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Opposite regulation of ANP and renin in hyperleptinemic rats
Author(s) -
Yuan Kuichang,
Yu Jiahua,
Kim Sun Young,
Han Jeong Hee,
Park ByungHyun,
Kim Sung Zoo,
Kim Suhn Hee
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.947.6
Subject(s) - medicine , endocrinology , leptin , kidney , chemistry , plasma renin activity , atrial natriuretic peptide , receptor , contractility , renin–angiotensin system , biology , obesity , blood pressure
The kidney expresses the leptin receptor, and various renal effects of leptin have been reported. This study is aimed to investigate the effects of leptin on regulation of body fluid. Sprague‐Dawley rats were received adenovirus containing the rat leptin cDNA (AdCMV‐leptin) or b‐galactosidase gene (AdCMV‐bGal) and their metabolism was observed for 2–4weeks. Food intake and body weight were markedly decreased in hyperleptinemic rats. However, no significant differences in water balance and urinary excretions of electrolytes were observed between hyperleptinemic rats and pair‐feeding rats. Plasma renin activity was increased whereas plasma ANP level was decreased. No significant change in ANP binding density in kidney was observed. The ratio between plasma cAMP and cGMP levels was decreased. In isolated perfused beating atria from hyperleptinemic rats, no differences in basal ANP release, contractility and ECF translocation were observed. The response of isoproterenol‐induced decrease of ANP release was similar. These results suggest that leptin may stimulate renin secretion rate from kidney, which was followed by water retention and suppression of ANP release. Supported by KRF‐2005‐204‐E0007 and the KOSEF (R01‐2006‐000‐10554‐0).