Mozaffari M S, Roysommuti S, Shao Z H, Wyss J M
Department of Oral Biology/Pharmacology, School of Dentistry, Medical College of Georgia, Augusta 30912-1128, USA.
Am J Med Sci. 1997 Dec;314(6):370-6. doi: 10.1097/00000441-199712000-00003.
In Wistar Kyoto (WKY) and Sprague Dawley rats, high dietary sodium chloride (NaCl) increases natriuretic and diuretic responses to acute isotonic saline infusion, but in NaCl-sensitive spontaneously hypertensive rats (SHR-S), a high-NaCl diet causes negligible increases in natriuretic and diuretic responses. To investigate whether this deficit in sodium and fluid excretion in SHR-S is stimulus (volume)-specific or because of a more generalized alteration in renal function, the present study measured, in SHR-S and Wistar Kyoto rats, natriuretic and diuretic responses to a hypertonic saline infusion (the amount of sodium infused was equal to that infused in a previous, isotonic experiment). Eight-week-old Wistar Kyoto rats, SHR-S, and salt-resistant SHR were given a basal (1%) or high (8%)-NaCl diet for 2 weeks. Intravenous infusion of hypertonic saline increased mean arterial pressure and reduced heart rate in all groups. Baseline sodium excretion was lower in SHR-S compared with salt-resistant SHR with either diet, but after infusion of hypertonic saline, all 6 groups displayed significant increases in sodium and fluid excretion, glomerular filtration rate, and effective renal blood flow (ERBF). The percent-sodium excretion in response to hypertonic saline infusion was slightly, but significantly, lower in SHR-S (compared with salt-resistant SHR) for either the basal or the high-NaCl diet. We conclude that renal responses to hypertonic saline infusion are affected minimally in SHR-S compared with salt-resistant SHR or Wistar Kyoto rats. Therefore, the deficits in renal function observed in SHR-S after volume loading are not reflected in a renal deficit to hypertonic saline challenge.
在Wistar Kyoto(WKY)大鼠和Sprague Dawley大鼠中,高盐饮食(氯化钠)可增强对急性等渗盐水输注的利钠和利尿反应,但在盐敏感型自发性高血压大鼠(SHR-S)中,高盐饮食对利钠和利尿反应的增强作用可忽略不计。为了研究SHR-S中钠和液体排泄的这种缺陷是刺激(容量)特异性的,还是由于更普遍的肾功能改变,本研究测量了SHR-S和Wistar Kyoto大鼠对高渗盐水输注的利钠和利尿反应(输注的钠量与之前等渗实验中输注的量相等)。给8周龄的Wistar Kyoto大鼠、SHR-S和盐抵抗型SHR喂食基础(1%)或高(8%)盐饮食2周。静脉输注高渗盐水使所有组的平均动脉压升高,心率降低。与任一饮食的盐抵抗型SHR相比,SHR-S的基线钠排泄较低,但输注高渗盐水后,所有6组的钠和液体排泄、肾小球滤过率和有效肾血流量(ERBF)均显著增加。对于基础或高盐饮食,SHR-S(与盐抵抗型SHR相比)对高渗盐水输注的钠排泄百分比略有但显著降低。我们得出结论,与盐抵抗型SHR或Wistar Kyoto大鼠相比,SHR-S对高渗盐水输注的肾脏反应受到的影响最小。因此,容量负荷后SHR-S中观察到的肾功能缺陷在高渗盐水刺激的肾脏缺陷中未得到体现。