Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia
Healthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion cha...
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | Stroke Research and Treatment |
| Online Access: | http://dx.doi.org/10.1155/2012/382146 |
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| author | Marcel A. Kamp Maxine Dibué Toni Schneider Hans-Jakob Steiger Daniel Hänggi |
| author_facet | Marcel A. Kamp Maxine Dibué Toni Schneider Hans-Jakob Steiger Daniel Hänggi |
| author_sort | Marcel A. Kamp |
| collection | DOAJ |
| description | Healthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion channel expression and function is initiated, with acute and long-term effects differing from each other. Initial hypoperfusion after exposure of cerebral vessels to oxyhemoglobin correlates with a suppression of voltage-gated potassium channel activity, whereas delayed cerebral vasospasm involves changes in other potassium channel and voltage-gated calcium channels expression and function. Furthermore, expression patterns and function of ion channels appear to differ between main and small peripheral vessels, which may be key in understanding mechanisms behind subarachnoid hemorrhage-induced vasospasm. Here, changes in calcium and potassium channel expression and function in animal models of subarachnoid hemorrhage and transient global ischemia are systematically reviewed and their clinical significance discussed. |
| format | Article |
| id | doaj-art-c9cf5e03b4974e33bd6bfedaf05d088e |
| institution | OA Journals |
| issn | 2090-8105 2042-0056 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Stroke Research and Treatment |
| spelling | doaj-art-c9cf5e03b4974e33bd6bfedaf05d088e2025-08-20T02:19:35ZengWileyStroke Research and Treatment2090-81052042-00562012-01-01201210.1155/2012/382146382146Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global IschemiaMarcel A. Kamp0Maxine Dibué1Toni Schneider2Hans-Jakob Steiger3Daniel Hänggi4Department for Neurosurgery, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, GermanyDepartment for Neurosurgery, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, GermanyInstitute for Neurophysiology, University of Cologne, Robert-Koch-Straße 39, 50931 Cologne, GermanyDepartment for Neurosurgery, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, GermanyDepartment for Neurosurgery, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, GermanyHealthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion channel expression and function is initiated, with acute and long-term effects differing from each other. Initial hypoperfusion after exposure of cerebral vessels to oxyhemoglobin correlates with a suppression of voltage-gated potassium channel activity, whereas delayed cerebral vasospasm involves changes in other potassium channel and voltage-gated calcium channels expression and function. Furthermore, expression patterns and function of ion channels appear to differ between main and small peripheral vessels, which may be key in understanding mechanisms behind subarachnoid hemorrhage-induced vasospasm. Here, changes in calcium and potassium channel expression and function in animal models of subarachnoid hemorrhage and transient global ischemia are systematically reviewed and their clinical significance discussed.http://dx.doi.org/10.1155/2012/382146 |
| spellingShingle | Marcel A. Kamp Maxine Dibué Toni Schneider Hans-Jakob Steiger Daniel Hänggi Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia Stroke Research and Treatment |
| title | Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia |
| title_full | Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia |
| title_fullStr | Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia |
| title_full_unstemmed | Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia |
| title_short | Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia |
| title_sort | calcium and potassium channels in experimental subarachnoid hemorrhage and transient global ischemia |
| url | http://dx.doi.org/10.1155/2012/382146 |
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