Renal interstitial hydrostatic pressure during pressure natriuresis in hypertension

Abstract

The objective of this study was to test the hypothesis that changes in renal perfusion pressure (RPP) are not fully transmitted to the renal interstitium in spontaneous hypertension in comparison with normotensive states. Okamoto spontaneously hypertensive and normotensive Wistar-Kyoto rats were used in this study. Renal interstitial hydrostatic pressure (RIHP) was measured directly and continuously via a polyethylene matrix that was implanted chronically in the left kidney 3 wk before RIHP measurement. When RPP was allowed to increase from 136 +/- 0.5 to 162 +/- 1.3 mmHg in male spontaneously hypertensive rats, RIHP was not significantly changed from 3.7 +/- 0.9 to 4.6 +/- 1.1 mmHg, and fractional excretion of sodium (FENa) increased significantly from 0.26 +/- 0.12 to 0.65 +/- 0.15% (P less than 0.05). When RPP was allowed to change from 104 +/- 0.9 to 127 +/- 1.3 mmHg in male Wistar-Kyoto rats, RIHP increased markedly from 4.0 +/- 0.3 to 7.2 +/- 0.4 mmHg (P less than 0.05), and FENa was significantly elevated from 0.27 +/- 0.08 to 2.02 +/- 0.55% (P less than 0.05). In conclusion, spontaneously hypertensive rats have a blunted increase in RIHP and pressure natriuresis response in comparison with Wistar-Kyoto rats. Thus, in Okamoto spontaneously hypertensive rats, the effect of RPP on RIHP is attenuated, leading to a blunted pressure natriuresis response.