Philipsen E K, Myhre J, Larsen S, Damkjaer Nielsen M, Holst J J, Hilsted J
Medical Department F, Glostrup Hospital, Denmark.
Acta Endocrinol (Copenh). 1990 Jan;122(1):115-20. doi: 10.1530/acta.0.1220115.
To test the hypothesis that increments in plasma cyclic AMP during beta-adrenergic stimulation reflect integrated second messenger function of the tissues activated by the agonist, graded adrenaline infusion resulting in plasma adrenaline concentrations within the physiological range was performed in 8 healthy subjects with and without concomitant beta-adrenoceptor blockade by iv propranolol. A significant correlation was found between increments in plasma adrenaline and plasma cyclic AMP in the experiments without beta-blockade; during concomitant beta-blockade the increase in plasma cyclic AMP concentrations at low adrenaline infusion rates was prevented, whereas a small increase in cyclic AMP was found at high adrenaline infusion rates, probably owing to incomplete beta-receptor blockade. Likewise, the adrenaline-induced increments in blood substrates (glucose, lactate, glycerol and beta hydroxybutyric acid) were significantly reduced but not completely prevented by beta-blockade. We conclude that an altered relationship between beta-agonist concentrations and plasma cyclic AMP may provide evidence for the existence of differences in beta-adrenergic sensitivity in man.
为了验证β-肾上腺素能刺激期间血浆环磷酸腺苷(cAMP)的增加反映了激动剂激活组织的整合第二信使功能这一假设,在8名健康受试者中进行了分级肾上腺素输注,使血浆肾上腺素浓度处于生理范围内,其中部分受试者静脉注射普萘洛尔进行β-肾上腺素能受体阻滞,部分未进行。在未进行β-受体阻滞的实验中,发现血浆肾上腺素的增加与血浆环磷酸腺苷之间存在显著相关性;在同时进行β-受体阻滞时,低肾上腺素输注速率下血浆环磷酸腺苷浓度的增加被阻止,而在高肾上腺素输注速率下发现环磷酸腺苷有小幅增加,这可能是由于β-受体阻滞不完全所致。同样,β-受体阻滞显著降低了肾上腺素诱导的血液底物(葡萄糖、乳酸、甘油和β-羟基丁酸)的增加,但并未完全阻止。我们得出结论,β-激动剂浓度与血浆环磷酸腺苷之间关系的改变可能为人类β-肾上腺素能敏感性存在差异提供证据。