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High Salt Exacerbates Proteinuria in Chronic Angiotensin‐II Infused Rats.
Author(s) -
Lowenburg Benjamin M,
Planchard Jeffrey A,
Martin Victoria L,
Davis Porcha D,
Botros Fady T,
Mitchell Kenneth D,
Navar L Gabriel,
Prieto Minolfa C
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.1016.1
Subject(s) - losartan , proteinuria , medicine , endocrinology , angiotensin ii , blood pressure , kidney , renin–angiotensin system , angiotensin receptor
This study examined the effect of a high salt (HS) diet on systolic blood pressure (SBP) and proteinuria in chronic Ang II‐infused hypertensive rats with and without RAS blockade with an Ang II type I receptor blocker, losartan (LOS). Male Sprague‐Dawley rats divided into four groups: 1) Sham+HS [n=5]; 2) Ang II [n=3]; 3) AngII+HS [n=5]; 4) Ang II+HS+LOS [n=5] were infused with Ang II (80 ng/min) for 14 days, fed with HS diet (8% NaCl) and treated with LOS (30 mg/L, drinking water). SBP progressively increased in Ang II and Ang II+HS rats up to 228±9mmHg and 228±10mmHg, respectively, compared to Sham+HS (128±7mmHg). Losartan attenuated the increases in SBP during the two‐weeks of treatment (144±9mmHg). Rats receiving Ang II+HS showed marked proteinuria measured in 24h‐urine collections (79±26mg/day) which was greater than in the Ang II group. Proteinuria decreased in the Ang II+HS+LOS, but not to levels of Sham+HS (29±2mg/day vs. 18±1mg/day), indicating a partial beneficial effect of LOS on proteinuria. The lack of difference between SBP in rats with Ang II‐induced hypertension and those that also received HS suggest that HS does not exert an additive effect on SBP. However, the presence of marked proteinuria in Ang II+HS rats indicates that HS might contribute to glomerular kidney damage independently of SBP and Ang II effects suggesting a direct action on glomerular protein barrier. Support from NIH and Merck & Co., Inc.