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Guldbrandsen HO, Staehr C, Iversen NK, et al. Does Src Kinase Mediated Vasoconstriction Impair Penumbral Reperfusion?. Stroke. 2021;52(6):e250-e258doi: 10.1161/STROKEAHA.120.032737.
Guldbrandsen, H. O., Staehr, C., Iversen, N. K., Postnov, D. D., & Matchkov, V. V. (2021). Does Src Kinase Mediated Vasoconstriction Impair Penumbral Reperfusion?. Stroke, 52(6), e250-e258. https://doi.org/10.1161/STROKEAHA.120.032737
Guldbrandsen, Halvor Osterby, et al. "Does Src Kinase Mediated Vasoconstriction Impair Penumbral Reperfusion?." Stroke vol. 52,6 (2021): e250-e258. doi: https://doi.org/10.1161/STROKEAHA.120.032737
Guldbrandsen HO, Staehr C, Iversen NK, Postnov DD, Matchkov VV. Does Src Kinase Mediated Vasoconstriction Impair Penumbral Reperfusion?. Stroke. 2021 Jun;52(6):e250-e258. doi: 10.1161/STROKEAHA.120.032737. Epub 2021 May 05. PMID: 33947213.
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Stroke. 2021 Jun;52(6):e250-e258. doi: 10.1161/STROKEAHA.120.032737. Epub 2021 May 05.

Does Src Kinase Mediated Vasoconstriction Impair Penumbral Reperfusion?.

Stroke

Halvor Osterby Guldbrandsen, Christian Staehr, Nina Kerting Iversen, Dmitry D Postnov, Vladimir V Matchkov

Affiliations

  1. Department of Biomedicine, MEMBRANES, Health (H.O.G., C.S., V.V.M.), Aarhus University, Denmark.
  2. Center of Functionally Integrative Neuroscience, Institute for Clinical Medicine (N.K.I.), Aarhus University, Denmark.
  3. Department of Biomedical Sciences, Faculty of Health and Medical Sciences, Copenhagen University, Denmark (D.D.P.).

PMID: 33947213 DOI: 10.1161/STROKEAHA.120.032737

Abstract

Despite successful recanalization, a significant number of patients with ischemic stroke experience impaired local brain tissue reperfusion with adverse clinical outcome. The cause and mechanism of this multifactorial complication are yet to be understood. At the current moment, major attention is given to dysfunction in blood-brain barrier and capillary blood flow but contribution of exaggerated constriction of cerebral arterioles has also been suggested. In the brain, arterioles significantly contribute to vascular resistance and thus control of perfusion. Accordingly, pathological changes in arteriolar wall function can, therefore, limit sufficient reperfusion in ischemic stroke, but this has not yet received sufficient attention. Although an increased vascular tone after reperfusion has been demonstrated in several studies, the mechanism behind it remains to be characterized. Importantly, the majority of conventional mechanisms controlling vascular contraction failed to explain elevated cerebrovascular tone after reperfusion. We propose here that the Na,K-ATPase-dependent Src kinase activation are the key mechanisms responsible for elevation of cerebrovascular tone after reperfusion. The Na,K-ATPase, which is essential to control intracellular ion homeostasis, also executes numerous signaling functions. Under hypoxic conditions, the Na,K-ATPase is endocytosed from the membrane of vascular smooth muscle cells. This initiates the Src kinase signaling pathway that sensitizes the contractile machinery to intracellular Ca

Keywords: blood-brain barrier; homeostasis; ischemic stroke; reperfusion; smooth muscle; sodium-potassium-exchanging ATPase; src-family kinases

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