{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T16:40:17Z","timestamp":1791909617327,"version":"4.3.4"},"reference-count":44,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:p>Chronic hypertension induces cardiac remodeling, including left ventricular hypertrophy and fibrosis, through a combination of both hemodynamic and humoral factors. In previous studies, we showed that the heptapeptide ANG-(1\u20137) prevented mitogen-stimulated growth of cardiac myocytes in vitro, through a reduction in the activity of the MAPKs ERK1 and ERK2. In this study, saline- or ANG II-infused rats were treated with ANG-(1\u20137) to determine whether the heptapeptide reduces myocyte hypertrophy in vivo and to identify the signaling pathways involved in the process. ANG II infusion into normotensive rats elevated systolic blood pressure &gt;50 mmHg, in association with increased myocyte cross-sectional area, ventricular atrial natriuretic peptide mRNA, and ventricular brain natriuretric peptide mRNA. Although infusion with ANG-(1\u20137) had no effect on the ANG II-stimulated elevation in blood pressure, the heptapeptide hormone significantly reduced the ANG II-mediated increase in myocyte cross-sectional area, interstitial fibrosis, and natriuretic peptide mRNAs. ANG II increased phospho-ERK1 and phospho-ERK2, whereas cotreatment with ANG-(1\u20137) reduced the phosphorylation of both MAPKs. Neither ANG II nor ANG-(1\u20137) altered the ERK1\/2 MAPK kinase MEK1\/2. However, ANG-(1\u20137) infusion, with or without ANG II, increased the MAPK phosphatase dual-specificity phosphatase (DUSP)-1; in contrast, treatment with ANG II had no effect on DUSP-1, suggesting that ANG-(1\u20137) upregulates DUSP-1 to reduce ANG II-stimulated ERK activation. These results indicate that ANG-(1\u20137) attenuates cardiac remodeling associated with a chronic elevation in blood pressure and upregulation of a MAPK phosphatase and may be cardioprotective in patients with hypertension.<\/jats:p>","DOI":"10.1152\/ajpheart.00908.2011","type":"journal-article","created":{"date-parts":[[2011,12,3]],"date-time":"2011-12-03T19:47:29Z","timestamp":1322941649000},"page":"H801-H810","source":"Crossref","is-referenced-by-count":74,"title":["Angiotensin-(1\u20137) attenuates angiotensin II-induced cardiac remodeling associated with upregulation of dual-specificity phosphatase 1"],"prefix":"10.1152","volume":"302","author":[{"given":"LaTronya T.","family":"McCollum","sequence":"first","affiliation":[{"name":"The Hypertension and Vascular Research Center, Wake Forest School of Medicine, Winston-Salem, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia 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