Abstract
We previously demonstrated that rats infused chronically with Val5‐Ang II exhibited increased urinary excretion of endogenous Ile5‐Ang II by the 12th day of infusion suggesting the stimulation of endogenous Ang II formation by Val5‐Ang II infusion. To determine the time course of increased urinary Ang II excretion and the effects of AT1 receptor blockade (candesartan, 0.69 ± 0.04 mg/day) on the urinary excretion rates of Ile5‐Ang II in Val5‐Ang II infused rats, Sham (6), Val5‐Ang II infused (5), and Val5‐Ang II infused rats treated with candesartan (6) were evaluated. Val5‐Ang II was infused for 13 days, and Ile5‐Ang II was separated from Val5‐Ang II in urine by HPLC and measured by RIA. SBP increased progressively (206 ± 3.8 mmHg) in Val5‐Ang II infused rats while the candesartan treated group remained normotensive (129.5 ± 6.0 mmHg). Urinary endogenous Ile5‐Ang II excretion rates were elevated by day 9 (2185.7 ± 283.2 fmol/24hr) in Val5‐Ang II infused rats but not in candesartan treated rats (740.6 ± 110.3 fmol/24hr). Thus, AT1 receptor blockade prevented the increase in urinary excretion of endogenous Ang II. These data indicate that the increased urinary endogenous Ang II excretion in Val5‐Ang II infused rats is not due to filtration but is due to secretion into and/or de novo formation of Ang II within the tubular lumen, which is mediated by AT1 receptors.
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