{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:50:33Z","timestamp":1771627833523,"version":"3.50.1"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1989,3,1]],"date-time":"1989-03-01T00:00:00Z","timestamp":604713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1989,3]]},"abstract":"<jats:p>1. Conventional microelectrodes, the Na+ channel blocker amiloride (0.1 mM), and the K+ channel blocker tetraethylammonium chloride (TEA, 30 mM) were used to examine the effects of corticosteroid hormones administered in vivo on the Na+ and K+ transport properties of isolated rat distal colon. The cell membrane changes induced by aldosterone (a specific mineralocorticoid), RU 28362 (a synthetic glucocorticoid with negligible affinity for mineralocorticoid receptors), and dexamethasone (an activator of both mineralocorticoid and glucocorticoid receptors) were compared. 2. In control animals, there was no amiloride\u2010sensitive apical Na+ conductance, and only a relatively small TEA\u2010sensitive apical K+ conductance. 3. Hyperaldosteronism secondary to dietary Na+ depletion for 10\u201014 days, dexamethasone (600 micrograms 100 g\u20101 day\u20101 for 3 days), and RU 28362 (600 micrograms 100 g\u20101 day\u20101 for 3 days) induced amiloride\u2010sensitive electrogenic Na+ transport, with the potency of aldosterone greater than dexamethasone greater than RU 28362. 4. With each corticosteroid, increased electrogenic Na+ transport reflected enhanced apical Na+ conductance, and in the case of aldosterone and dexamethasone, 3.3\u2010fold and 2\u2010fold increases respectively in the maximum activity of the basolateral Na+\u2010K+ pump. In contrast, RU 28362 suppressed the maximum activity of the basolateral Na+\u2010K+ pump by 45%. 5. All three corticosteroids enhanced the K+ conductance of the apical membrane, with the potency of aldosterone greater than dexamethasone greater than RU 28362. 6. Co\u2010administration of spironolactone (5 mg 100 g\u20101 day\u20101) inhibited the effects of aldosterone on Na+ and K+ transport, but in dexamethasone\u2010treated animals spironolactone resulted in a pattern of response similar to that found in RU 28362\u2010treated animals. 7. The results support the view that mineralocorticoid receptors mediate changes in colonic Na+ and K+ transport which differ quantitatively and qualitatively from those mediated by glucocorticoid receptors. Dexamethasone and similar \u2018glucocorticoids\u2019 activate both types of receptor, with an overall epithelial response which mimics that induced by aldosterone.<\/jats:p>","DOI":"10.1113\/jphysiol.1989.sp017542","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T03:36:58Z","timestamp":1418960218000},"page":"425-441","source":"Crossref","is-referenced-by-count":40,"title":["Effects of corticosteroid hormones on the electrophysiology of rat distal colon: implications for Na+ and K+ transport."],"prefix":"10.1113","volume":"410","author":[{"given":"H J","family":"Binder","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F","family":"McGlone","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G I","family":"Sandle","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1989,3]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1989.sp017542","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1989.sp017542","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,22]],"date-time":"2023-10-22T00:55:11Z","timestamp":1697936111000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1989.sp017542"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1989,3]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1989,3]]}},"alternative-id":["10.1113\/jphysiol.1989.sp017542"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1989.sp017542","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1989,3]]}}}