Valcavi R, Dieguez C, Page M D, Zini M, Casoli P, Portioli I, Scanlon M F
2a Divisione di Medicina Generale, Arcispedale, S. Maria Nuova, Reggio Emilia, Italy.
Clin Endocrinol (Oxf). 1988 Sep;29(3):309-16. doi: 10.1111/j.1365-2265.1988.tb01229.x.
Administration of a supramaximal dose of GRF 1-44 (200 micrograms, i.v.) to normal human volunteers increased GH levels while a further bolus of GRF (200 micrograms i.v.) given 2 hours later failed to increase plasma GH levels. In contrast, alpha-adrenergic receptor agonism with either propranolol-adrenaline infusion or clonidine increased plasma GH levels at a time when GH responses to this supramaximal dose of GRF were absent. This indicates that alpha-adrenergic pathways stimulate GH secretion through a non-GRF-dependent mechanism in normal human subjects.
给正常人类志愿者静脉注射超最大剂量的生长激素释放因子1-44（200微克）可使生长激素水平升高，而2小时后再静脉注射一次生长激素释放因子（200微克）未能使血浆生长激素水平升高。相比之下，在对该超最大剂量生长激素释放因子无生长激素反应时，通过普萘洛尔-肾上腺素输注或可乐定进行α-肾上腺素能受体激动可使血浆生长激素水平升高。这表明在正常人类受试者中，α-肾上腺素能途径通过非生长激素释放因子依赖的机制刺激生长激素分泌。
