Nakamura T, Sakamaki T, Kurashina T, Sato K, Ono Z, Murata K
Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
Hypertension. 1995 Apr;25(4 Pt 2):866-71. doi: 10.1161/01.hyp.25.4.866.
Renal interstitial hydrostatic pressure (RIHP) has recently been cited as an important mediator of pressure natriuresis. Our objective was to determine the roles of vasopressin V1 and V2 receptors in mediating the effects of renal perfusion pressure (RPP) on RIHP and sodium excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and UNaV were assessed in control Wistar rats (n = 10) and in rats pretreated with intravenous infusion of the specific nonpeptide vasopressin V1 antagonist OPC-21268 (100 micrograms.kg-1.min-1; n = 8) and the V2 antagonist OPC-31260 (40 micrograms.kg-1.min-1; n = 10). Increasing RPP from 95 to 118 mm Hg in control rats increased RIHP (6.4 +/- 1.0 to 9.9 +/- 1.3 mm Hg), UNaV (0.29 +/- 0.03 to 0.52 +/- 0.05 muEq.min-1.g-1), urine flow rate (UFR) (5.2 +/- 0.3 to 7.6 +/- 0.6 microL.min-1.g-1), and the fractional excretion of sodium (FENa). In rats pretreated with V1 antagonist, similar results were obtained for urine osmolality and the responses of RIHP, UNaV, UFR, and FENa to RPP. V2 antagonist reduced urine osmolality (392 +/- 47 compared with 979 +/- 88 mOsm.kg-1 in control rats) and enhanced the responses of UNaV (0.43 +/- 0.08 to 1.32 +/- 0.32 microEq.min-1), UFR (17.8 +/- 3.2 to 29.2 +/- 3.8 microL.min-1.g-1), and FENa to RPP, but the RIHP response resembled that observed in the control and V1 antagonist groups. Renal blood flow and glomerular filtration rate did not differ among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
肾间质静水压（RIHP）最近被认为是压力性利尿的重要介导因素。我们的目的是确定血管加压素V1和V2受体在介导肾灌注压（RPP）对RIHP和钠排泄（UNaV）影响中的作用。在对照Wistar大鼠（n = 10）以及经静脉输注特异性非肽类血管加压素V1拮抗剂OPC - 21268（100微克·千克⁻¹·分钟⁻¹；n = 8）和V2拮抗剂OPC - 31260（40微克·千克⁻¹·分钟⁻¹；n = 10）预处理的大鼠中，评估了RPP对肾血流动力学、RIHP和UNaV的影响。在对照大鼠中，将RPP从95毫米汞柱提高到118毫米汞柱会增加RIHP（从6.4±1.0毫米汞柱增加到9.9±1.3毫米汞柱）、UNaV（从0.29±0.03微当量·分钟⁻¹·克⁻¹增加到0.52±0.05微当量·分钟⁻¹·克⁻¹）、尿流率（UFR）（从5.2±0.3微升·分钟⁻¹·克⁻¹增加到7.6±0.6微升·分钟⁻¹·克⁻¹）以及钠分数排泄（FENa）。在用V1拮抗剂预处理的大鼠中，尿渗透压以及RIHP、UNaV、UFR和FENa对RPP的反应得到了类似结果。V2拮抗剂降低了尿渗透压（对照大鼠为979±88毫渗摩尔·千克⁻¹，与之相比为392±47毫渗摩尔·千克⁻¹），并增强了UNaV（从0.43±0.08微当量·分钟⁻¹增加到1.32±0.32微当量·分钟⁻¹）、UFR（从17.8±3.2微升·分钟⁻¹·克⁻¹增加到29.2±3.8微升·分钟⁻¹·克⁻¹）和FENa对RPP的反应，但RIHP反应与在对照和V1拮抗剂组中观察到的相似。三组之间的肾血流量和肾小球滤过率没有差异。（摘要截断于250字）
