Ballé C, Jungermann K
Eur J Biochem. 1986 Jul 1;158(1):13-8. doi: 10.1111/j.1432-1033.1986.tb09714.x.
The nervous control of hepatic urea and glutamine release and of ammonia uptake was studied in the rat liver perfused in situ. Electrical stimulation of the nerve bundles around the hepatic artery and the portal vein resulted in a reduction of urea release, of glutamine output and of ammonia uptake. At the same time, as observed before [Hartmann et al. (1982) Eur. J. Biochem. 123, 521-526], nerve stimulation led to a decrease of portal flow as well as to an increase of glucose release and a shift of lactate uptake to output. Noradrenaline infusion mimicked the nerve-dependent metabolic and hemodynamic changes in a first approximation only at the highly unphysiological concentration of 0.1 microM. It was without effect at 0.01 microM, which might be reached in the sinusoids as a result of overflow from the vasculature. In the presence of sodium nitroprusside nerve stimulation no longer reduced urea output, glutamine release and ammonia uptake or portal flow, yet it still increased glucose and lactate release. Phentolamine clearly reduced the alterations after nervous stimulation of urea output, ammonia uptake and portal flow, while propranolol was essentially not effective. The nerve-stimulation-dependent reduction of glutamine release was almost abolished in the presence of phentolamine and lowered to 50% by propranolol. Glucagon stimulated urea output but had no influence on glutamine release, ammonia uptake and portal flow. Nerve stimulation antagonized the glucagon-stimulated urea release. The present results suggest that in the perfused liver alpha-sympathetic hepatic nerves regulate urea release, glutamine output and ammonia uptake predominantly by an indirect mechanism via hemodynamic alterations, but glucose release by a direct mechanism also in the absence of circulatory changes.
在原位灌注的大鼠肝脏中研究了肝脏尿素和谷氨酰胺释放以及氨摄取的神经控制。电刺激肝动脉和门静脉周围的神经束导致尿素释放、谷氨酰胺输出和氨摄取减少。同时，如之前所观察到的[Hartmann等人（1982年），《欧洲生物化学杂志》123卷，521 - 526页]，神经刺激导致门静脉血流减少，以及葡萄糖释放增加和乳酸摄取向输出的转变。仅在0.1微摩尔这种高度非生理浓度下，去甲肾上腺素输注大致模拟了神经依赖性的代谢和血流动力学变化。在0.01微摩尔时它没有作用，而这一浓度可能因血管系统中的溢出而在肝血窦中达到。在硝普钠存在的情况下，神经刺激不再降低尿素输出、谷氨酰胺释放和氨摄取或门静脉血流，但仍会增加葡萄糖和乳酸释放。酚妥拉明明显减轻了神经刺激后尿素输出、氨摄取和门静脉血流的改变，而普萘洛尔基本上没有效果。在酚妥拉明存在的情况下，神经刺激依赖性的谷氨酰胺释放减少几乎被消除，而普萘洛尔使其降低到50%。胰高血糖素刺激尿素输出，但对谷氨酰胺释放、氨摄取和门静脉血流没有影响。神经刺激拮抗了胰高血糖素刺激的尿素释放。目前的结果表明，在灌注的肝脏中，α - 交感肝神经主要通过血流动力学改变的间接机制调节尿素释放、谷氨酰胺输出和氨摄取，但在没有循环变化的情况下，也通过直接机制调节葡萄糖释放。
