{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:12:55Z","timestamp":1765545175532},"reference-count":24,"publisher":"The Endocrine Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>There is increasing evidence that the trigger for cardiac fibrosis in response to mineralocorticoid\/salt administration is coronary vasculitis and that effects can be seen within days of deoxycorticosterone acetate (DOCA) administration. Furthermore, rapid, nongenomic mineralocorticoid effects on the sodium-hydrogen exchanger (NHE-1) in vascular smooth muscle cells have recently been described. That this mechanism may act as an inflammatory or profibrotic signal was tested by comparing the specific NHE-1 antagonist cariporide and the mineralocorticoid receptor antagonist K canrenoate in the rat model of mineralocorticoid\/salt perivascular fibrosis over 8 d of DOCA\/salt administration. Interstitial collagen, inflammatory cell infiltration, and inflammatory markers were determined. DOCA elevated blood pressure above control, cariporide +DOCA, or K canrenoate +DOCA rats, without cardiac hypertrophy. At 8 d interstitial collagen was significantly elevated in the DOCA-alone group, with levels in cariporide- and K canrenoate-treated rats not different from control. Expression of osteopontin, cyclooxygenase-2, and ED-1 were elevated by DOCA treatment, blocked by potassium canrenoate, and (for ED-1 and osteopontin) partially reduced by cariporide. These results suggest mineralocorticoid\/salt-induced cardiac fibrosis may involve coronary vascular smooth muscle cell NHE-1 activity as a possible contributor to the cascade of transcriptional events that produce the characteristic coronary vasculitis seen with excess mineralocorticoid and salt.<\/jats:p>","DOI":"10.1210\/en.2003-0039","type":"journal-article","created":{"date-parts":[[2003,6,4]],"date-time":"2003-06-04T01:24:40Z","timestamp":1054689880000},"page":"3848-3851","source":"Crossref","is-referenced-by-count":40,"title":["Mineralocorticoid Action and Sodium-Hydrogen Exchange: Studies in Experimental Cardiac Fibrosis"],"prefix":"10.1210","volume":"144","author":[{"given":"Morag","family":"Young","sequence":"first","affiliation":[{"name":"Prince Henry\u2019s Institute of Medical Research, Clayton, Victoria 3168, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Funder","sequence":"additional","affiliation":[{"name":"Prince 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