ArticleActa neurochirurgica. Supplement2013
SAH-induced suppression of voltage-gated K(+) (K (V)) channel currents in parenchymal arteriolar myocytes involves activation of the HB-EGF/EGFR pathway.
Article in Acta neurochirurgica. Supplement, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Causal association between gut microbiomes and different types of aneurysms: a Mendelian randomization study.Frontiers in microbiology · 2024Article
- Cerebral Autoregulation in Subarachnoid Hemorrhage.Frontiers in neurology · 2021Review
- Anti-vasospastic Effects of Epidermal Growth Factor Receptor Inhibitors After Subarachnoid Hemorrhage in Mice.Molecular neurobiology · 2019Article
- Cerebral artery myogenic reactivity: The next frontier in developing effective interventions for subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- The yin and yang of KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Effect of subarachnoid hemorrhage on voltage-dependence calcium channel current in cerebral artery smooth muscle cells.International journal of clinical and experimental medicine · 2015Article
- Subarachnoid hemorrhage: a review of experimental studies on the microcirculation and the neurovascular unit.Translational stroke research · 2014Review
- Controversies and evolving new mechanisms in subarachnoid hemorrhage.Progress in neurobiology · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Potassium channels play an important role in the regulation of arterial tone, and decreased activity of these ion channels has been linked to pial artery vasospasm after subarachnoid hemorrhage (SAH). Our previous work has shown that acute application of a blood component, oxyhemoglobin, caused suppression of voltage-gated K(+) (K(V)) channels through heparin-binding epidermal growth factor-like growth factor (HB-EGF)-mediated activation of epidermal growth factor receptor (EGFR). Using patch clamp electrophysiology, we have now examined whether this pathway of K(V) channel suppression is activated in parenchymal arteriolar myocytes following long-term in vivo exposure to subarachnoid blood. We have found that K(V) currents, but not large conductance Ca(2+) activated or inwardly rectifying K(+) channel currents, were decreased in parenchymal arteriolar myocytes freshly isolated from day 5 SAH model rabbits. Interestingly, parenchymal arteriolar myocytes from control animals were more sensitive to exogenous HB-EGF (half-maximal inhibitory concentration [IC(50)] 0.2 ± 0.4 ng/ml) compared to pial arterial myocytes (IC(50) 2.4 ± 1.3 ng/ml). However, HB-EGF and oxyhemoglobin failed to decrease K(V) currents in parenchymal arteriolar myocytes from SAH animals, consistent with EGFR activation and K(V) current suppression by SAH. These data suggest that HB-EGF/EGFR pathway activation contributes to K(V) current suppression and enhanced parenchymal arteriolar constriction after SAH.
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