Skov Olsen P, Kirkegaard P, Poulsen S S, Nexø E
Regul Pept. 1985 May;11(1):17-25. doi: 10.1016/0167-0115(85)90027-8.
Urinary epidermal growth factor (EGF) has been demonstrated recently to originate from the kidneys. The present study was undertaken to investigate the adrenergic and cholinergic influence on secretion of renal EGF. beta-Adrenergic agonists increased the level of urinary EGF, while propranolol, a beta-adrenergic blocking agent, decreased basal and beta-adrenergic stimulated total output of urinary EGF. Acetylcholine and the anticholinergic agent atropine had no effect on the output of EGF in urine. Also chemical sympathectomy induced by 6-hydroxydopamine reduced the urinary output of EGF. None of the experimental groups had a median serum concentration above the detection limit of the assay. The present study shows that secretion of renal EGF is under the influence of the sympathetic nervous system and release of EGF is stimulated by activation of beta-adrenergic receptors in the kidneys.
最近已证实尿表皮生长因子（EGF）源自肾脏。本研究旨在探讨肾上腺素能和胆碱能对肾EGF分泌的影响。β-肾上腺素能激动剂可提高尿EGF水平，而β-肾上腺素能阻滞剂普萘洛尔则降低尿EGF的基础分泌量以及β-肾上腺素能刺激后的总分泌量。乙酰胆碱和抗胆碱能药物阿托品对尿中EGF的分泌量无影响。此外，6-羟基多巴胺诱导的化学性交感神经切除术可降低尿EGF的分泌量。各实验组的血清浓度中位数均未超过检测限。本研究表明，肾EGF的分泌受交感神经系统的影响，肾脏中β-肾上腺素能受体的激活可刺激EGF的释放。
