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REGULATION OF RENAL AQUAPORINS AND SALT TRANSPORTERS IN LOW SODIUM DIET RATS WITH EXPERIMENTALLY INDUCED HEART FAILURE
Author(s) -
Lütken Sophie Constantin,
Praphaphimon Pariwat,
Kwon TaeHwan,
Bie Peter,
Frøkiær Jørgen,
Nielsen Søren
Publication year - 2009
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.23.1_supplement.1006.5
Subject(s) - sodium , aquaporin 2 , medicine , endocrinology , vasopressin , heart failure , kidney , myocardial infarction , low sodium diet , hyponatremia , transporter , sed , chemistry , cardiology , renin–angiotensin system , biochemistry , blood pressure , organic chemistry , gene , mechanical engineering , water channel , engineering , inlet
Heart failure (HF) is a common complication to myocardial infarction (MI) and is associated with increased plasma vasopressin levels and renal AQP2 protein abundance as well as sodium and water retention. Thus reduced sodium intake is often recommended to patients with HF. To examine the underlying renal molecular mechanisms in low‐output HF, male rats were subjected to ligation of the left anterior descending artery. The following MI and HF were confirmed with echocardiography at day seven. During the last seven days of experiment all the rats were fed a low sodium diet and treated with dDAVP (20 ng/h s.c.) or vehicle. The rats were divided into four groups: Sham (n=6); Sham+dDAVP (n=6); HF (n=5), HF+dDAVP (n=6). In dDAVP treated groups the protein abundance of AQP2, p(S256)‐AQP2 and renal sodium transporters increased. Surprisingly vehicle‐treated HF rats failed to increase or even decreased protein abundance of water and sodium transporters, the finding being most profound in inner medulla. In conclusion, the findings support that sodium restriction may be important as a powerful clinical tool against renal water and sodium retention associated with low‐output HF.Danish Medical Research Council