Nimodipine - CAS 66085-59-4
Catalog number: 66085-59-4
Category: Inhibitor
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Calcium Channel
Nimodipine is a dihydropyridine derivative and an analogue of the calcium channel blocker nifedipine, with antihypertensive activity.Nimodipine decreases intracellular free Ca2+,Beclin-1 and autophagy.
LY127809; LY 127809; LY-127809; Nimodipine, Nimotop, Periplum, BAY E 9736, BAY-E-9736, BAYE9736
Canonical SMILES:
1.A Systematic Review of Diuretics in the Medical Management of Ménière's Disease.
Crowson MG1, Patki A2, Tucci DL2. Otolaryngol Head Neck Surg. 2016 Mar 1. pii: 0194599816630733. [Epub ahead of print]
OBJECTIVE: (1) Review evidence for the use of oral diuretic medications in the management of Ménière's disease. (2) Analyze therapy-related hearing and vertigo outcomes.
2.Is intra arterial nimodipine really beneficial in vasospasm following aneurysmal subarachnoid haemorrhage?
Goel R1, Aggarwal A1, Salunke P1, Kumar A2, Chhabra R1. Br J Neurosurg. 2016 Mar 21:1-4. [Epub ahead of print]
Object/Background: Vasospasm is a common cause of mortality and morbidity following rupture of intracranial aneurysm. Hemodynamic therapy instituted in these patients in the past has been replaced by direct manipulation of the spastic vessels by angioplasty and intra-arterial infusion of vasodilators. However, no case control studies exist proving its superiority. The purpose of our study was to compare the efficacy of intra-arterial nimodipine (IAN) to that of hemodynamic therapy in patients with vasospasm following aSAH.
3.Endovascular therapy for vasospasm after aneurysmatic subarachnoid hemorrhage.
Kerz T1, Boor S2, Ulrich A3, Beyer C1, Hechtner M4, Mueller-Forell W2. Br J Neurosurg. 2016 Apr 15:1-5. [Epub ahead of print]
INTRODUCTION: Balloon angioplasty and/or selective intra-arterial vasodilator therapies are treatment options in patients with vasospasm after subarachnoid hemorrhage (SAH). We analyzed the effect of balloon angioplasty and/or selective intra-arterial vasodilator therapy in our patients.
4.Sequential ionic and conformational signaling by calcium channels drives neuronal gene expression.
Li B1, Tadross MR2, Tsien RW3. Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.
Voltage-gated CaV1.2 channels (L-type calcium channel α1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VΔC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VΔC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VΔC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VΔC by 10 to 20 seconds. CaV1.2 VΔC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VΔC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VΔC signaling is vital to the function of CaV1.
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CAS 66085-59-4 Nimodipine

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