{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T16:36:09Z","timestamp":1791477369158,"version":"4.3.4"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2020,3,26]],"date-time":"2020-03-26T00:00:00Z","timestamp":1585180800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"National Health and Medical Research Council of Australia","award":["GNT1064686"],"award-info":[{"award-number":["GNT1064686"]}]},{"name":"National Health and Medical Research Council of Australia","award":["GNT1085323"],"award-info":[{"award-number":["GNT1085323"]}]},{"DOI":"10.13039\/501100000925","name":"NHMRC","doi-asserted-by":"publisher","award":["GNT1079467"],"award-info":[{"award-number":["GNT1079467"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,2,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>The G protein-coupled estrogen receptor 1 (GPER) may modulate some effects of aldosterone. In addition, G-1 (a GPER agonist) can lower blood pressure (BP) and promote T cell-mediated anti-inflammatory responses. This study aimed to test the effects of G-1 and G-15 (a GPER antagonist) on aldosterone-induced hypertension in mice and to examine the cellular mechanisms involved.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>C57Bl\/6 (wild-type, WT), RAG1-deficient and GPER-deficient mice were infused with vehicle, aldosterone (0.72\u2009mg\/kg\/day S.C. plus 0.9% NaCl for drinking) \u00b1 G-1 (0.03\u2009mg\/kg\/day S.C.) \u00b1 G-15 (0.3\u2009mg\/kg\/day S.C.) for 14 days. G-1 attenuated aldosterone-induced hypertension in male WT but not male GPER-deficient mice. G-15 alone did not alter hypertension but it prevented the anti-hypertensive effect of G-1. In intact female WT mice, aldosterone-induced hypertension was markedly delayed and suppressed compared with responses in males, with BP remaining unchanged until after Day 7. In contrast, co-administration of aldosterone and G-15 fully increased BP within 7 days in WT females. Similarly, aldosterone robustly increased BP by Day 7 in ovariectomized WT females, and in both sexes of GPER-deficient mice. Whereas aldosterone had virtually no effect on BP in RAG1-deficient mice, adoptive transfer of T cells from male WT or male GPER-deficient mice into male RAG1-deficient mice restored the pressor response to aldosterone. This pressor effect could be attenuated by G-1 in RAG1-deficient mice that were reconstituted with either WT or GPER-deficient T cells, suggesting that G-1 does not act via T cells to lower BP.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings indicate that although aldosterone-induced hypertension is largely mediated by T cells, it can be attenuated by activation of GPER on non-T cells, which accounts for the sex difference in sensitivity to the pressor effect.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvaa075","type":"journal-article","created":{"date-parts":[[2020,3,20]],"date-time":"2020-03-20T08:25:59Z","timestamp":1584692759000},"page":"960-970","source":"Crossref","is-referenced-by-count":29,"title":["Aldosterone-induced hypertension is sex-dependent, mediated by T cells and sensitive to GPER activation"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2585-7329","authenticated-orcid":false,"given":"Quynh Nhu","family":"Dinh","sequence":"first","affiliation":[{"name":"Department of Physiology, Anatomy and Microbiology and Centre for Cardiovascular Biology and Disease Research, School of Life Sciences, La Trobe University, Bundoora, VIC 3086, Australia"},{"name":"Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Clayton, VIC 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8367-6134","authenticated-orcid":false,"given":"Antony","family":"Vinh","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Microbiology and Centre for Cardiovascular Biology and Disease Research, School of Life Sciences, La Trobe University, Bundoora, VIC 3086, Australia"},{"name":"Cardiovascular Disease 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Disease Program, Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Clayton, VIC 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7079-625X","authenticated-orcid":false,"given":"Courtney P","family":"Judkins","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Microbiology and Centre for Cardiovascular Biology and Disease Research, School of Life Sciences, La Trobe University, Bundoora, VIC 3086, Australia"},{"name":"Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Clayton, VIC 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8556-9738","authenticated-orcid":false,"given":"Grant R","family":"Drummond","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Microbiology and Centre for Cardiovascular 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