Calcium-channel blockers in the treatment of migraine

Gelmers, H. J.

doi:10.1016/0002-9149(85)90622-8

Cited by 49 publications

(23 citation statements)

References 26 publications

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“…As an example, nimodipine has been used as a neurological therapeutic to reduce vasospasm associated with subarachnoid hemorrhage (Allen et al, 1983). Through blockade of calcium channels, dihydropyridines have primarily been used to reduce cardiovascular symptoms of hypertension and angina, treat bipolar disorder and alleviate migraine (Gelmers, 1985; Goodnick, 2000; Rosendorff, 2007). In addition, recent studies reviewing the incidence of Parkinson’s disease revealed a risk reduction for individuals taking centrally acting L-type calcium channel blockers (Becker et al 2008, Ritz et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Progesterone blocks multiple routes of ion flux

Kelley

Mermelstein

2011

Molecular and Cellular Neuroscience

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The administration of progesterone as a neuroprotective agent following traumatic brain injury has recently entered phase III clinical trials. Previous work has demonstrated that therapeutic concentrations of progesterone decrease excitotoxicity through direct inhibition of voltage-gated calcium channels, an action independent of the nuclear progesterone receptor. Here we report using cultured rat striatal neurons that these same concentrations of progesterone also block voltage-gated potassium channels, sodium channels and GABAA currents. The actions of progesterone act at the surface membrane of neurons in a steroid specific, voltage-independent, concentration-dependent manner. Notably, these broad actions of progesterone on ion channel and neurotransmitter receptor function mirror those of dihydropyridines, and indicate potential shared mechanisms of action, the prospective of additional therapeutic applications, and possibly, untoward effects.

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Section: Discussionmentioning

confidence: 99%

Progesterone blocks multiple routes of ion flux

Kelley

Mermelstein

2011

Molecular and Cellular Neuroscience

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“…Nimodipine is a dihydropyridine calcium antagonist with therapeutic indications for cerebrovascular spasm, stroke, and migraine (1,2). Nowadays, nimodipine is administered by oral soft capsules and capsules clinically; however, there are several unfavorable properties which limited their clinical efficacy, including the low bioavailability, large dosage and many adverse effects (3,4).…”

Section: Introductionmentioning

confidence: 99%

Liquid Proliposomes of Nimodipine Drug Delivery System: Preparation, Characterization, and Pharmacokinetics

Sun

Liu

et al. 2013

AAPS PharmSciTech

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Abstract. To investigate the possibility of liquid proliposomes being carriers for oral delivery, nimodipine liquid proliposomes-based soft capsules (NPSC) were prepared. Nimodipine proliposomes were characterized by transmission electron microscopy (TEM), conversion rate from proliposomes to liposomes, entrapment efficiency, particle size, and zeta potential. Accelerated stability testing of NPSC was carried out for 3 months at 40±2°C, 75±5% RH. The concentration of nimodipine in plasma of New Zealand rabbits of NPSC, nimodipine soft capsules, and hydrated liposomes was studied. Results showed that nimodipine proliposomes were automatically converted into liposomes when exposed to a water phase in 30 s. The average diameter was 378.6±26.5 nm in distilled water with entrapment efficiency (EE%) of 84.7±5.9%, while the average diameter was 316.9±34.6 nm in 0.1 M hydrochloric acid solution with EE% of 72.8±4.7%. Accelerated stability test showed that there was no change in drug content, particle size, and EE% except for a decrease in dissolution of nimodipine. In vivo experiments, areas under the plasma level-time curve of NPSC and nimodipine-hydrated liposomes increased 2.41 and 2.34 times more than that of nimodipine soft capsules, peak concentration increased 2.87 and 2.92 times, time of peak concentration from 0.75 to 2 and 1 h, respectively. Nimodipine-hydrated liposomes presented similar pharmacokinetic parameters compared with NPSC. Results suggested that NPSC offered a potential way to improve oral delivery of nimodipine.

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“…Cellular hypoxia, in turn, can cause an increase in the flow of calcium from the extracellular fluid to the intracellular space, resulting in calcium overload and cellular dysfunction. The piperazine derivative flunarizine, a non-selective calcium antagonist [17], shown in many controlled clinical studies to be effective in migraine prophylaxis [18–26], has been found to protect brain tissue against hypoxic damage [27]. Therefore, the purpose of this study is to explore whether cerebral mitochondrial injury is related to CSD under both normoxic and hypoxic conditions and to find whether flunarizine has a protective effect on cerebral mitochondria.…”

Section: Introductionmentioning

confidence: 99%

Protection of flunarizine on cerebral mitochondria injury induced by cortical spreading depression under hypoxic conditions

Qiu

Dong

et al. 2011

J Headache Pain

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A rat cortical spreading depression (CSD) model was established to explore whether cerebral mitochondria injury was induced by CSD under both normoxic and hypoxic conditions and whether flunarizine had a protective effect on cerebral mitochondria. SD rats, which were divided into seven groups, received treatment as follows: no intervention (control Group I); 1 M NaCl injections (Group II); 1 M KCl injections (Group III); intraperitoneal flunarizine (3 mg/kg) 30 min before KCl injections (Group IV); 14% O2 inhalation before NaCl injections (Group V); 14% O2 inhalation followed by KCl injections (Group VI); 14% O2 inhalation and intraperitoneal flunarizine followed by KCl injections (Group VII). Following treatment, brains were removed for the analysis of mitochondria transmembrane potential (MMP) and oxidative respiratory function after recording the number, amplitude and duration of CSD. The duration of CSD was significantly longer in Group VI than that in Group III. The number and duration of CSD in Group VII was significantly lower than that in Group VI. MMP in Group VI was significantly lower than that in Group III, and MMP in Group VII was significantly higher than that in Group VI. State 4 respiration in Group VI was significantly higher than that in Group III, and state 3 respiration in Group VII was significantly higher than that in Group VI. Respiration control of rate in Group VII was also significantly higher than that in Group VI. Thus, we concluded that aggravated cerebral mitochondria injury might be attributed to CSD under hypoxic conditions. Flunarizine can alleviate such cerebral mitochondria injury under both normoxic and hypoxic conditions.

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Calcium-channel blockers in the treatment of migraine

Cited by 49 publications

References 26 publications

Progesterone blocks multiple routes of ion flux

Progesterone blocks multiple routes of ion flux

Liquid Proliposomes of Nimodipine Drug Delivery System: Preparation, Characterization, and Pharmacokinetics

Protection of flunarizine on cerebral mitochondria injury induced by cortical spreading depression under hypoxic conditions

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