Abstract

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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.