups. 3. In WKY, salt loading did not induce change in SBP or increase of cardiac ET-1 gene expression and ventricle mass. In these normotensive rats, lacidipine (1 mg kg-1 day-1) did not modulate the basal preproET-1-mRNA expression and did not affect SBP or heart weight. 4. The maximum binding capacity (Bmax) and the dissociation constant (KD) of [125I]-ET-1 binding and the relative proportion of low- and high-affinity binding sites for ET-3 were not significantly affected by salt loading or lacidipine treatment in SHRSP. 5. These results show that lacidipine exerted a dose-related inhibition of ventricle hypertrophy and preproET-1-mRNA expression in SHRSP and indicate that this effect was unrelated to SBP changes. The dose-dependency of this inhibition suggests that salt-induced cardiac hypertrophy could be related to ET-1 gene overexpression. The results further show that ET receptor changes are not involved in the pathophysiological process studied here.

Animals↗
PubMed1998

Effects of local administration of L-, N-, and P/Q-type calcium channel blockers on spontaneous dopamine release in the striatum and the substantia nigra: a microdialysis study in rat.

The pivotal role for voltage-sensitive calcium channels in initiating synaptic transmitter release is undisputed, but it is only partly known to what extent the different subtypes contribute in vivo. Their importance for the dendritic release of dopamine has not been investigated in vivo previously. To evaluate comprehensively the relative importance of different voltage-sensitive calcium channel subtypes for striatal dopamine release, and to further investigate the mechanism of dendritic dopamine release in the reticulate part of substantia nigra, dopamine was measured by in vivo microdialysis in the striatum or substantia nigra of awake rats. The calcium channel blockers nimodipine, omega-conotoxin-GVIA, omega-agatoxin-IVA, and neomycin were administered locally through the dialysis probes and compared with calcium-free perfusion. Results indicate that dopamine release in the striatum is mainly dependent on N- and P/Q-type channels, but the dendritic dopamine release in the substantia nigra is mediated mainly by some other calcium-dependent mechanism, for example, calcium mobilization through T-, O-, or R-type calcium channels. A portion of the dendritic release is calcium independent but can be inhibited partially by neomycin, which might suggest a role for inositol 4,5-bisphosphate breakdown products.

Administration, Topical↗
PubMedDate not supplied

Role of adrenal gland hormones in antiinflammatory effect of calcium channel blockers.

Effects of amlodipine, lacidipine and nicardipine on acute phase of inflammation in the carregeenan model in intact rats were investigated in this study. In addition, the most effective dose of nicardipine that had the highest anti-inflammatory impact was investigated in carregeenan test in adrenalectomized rats. The effective dose of nicardipine was tested in the chronic phase of inflammation in the model of cotton pellet granuloma, and its efficiency was compared with diclofenac sodium. Amlodipine at 5 and 10 mg/kg doses showed 61%, 80%, lacidipine 73%, 34% and nicardipine 38%, 87% inhibition of carrageenan-induced inflammation, respectively. Nicardipine (10 mg/kg) and diclofenac sodium (25 mg/kg) showed 11.6% and 16.2% inhibition, respectively against carrageenan-induced edema. Diclofenac at 10 mg/kg showed 43% inhibition of the inflammation. In cotton pellet test, antiproliferative effects of nicardipine (10 mg/kg) and diclofenac sodium (10 mg/kg) were evaluated as 60% and 39.5%, respectively. The obtained results showed that calcium channel blockers and diclofenac sodium significantly blocked acute and chronic phases of inflammation in intact rats, but in adrenalectomized rats calcium channel blockers and diclofenac sodium had no significant antiinflammatory effect.

Adrenal Glands↗