Renal interstitial hydrostatic pressure and natriuretic response to high doses of angiotensin II in pregnant rats

Background: Administration of high doses of angiotensin II (Ang II) results in natriuretic and diuretic responses that are mediated by increases in renal perfusion pressure (RPP). Elevations in renal interstitial hydrostatic pressure (RIHP) caused by increases in mean arterial pressure (MAP) or RPP are associated with significant increases in urinary sodium excretion (U_NaV) and urine flow rate (V). In pregnant rats the renin-angiotensin system (RAS) is activated and basal RIHP is reduced. The exact relationship among MAP, RIHP, U_NaV, and V in response to a high pressor dose of Ang II during normal pregnancy is not known. Methods: The objective of this study was to evaluate the relationship between MAP and RIHP, and determine the role of RIHP in the natriuretic and diuretic responses to administration of high dose of Ang II in midterm pregnant (MP) and nonpregnant (NP) Sprague-Dawley (SD) rats. Results: Intravenous infusion of Ang II (200 ng/kg/min) significantly increased MAP (ΔMAP), ΔU_NaV, and ΔV in anesthetized MP and NP rats. The ΔMAP, ΔU_NaV, and ΔV were 12 ± 2 mm Hg, 27.9 ± 2.7 μEq/min, and 197 ± 23 μL/min for MP rats and were similar (15 ± 3 mm Hg, 34.1 ± 4.3 μEq/min, and 242 ± 34 μL/min, respectively) for NP rats. The RIHP decreased significantly (P < .05) with Ang II infusion in NP (from 6.1 ± 0.2 to 3.9 ± 0.4 mm Hg) but not in MP (from 3.3 ± 0.3 to 4.1 ± 0.4 mm Hg) groups of rats. Acute renal decapsulation eliminated the change in RIHP mediated by high doses of Ang II infusion in the NP group, but did not affect MAP or the natriuretic and diuretic responses to Ang II in either the MP or NP groups of rats. Conclusions: The natriuretic and diuretic responses to high doses of Ang II are not mediated by changes in RIHP in pregnant or nonpregnant rats.