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G protein-coupled estrogen receptor agonist, G-1, attenuates BK channel activation in cerebral arterial smooth muscle cells.

Title: The G protein-coupled estrogen receptor agonist, G-1, attenuates BK channel activation in cerebral arterial smooth muscle cells.
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Name(s): Evanson, Kirk W, author
Goldsmith, Jacob A, author
Ghosh, Payal, author
Delp, Michael D, author
Type of Resource: text
Genre: Journal Article
Text
Date Issued: 2018-06-21
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: The G protein-coupled estrogen receptor (GPER) is a significant modulator of arterial contractility and blood flow. The GPER-specific activator, G-1, has been widely used to characterize GPER function in a variety of tissue types. Large conductance, calcium (Ca)-activated K (BK) channels are sensitive to 17β-estradiol (17β-E2) and estrogenic compounds (e.g., tamoxifen, ICI 182 780) that target estrogen receptors. The purpose of this study was to investigate the effects of G-1 on BK channel activation and function in cerebral arterial myocytes. Inside-out and perforated patch clamp were utilized to assess the effects of G-1 (50 nmol·L-5 μmol·L) on BK channel activation and currents in cerebral arterial myocytes. Pressurized artery myography was used to investigate the effects of G-1 on vasodilatory response and BK channel function of cerebral resistance size arteries. G-1 reduced BK channel activation in cerebral arterial myocytes through elevations in BK channel mean close times. Depressed BK channel activation following G-1 application resulted in attenuated physiological BK currents (transient BK currents). G-1 elicited vasodilation, but reduced BK channel function, in pressurized, endothelium-denuded cerebral arteries. These data suggest that G-1 directly suppresses BK channel activation and currents in cerebral arterial myocytes, BK channels being critically important in the regulation of myocyte membrane potential and arterial contractility. Thus, GPER-mediated vasodilation using G-1 to activate the receptor may underestimate the physiological function and relevance of GPER in the cardiovascular system.
Identifier: FSU_pmch_29938113 (IID), 10.1002/prp2.409 (DOI), PMC6011940 (PMCID), 29938113 (RID), 29938113 (EID), PRP2409 (PII)
Keywords: BK channel, BKca channel, GPER1, GPR30, G‐1, Estrogen receptor
Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6011940.
Persistent Link to This Record: http://purl.flvc.org/fsu/fd/FSU_pmch_29938113
Host Institution: FSU
Is Part Of: Pharmacology research & perspectives.
2052-1707
Issue: iss. 4, vol. 6

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Evanson, K. W., Goldsmith, J. A., Ghosh, P., & Delp, M. D. (2018). The G protein-coupled estrogen receptor agonist, G-1, attenuates BK channel activation in cerebral arterial smooth muscle cells. Pharmacology Research & Perspectives. Retrieved from http://purl.flvc.org/fsu/fd/FSU_pmch_29938113