{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T12:53:11Z","timestamp":1791118391068,"version":"4.1.0"},"reference-count":88,"publisher":"The Endocrine Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The steroid hormone aldosterone is important for salt and water homeostasis as well as for pathological tissue modifications in the cardiovascular system and the kidney. The mechanisms of action include a classical genomic pathway, but physiological relevant nongenotropic effects have also been described. Unlike for estrogens or progesterone, the mechanisms for these nongenotropic effects are not well understood, although pharmacological studies suggest a role for the mineralocorticoid receptor (MR). Here we investigated whether the MR contributes to nongenotropic effects. After transfection with human MR, aldosterone induced a rapid and dose-dependent phosphorylation of ERK1\/2 and c-Jun NH2-terminal kinase (JNK) 1\/2 kinases in Chinese hamster ovary or human embryonic kidney cells, which was reduced by the MR-antagonist spironolactone and involved cSrc kinase as well as the epidermal growth factor receptor. In primary human aortic endothelial cells, similar results were obtained for ERK1\/2 and JNK1\/2. Inhibition of MAPK kinase (MEK) kinase but not of protein kinase C prevented the rapid action of aldosterone and also reduced aldosterone-induced transactivation, most probably due to impaired nuclear-cytoplasmic shuttling of MR. Cytosolic Ca2+ was increased by aldosterone in mock- and in human MR-transfected cells to the same extend due to Ca2+ influx, whereas dexamethasone had virtually no effect. Spironolactone did not prevent the Ca2+ response. We conclude that some nongenotropic effects of aldosterone are MR dependent and others are MR independent (e.g. Ca2+), indicating a higher degree of complexity of rapid aldosterone signaling. According to this model, we have to distinguish three aldosterone signaling pathways: 1) genomic via MR, 2) nongenotropic via MR, and 3) nongenotropic MR independent.<\/jats:p>","DOI":"10.1210\/me.2004-0469","type":"journal-article","created":{"date-parts":[[2005,3,10]],"date-time":"2005-03-10T21:53:52Z","timestamp":1110491632000},"page":"1697-1710","source":"Crossref","is-referenced-by-count":164,"title":["Human Mineralocorticoid Receptor Expression Renders Cells Responsive for Nongenotropic Aldosterone Actions"],"prefix":"10.1210","volume":"19","author":[{"given":"Claudia","family":"Grossmann","sequence":"first","affiliation":[{"name":"Physiologisches Institut der Universita\u0308t Wu\u0308rzburg (C.G., A.B., R.F., S.M., B.G., M.G.), 97070 Wu\u0308rzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Benesic","sequence":"additional","affiliation":[{"name":"Physiologisches Institut der Universita\u0308t Wu\u0308rzburg (C.G., A.B., R.F., S.M., B.G., M.G.), 97070 Wu\u0308rzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander W.","family":"Krug","sequence":"additional","affiliation":[{"name":"Universita\u0308tsklinikum, Medical Clinic (A.W.K.), Technical University Dresden, 01062 Dresden, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth","family":"Freudinger","sequence":"additional","affiliation":[{"name":"Physiologisches Institut der Universita\u0308t Wu\u0308rzburg (C.G., A.B., R.F., S.M., B.G., M.G.), 97070 Wu\u0308rzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sigrid","family":"Mildenberger","sequence":"additional","affiliation":[{"name":"Physiologisches Institut der Universita\u0308t Wu\u0308rzburg (C.G., A.B., R.F., S.M., B.G., M.G.), 97070 Wu\u0308rzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Birgit","family":"Gassner","sequence":"additional","affiliation":[{"name":"Physiologisches Institut der Universita\u0308t Wu\u0308rzburg (C.G., A.B., R.F., S.M., B.G., M.G.), 97070 Wu\u0308rzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Gekle","sequence":"additional","affiliation":[{"name":"Physiologisches Institut der Universita\u0308t Wu\u0308rzburg (C.G., A.B., R.F., S.M., B.G., M.G.), 97070 Wu\u0308rzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","reference":[{"key":"2020071614154513300_R1","doi-asserted-by":"crossref","first-page":"877","DOI":"10.1146\/annurev.physiol.64.082101.143243","article-title":"Epithelial sodium channel and the control of sodium balance: interaction between genetic and environmental factors.","volume":"64","author":"Rossier","year":"2002","journal-title":"Annu Rev Physiol"},{"key":"2020071614154513300_R2","doi-asserted-by":"crossref","first-page":"1002","DOI":"10.1046\/j.1440-1681.2001.03586.x","article-title":"Mineralocorticoids and cardiac fibrosis: the decade in review.","volume":"28","author":"Funder","year":"2001","journal-title":"Clin Exp Pharmacol Physiol"},{"key":"2020071614154513300_R3","doi-asserted-by":"crossref","first-page":"677","DOI":"10.1016\/S0272-6386(01)80115-3","article-title":"Aldosterone as a mediator of progressive renal disease: pathogenetic and clinical implications.","volume":"37","author":"Epstein","year":"2001","journal-title":"Am J Kidney Dis"},{"key":"2020071614154513300_R4","doi-asserted-by":"crossref","first-page":"378","DOI":"10.1177\/014107680109400803","article-title":"Aldosterone as a determinant of cardiovascular and renal dysfunction.","volume":"94","author":"Epstein","year":"2001","journal-title":"J R Soc Med"},{"key":"2020071614154513300_R5","doi-asserted-by":"crossref","first-page":"351","DOI":"10.1016\/S0735-1097(01)01729-6","article-title":"Addition of spironolactone to angiotensin-converting enzyme inhibition in heart failure improves endothelial vasomotor dysfunction.","volume":"39","author":"Bauersachs","year":"2002","journal-title":"J Am Coll Cardiol"},{"key":"2020071614154513300_R6","doi-asserted-by":"crossref","first-page":"1791","DOI":"10.1046\/j.1523-1755.2003.00929.x","article-title":"Aldosterone\/salt induces renal inflammation and fibrosis in hypertensive rats.","volume":"63","author":"Blasi","year":"2003","journal-title":"Kidney Int"},{"key":"2020071614154513300_R7","doi-asserted-by":"crossref","first-page":"709","DOI":"10.1056\/NEJM199909023411001","article-title":"The effect of spironolactone on morbidity and mortality in patients with severe heart failure. 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