Granger J P, Scott J W
Department of Physiology, Eastern Virginia Medical School, Norfolk 23501.
Am J Physiol. 1988 Nov;255(5 Pt 2):F828-33. doi: 10.1152/ajprenal.1988.255.5.F828.
Renal vasodilation has a marked effect on the pressure-natriuresis relationship. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating the effect of renal perfusion pressure (RPP) on urinary sodium excretion rate (UNaV) in control and vasodilated kidneys. The effects of RPP on UNaV and RIHP were determined in dogs under control conditions and during renal vasodilation with acetylcholine (Ach, 2.0 micrograms.kg-1.min-1) or secretin (SEC, 0.025 micrograms.kg-1.min-1). Decreases in RPP in control kidneys from 130 to 60 mmHg decreased UNaV from 2.9 +/- 0.1 to 0.6 +/- 0.3 microeq/min and fractional excretion of Na (FENa) from 0.15 +/- 0.08 to 0.06 +/- 0.04%. These changes were associated with significant reductions in RIHP (8.9 +/- 0.6 to 5.6 +/- 1.2 mmHg). In Ach-vasodilated kidneys, reductions in RPP from 130 to 60 mmHg decreased UNaV from 149.8 +/- 52.4 to 0.2 +/- 0.1 microeq/min and FENa from 3.42 +/- 1.18 to 0.012 +/- 0.01%. RIHP decreased from 17.8 +/- 3.4 to 8.4 +/- 1.3 mmHg, despite autoregulation of RBF. Renal vasodilation with SEC, which did not affect RIHP, had only a small effect on the relationship between RPP and UNaV. These data suggest that RIHP may be playing an important role in mediating the effect of RPP on UNaV.
肾血管舒张对压力-利钠关系有显著影响。本研究的目的是确定肾间质静水压（RIHP）在介导肾灌注压（RPP）对正常和血管舒张肾脏尿钠排泄率（UNaV）的影响中所起的作用。在对照条件下以及用乙酰胆碱（Ach，2.0微克·千克⁻¹·分钟⁻¹）或促胰液素（SEC，0.025微克·千克⁻¹·分钟⁻¹）进行肾血管舒张期间，测定了犬RPP对UNaV和RIHP的影响。正常肾脏的RPP从130 mmHg降至60 mmHg时，UNaV从2.9±0.1微当量/分钟降至0.6±0.3微当量/分钟，钠分数排泄（FENa）从0.15±0.08降至0.06±0.04%。这些变化与RIHP的显著降低（从8.9±0.6 mmHg降至5.6±1.2 mmHg）相关。在Ach血管舒张的肾脏中，RPP从130 mmHg降至60 mmHg时，UNaV从149.8±52.4微当量/分钟降至0.2±0.1微当量/分钟，FENa从3.42±1.18降至0.012±0.01%。尽管肾血流量（RBF）有自身调节，但RIHP仍从17.8±3.4 mmHg降至8.4±1.3 mmHg。用SEC进行肾血管舒张，其不影响RIHP，对RPP与UNaV之间的关系仅有微小影响。这些数据表明，RIHP可能在介导RPP对UNaV的影响中起重要作用。
