{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:57:43Z","timestamp":1777859863248,"version":"3.51.4"},"reference-count":34,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2015,5,21]],"date-time":"2015-05-21T00:00:00Z","timestamp":1432166400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:sec>\n                    <jats:title>Introduction:<\/jats:title>\n                    <jats:p>\n                      Aldosterone can induce changes in the expression or activity of Na\n                      <jats:sup>+<\/jats:sup>\n                      \/H\n                      <jats:sup>+<\/jats:sup>\n                      exchanger isoform 1 (NHE\u20131) in vascular smooth muscle cells. We aimed to clarify whether chronic mineralocorticoid receptor activation exerts an effect on the activity of NHE\u20131 in the aorta of mineralocorticoid-induced hypertensive rats.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Uninephrectomized male Sprague-Dawley rats received subcutaneously 10 mg\/week of desoxycorticosterone (DOCA) with or without 20 mg\/kg of spironolactone, or vehicle alone ( n = 20). After four weeks of treatment, the animals were sacrificed; the aorta was excised for subsequent studies, including histological analysis, RT-PCR, Western blot, measurement of NHE-1 activity and vascular contractility in the presence or absence of the selective NHE-1 inhibitor ethyl-isopropyl amiloride (EIPA).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Chronic DOCA treatment increased the NHE-1 activity, systolic and diastolic blood pressure, and aortic wall thickness. All these effects were prevented by co-treatment with Spironolactone ( p &lt; 0.05). Phenylephrine-induced vascular contractility was significantly reduced in the DOCA group when EIPA was added in the media ( p &lt; 0.05). No significant differences in NHE-1 mRNA or protein levels were detected between groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Chronic DOCA administration induced functional and morphological alterations in the rat aorta that are partially explained by enhanced NHE-1 activity and prevented by spironolactone. However, we did not observe changes in the NHE-1 transcript or protein levels, suggesting that the effect may be due to post-transcriptional modifications induced by mineralocorticoid receptor activation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1470320315587193","type":"journal-article","created":{"date-parts":[[2015,5,21]],"date-time":"2015-05-21T21:35:21Z","timestamp":1432244121000},"page":"1225-1231","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":5,"title":["Spironolactone inhibits the activity of the Na\n                    <sup>+<\/sup>\n                    \/H\n                    <sup>+<\/sup>\n                    exchanger in the aorta of mineralocorticoid-induced hypertensive rats"],"prefix":"10.1177","volume":"16","author":[{"given":"Juan E","family":"Carre\u00f1o","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fernando J","family":"Verdugo","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Felipe","family":"Contreras","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Felipe A","family":"Montellano","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sebastian","family":"Veloso","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kurt A","family":"Schalper","sequence":"additional","affiliation":[{"name":"Department of Pathology, Yale School of Medicine, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mauricio","family":"Sandoval","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandra","family":"Villanueva","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elisa","family":"Marusic","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carlos E","family":"Irarrazabal","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Physiology, Faculty of Medicine, Universidad de los Andes, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2015,5,21]]},"reference":[{"key":"bibr1-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa033263"},{"key":"bibr2-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.106.634626"},{"key":"bibr3-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1159\/000345243"},{"key":"bibr4-1470320315587193","doi-asserted-by":"publisher","DOI":"10.2174\/157016111796642689"},{"key":"bibr5-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1998.275.6.E1072"},{"key":"bibr6-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1210\/en.2002-220950"},{"key":"bibr7-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsbmb.2008.03.005"},{"key":"bibr8-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1007\/BF00234570"},{"key":"bibr9-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.254.2.C213"},{"key":"bibr10-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(95)00447-5"},{"key":"bibr11-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.5.1099"},{"key":"bibr12-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000194122.27475.6c"},{"key":"bibr13-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.096289"},{"key":"bibr14-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1177\/1470320308096367"},{"key":"bibr15-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0039665"},{"key":"bibr16-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1130"},{"key":"bibr17-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.112.000034"},{"key":"bibr18-1470320315587193","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1771"},{"key":"bibr19-1470320315587193","first-page":"709","volume":"60","author":"Cingolani 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