{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T05:18:10Z","timestamp":1715577490563},"reference-count":32,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:p>Leptin is a regulator of body weight and affects nitric oxide (NO) production. This study was designed to determine whether the myocardial NO-cGMP signal transduction system was altered in leptin-deficient obese mice. Contractile function, guanylyl cyclase activity, and cGMP-dependent protein phosphorylation were assessed in ventricular myocytes isolated from genetically obese (B6.V-Lep<jats:sup>ob<\/jats:sup>) and age-matched lean (C57BL\/6J) mice. There were no differences in baseline contraction between the lean and obese groups. After stimulation with the NO donor S-nitroso- N-acetyl-penicillamine (SNAP, 10<jats:sup>\u20136<\/jats:sup>and 10<jats:sup>\u20135<\/jats:sup>M) or a membrane-permeable cGMP analog 8-bromo-cGMP (8-Br-cGMP, 10<jats:sup>\u20136<\/jats:sup>and 10<jats:sup>\u20135<\/jats:sup>M), cell contractility was depressed. However, 8-Br-cGMP had significantly greater effects in obese mice than in lean controls with percent shortening reduced by 47 vs. 39% and maximal rate of shortening decreased by 46 vs. 36%. The negative effects of SNAP were similar between the two groups. Soluble guanylyl cyclase activity was not attenuated. This suggests that the activity of the cGMP-independent NO pathway may be enhanced in obesity. The phosphorylated protein profile of cGMP-dependent protein kinase showed that four proteins were more intensively phosphorylated in obese mice, which suggests an explanation for the enhanced effect of cGMP. These results indicate that the NO-cGMP signaling pathway was significantly altered in ventricular myocytes from the leptin-deficient obese mouse model.<\/jats:p>","DOI":"10.1152\/ajpheart.00316.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:13:37Z","timestamp":1425413617000},"page":"H2111-H2117","source":"Crossref","is-referenced-by-count":9,"title":["Alterations in nitric oxide-cGMP pathway in ventricular myocytes from obese leptin-deficient mice"],"prefix":"10.1152","volume":"285","author":[{"given":"Jun","family":"Su","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shengjun","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James","family":"Tse","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter 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