Direct renal intestitial volume expansion causes exaggerated natriuresis in SHR

In Okamoto spontaneously hypertensive rats (SHR), elevated arterial blood pressure is not transmitted to the renal interstitium, and therefore pressure natriuretic and diuretic responses are attenuated. The objective of this study was to determine the effect of increasing renal interstitial hydrostatic pressure (RIHP) by direct renal interstitial volume expansion (DRIVE) on natriuresis and diuresis of SHR and Wistar-Kyoto rats (WKY). Unilateral nephrectomy and implantation of two polyethylene (PE) matrices were performed 3-4 wk before the acute experiment. Four groups of rats, two experimental and two time control, were used. A control clearance period was taken in all groups. In experimental groups and at the beginning and middle of the second period DRIVE was accomplished by bolus injection of a solution of 2.5% human albumin in saline directly into interstitium through one of the PE matrices. In time-control groups saline was infused in renal interstitium at the beginning of the second period. The second PE matrix was used to continuously measure RIHP in all groups. In experimental groups, DRIVE produced a significant increase in RIHP from 3.8 ± 0.4 to 5.7 ± 0.8 mmHg (P < 0.05) in SHR and 4.3 ± 0.4 to 7.1 ± 0.5 mmHg (P < 0.05) in WKY. In both groups the significant increase in RIHP was associated with significant increases in urinary sodium excretion (U(Na)V̇), fractional excretion of sodium (FE(Na)), and urine flow rate (V̇). ΔU(Na)V̇/ΔRIHP, ΔFE(Na)/ΔRIHP, and ΔV̇/ΔRIHP were all significantly higher (P < 0.05) in SHR compared with WKY (2.72 ± 0.70 vs. 0.78 ± 22 μeq·min^-1·mmHg^-1; 1.39 ± 0.48 vs. 0.27 ± 0.06%/mmHg; and 15.69 ± 3.89 vs. 4.95 ± 0.79 μl·min^-1·mmHg^-1, respectively). We conclude that the natriuretic response to increases in RIHP is exaggerated in SHR and that the sensitivities of natriuretic and diuretic responses of SHR to direct increases in RIHP are higher than those of WKY.