Zeigler D W, Patel K P
Department of Physiology and Pharmacology, University of South Dakota School of Medicine, Vermillion 57069.
Am J Physiol. 1991 Sep;261(3 Pt 2):R712-8. doi: 10.1152/ajpregu.1991.261.3.R712.
The purpose of this study was to determine if the reflex response to a saline load is altered in the obese Zucker rat. The obese Zucker rat is a genetic model of obesity and insulin-resistant diabetes that has been reported to have high blood pressure. We examined the reflux renal responses to volume expansion in both anesthetized obese and lean Zucker rats. Initial blood pressure was significantly elevated in the obese Zucker rats compared with the lean controls. Urine flow and sodium excretion from innervated and denervated kidneys were measured before and after volume expansion with normal saline. Volume expansion resulted in significantly less urine flow and sodium excretion in the obese than the lean Zucker rats. This response was evident in both the intact and denervated kidneys. Rats were then infused with atrial natriuretic peptide (ANP) to determine if natriuretic and diuretic responses were altered in these rats. The diuretic action of ANP was not significantly reduced in the obese Zucker rat. However, the natriuretic action of ANP was significantly attenuated in the obese rats. These results indicate that the reflux response to an acute saline load is attenuated in the obese Zucker rat and that this decreased response may be due to a reduction in the direct action of ANP on the kidney.
本研究的目的是确定肥胖 Zucker 大鼠对生理盐水负荷的反射反应是否发生改变。肥胖 Zucker 大鼠是肥胖和胰岛素抵抗性糖尿病的遗传模型，据报道患有高血压。我们研究了麻醉状态下肥胖和瘦 Zucker 大鼠对容量扩张的肾反流反应。与瘦对照组相比，肥胖 Zucker 大鼠的初始血压显著升高。在用生理盐水进行容量扩张前后，测量了去神经和未去神经肾脏的尿流量和钠排泄量。与瘦 Zucker 大鼠相比，容量扩张导致肥胖大鼠的尿流量和钠排泄量显著减少。这种反应在完整和去神经的肾脏中均很明显。然后给大鼠注射心房利钠肽（ANP），以确定这些大鼠的利钠和利尿反应是否发生改变。肥胖 Zucker 大鼠中 ANP 的利尿作用没有显著降低。然而，肥胖大鼠中 ANP 的利钠作用显著减弱。这些结果表明，肥胖 Zucker 大鼠对急性生理盐水负荷的反流反应减弱，这种反应降低可能是由于 ANP 对肾脏的直接作用降低所致。
