Lappe R W, Henry D P, Willis L R
Can J Physiol Pharmacol. 1982 Aug;60(8):1067-72. doi: 10.1139/y82-153.
Increased activity of the renal sympathetic nerves may result in increased urinary excretion of norepinephrine (NE). In the present study, unilateral electrical stimulation of the renal nerves of the rabbit was employed to test this hypothesis. Stimulation of the renal nerves to one kidney at 2 Hz (group I) produced no significant alteration of plasma NE concentration, glomerular filtration rate (GFR), or NE excretion by either kidney. Stimulation at 4 Hz (group II) caused statistically significant reductions of GFR and urine flow in experimental kidneys, but the urinary excretion of NE, per millilitre GFR, and the CNE/GFR ratios were significantly greater than prestimulation values. In another group of animals (group III), an inhibitor of cation-specific tubular transport, cyanine 863 (6 mg/kg, i.v.), significantly reduced the prestimulation urinary excretion of NE by 60-70% when compared with that of groups I or II. Stimulation of the renal nerves (4 Hz) in the animals of group III caused a significant reduction in GFR in the experimental kidney but did not alter the urinary excretion of NE or the CNE/GFR ratios. The results of these studies indicate that an increase in renal nerve activity causes an increase in the urinary excretion of NE, and that tubular secretion is responsible for the excretion of the neuronally released catecholamine.
肾交感神经活动增强可能导致去甲肾上腺素(NE)尿排泄增加。在本研究中,采用对兔肾神经进行单侧电刺激来验证这一假设。以2 Hz刺激一侧肾脏的肾神经(I组),对血浆NE浓度、肾小球滤过率(GFR)或两侧肾脏的NE排泄均无显著影响。以4 Hz刺激(II组)导致实验侧肾脏的GFR和尿流量出现统计学显著降低,但每毫升GFR的NE尿排泄量以及CNE/GFR比值显著高于刺激前值。在另一组动物(III组)中,一种阳离子特异性肾小管转运抑制剂花菁863(6 mg/kg,静脉注射)与I组或II组相比,使刺激前NE尿排泄量显著降低60 - 70%。对III组动物的肾神经(4 Hz)进行刺激导致实验侧肾脏的GFR显著降低,但未改变NE尿排泄量或CNE/GFR比值。这些研究结果表明,肾神经活动增加会导致NE尿排泄增加,并且肾小管分泌是神经元释放的儿茶酚胺排泄的原因。