{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T23:55:36Z","timestamp":1789170936098,"version":"build-2803163510"},"reference-count":66,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,10,11]],"date-time":"2022-10-11T00:00:00Z","timestamp":1665446400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["#FS\/18\/41\/33762"],"award-info":[{"award-number":["#FS\/18\/41\/33762"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["FS\/18\/41\/33762"],"award-info":[{"award-number":["FS\/18\/41\/33762"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Purpose<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Kcnq<\/jats:italic>\n                      \u2010encoded K\n                      <jats:sub>V<\/jats:sub>\n                      7 channels (termed K\n                      <jats:sub>V<\/jats:sub>\n                      7.1\u20135) regulate vascular smooth muscle cell (VSMC) contractility at rest and as targets of receptor\u2010mediated responses. However, the current data are mostly derived from males. Considering the known effects of sex, the oestrous cycle and sex hormones on vascular reactivity, here we have characterised the molecular and functional properties of K\n                      <jats:sub>V<\/jats:sub>\n                      7 channels from renal and mesenteric arteries from female Wistar rats separated into di\u2010oestrus and met\u2010oestrus (F\u2010D\/M) and pro\u2010oestrus and oestrus (F\u2010P\/E).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      RT\u2010qPCR, immunocytochemistry, proximity ligation assay and wire myography were performed in renal and mesenteric arteries. Circulating sex hormone concentrations were determined by liquid chromatography\u2013tandem mass spectrometry. Whole\u2010cell electrophysiology was undertaken on cells expressing K\n                      <jats:sub>V<\/jats:sub>\n                      7.4 channels in association with G\u2010protein\u2010coupled oestrogen receptor 1 (GPER1).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      The K\n                      <jats:sub>V<\/jats:sub>\n                      7.2\u20135 activators S\u20101 and ML213 and the pan\u2010K\n                      <jats:sub>V<\/jats:sub>\n                      7 inhibitor linopirdine were more effective in arteries from F\u2010D\/M compared with F\u2010P\/E animals. In VSMCs isolated from F\u2010P\/E rats, exploratory evidence indicates reduced membrane abundance of K\n                      <jats:sub>V<\/jats:sub>\n                      7.4 but not K\n                      <jats:sub>V<\/jats:sub>\n                      7.1, K\n                      <jats:sub>V<\/jats:sub>\n                      7.5 and Kcne4 when compared with cells from F\u2010D\/M. Plasma oestradiol was higher in F\u2010P\/E compared with F\u2010D\/M, and progesterone showed the converse pattern. Oestradiol\/GPER1 agonist G\u20101 diminished K\n                      <jats:sub>V<\/jats:sub>\n                      7.4 encoded currents and ML213 relaxations and reduced the membrane abundance of K\n                      <jats:sub>V<\/jats:sub>\n                      7.4 and interaction between K\n                      <jats:sub>V<\/jats:sub>\n                      7.4 and heat shock protein 90 (HSP90), in arteries from F\u2010D\/M but not F\u2010P\/E.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      GPER1 signalling decreased K\n                      <jats:sub>V<\/jats:sub>\n                      7.4 membrane abundance in conjunction with diminished interaction with HSP90, giving rise to a \u2018pro\u2010contractile state\u2019.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.15947","type":"journal-article","created":{"date-parts":[[2022,9,9]],"date-time":"2022-09-09T23:20:06Z","timestamp":1662765606000},"page":"174-193","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Marked oestrous cycle\u2010dependent regulation of rat arterial K\n                    <sub>V<\/sub>\n                    7.4 channels driven by GPER1"],"prefix":"10.1111","volume":"180","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3796-6090","authenticated-orcid":false,"given":"Samuel N.","family":"Baldwin","sequence":"first","affiliation":[{"name":"Vascular Biology Research Centre, Institute of Molecular and Clinical Sciences St George's University of London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth A.","family":"Forrester","sequence":"additional","affiliation":[{"name":"Vascular Biology Research Centre, Institute of Molecular and Clinical Sciences St George's University of London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalie Z. M.","family":"Homer","sequence":"additional","affiliation":[{"name":"Mass Spectrometry Core Laboratory, Edinburgh Clinical Research Facility, Queen's Medical Research Institute University of Edinburgh  Edinburgh UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6916-2994","authenticated-orcid":false,"given":"Ruth","family":"Andrew","sequence":"additional","affiliation":[{"name":"Mass Spectrometry Core Laboratory, Edinburgh Clinical Research Facility, Queen's Medical Research Institute University of Edinburgh  Edinburgh UK"},{"name":"BHF Centre for Cardiovascular Science, Queen's Medical Research Institute University of Edinburgh  Edinburgh UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincenzo","family":"Barrese","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Reproductive Sciences and Dentistry University of Naples Federico II  Naples Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer B.","family":"Stott","sequence":"additional","affiliation":[{"name":"Vascular Biology Research Centre, Institute of Molecular and Clinical Sciences St George's University of London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7692-6294","authenticated-orcid":false,"given":"Brant E.","family":"Isakson","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology and Biophysics, Robert M. 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