Magnesium sulfate suppresses L-type calcium currents on the basilar artery smooth muscle cells in rabbits

Sharma, Naveen; Cho, Dong Hyu; Kim, Sun Young; Bhattarai, Janardhan P.; Hwang, Pyoung Han; Han, Seong Kyu

doi:10.1179/1743132812y.0000000016

Cited by 10 publications

(11 citation statements)

References 38 publications

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“…They extrapolated from their data that serum concentration higher than 3 mmol/L should not be attempted [112]. Recently, Sharma et al [113] investigated, in an animal experimental study, the role of L-type Ca ++ channels in themagnesium-induced relaxation of basilar smooth muscle cells. Their results demonstrate that L-type Ca ++ channels are functionally expressed in rabbit basilar smooth muscle cells, and they suggest that L-type Ca ++ channels may play a pivotal role formagnesium-induced vascular relaxation.…”

Section: Resultsmentioning

confidence: 99%

Cerebral Vasospasm Pharmacological Treatment: An Update

Siasios

Kapsalaki

Fountas

2013

Neurology Research International

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Aneurysmal subarachnoid hemorrhage- (aSAH-) associated vasospasm constitutes a clinicopathological entity, in which reversible vasculopathy, impaired autoregulatory function, and hypovolemia take place, and lead to the reduction of cerebral perfusion and finally ischemia. Cerebral vasospasm begins most often on the third day after the ictal event and reaches the maximum on the 5th–7th postictal days. Several therapeutic modalities have been employed for preventing or reversing cerebral vasospasm. Triple “H” therapy, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators, administration of substances like magnesium sulfate, statins, fasudil hydrochloride, erythropoietin, endothelin-1 antagonists, nitric oxide progenitors, and sildenafil, are some of the therapeutic protocols, which are currently employed for managing patients with aSAH. Intense pathophysiological mechanism research has led to the identification of various mediators of cerebral vasospasm, such as endothelium-derived, vascular smooth muscle-derived, proinflammatory mediators, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Oral, intravenous, or intra-arterial administration of antagonists of these mediators has been suggested for treating patients suffering a-SAH vasospam. In our current study, we attempt to summate all the available pharmacological treatment modalities for managing vasospasm.

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Section: Resultsmentioning

confidence: 99%

Cerebral Vasospasm Pharmacological Treatment: An Update

Siasios

Kapsalaki

Fountas

2013

Neurology Research International

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“…In the cerebral vasculature, Mg exhibits direct effects on large, medium, and small vessels by inhibiting the actions of endothelin-1, neuropeptide Y, and angiotensin II (9, 10). In rabbit models, inhibition of L-type smooth muscle Ca channels suggests a potential role in vasospasm prevention (11). Augmentation of cerebral blood flow via vasodilatation results in improved outcomes following experimental middle cerebral artery occlusion in animal models (12).…”

Section: Pre-clinical Data For Magnesiummentioning

confidence: 99%

Magnesium: Potential Roles in Neurovascular Disease

et al. 2014

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Objective: Magnesium therapy has been studied extensively in pre-clinical and clinical trials in multiple organ systems. Cerebrovascular diseases may benefit from its neuroprotective properties. This review summarizes current studies of magnesium in a wide range of neurovascular diseases.Methods: We searched relevant terms in the National Library of Medicine PubMed database and selected research including basic science, translational reports, meta-analyses, and clinical studies.Results: Studies examining magnesium administration in ischemic stroke have failed to show any benefit in clinical outcome. Data on magnesium for intracerebral hemorrhage (ICH) are limited. Preliminary investigations in subarachnoid hemorrhage (SAH) were promising, but definitive studies did not reveal differences in clinical outcome between magnesium and placebo-treated groups. Studies examining magnesium administration in global ischemia following cardiac arrest suggest a trend toward improved clinical outcome. The strongest evidence for clinically relevant neuroprotection following magnesium administration derives from studies of pre-term infants and patients undergoing cardiac bypass and carotid endarterectomy procedures. Magnesium was found to have an excellent safety profile across all investigations.Conclusion: Magnesium is easy to administer and possesses a favorable safety profile. Its utility as a neuroprotectant in cardiac surgery, carotid endarterectomy, and pre-term infant hypoxia remain promising. Value as a therapeutic agent in ischemic stroke, ICH, and SAH is unclear and appears to be limited by late administration. Ongoing clinical trials assessing magnesium administration in the first hours following symptom onset may help clarify the role of magnesium therapy in these disease processes.

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“…The sustained calcium influx via L-type calcium channels into vascular smooth muscle leads the activation of various second messenger systems that results in vasoconstriction. Magnesium sulfate suppressed the calcium currents through L-type calcium channels in smooth muscle cells isolated from rabbit basilar artery (Sharma et al, 2012). More studies are needed to explore this hypothesis.…”

Section: Magnesium-vasodilation and Potassium Channel Activation On Vascular Smooth Muscle Cellsmentioning

confidence: 98%

Mechanisms of magnesium‐induced vasodilation in cerebral penetrating arterioles

Murata¹,

Dietrich

Horiuchi³

et al. 2015

FASEB j.

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We investigated in cerebral penetrating arterioles the signaling mechanisms and dose-dependency of extracellular magnesium-induced vasodilation and also its vasodilatory effects in vessels preconstricted with agonists associated with delayed cerebral vasospasm following SAH. Male rat penetrating arterioles were cannulated. Their internal diameters were monitored. To investigate mechanisms of magnesium-induced vasodilation, inhibitors of endothelial function, potassium channels and endothelial impairment were tested. To simulate cerebral vasospasm we applied several spasmogenic agonists. Increased extracellular magnesium concentration produced concentration-dependent vasodilation, which was partially attenuated by non-specific calciumsensitive potassium channel inhibitor tetraethylammonium, but not by other potassium channel inhibitors. Neither the nitric oxide synthase inhibitor L-NNA nor endothelial impairment induced by air embolism reduced the dilation. Although the magnesium-induced vasodilation was slightly attenuated by the spasmogen ET-1, neither application of PF 2α nor TXA 2 analog effect the vasodilation. Magnesium induced a concentration-and smooth muscle cell-dependent dilation in cerebral penetrating arterioles. Calcium-sensitive potassium channels of smooth muscle cells may play a key role in magnesium-induced vasodilation. Magnesium also dilated endothelium-impaired vessels as well as vessels preconstricted with spasmogenic agonists. These results provide a fundamental background for the clinical use of magnesium, especially in treatment against delayed cerebral ischemia or vasospasm following SAH.

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Magnesium sulfate suppresses L-type calcium currents on the basilar artery smooth muscle cells in rabbits

Abstract: These results demonstrate that L-type Ca(2+) channels are functionally expressed in rabbit basilar smooth muscle cells and suggest that L-type Ca(2+) channels may play a pivotal role for magnesium-induced relaxation.

Cited by 10 publications

References 38 publications

Cerebral Vasospasm Pharmacological Treatment: An Update

Cerebral Vasospasm Pharmacological Treatment: An Update

Magnesium: Potential Roles in Neurovascular Disease

Mechanisms of magnesium‐induced vasodilation in cerebral penetrating arterioles

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