Branco D, Garrett J
Arch Int Pharmacodyn Ther. 1985 Jul;276(1):50-9.
Intravenous adrenaline infusions (100 ng . kg-1 min-1) during 30 min resulted in an increase in dog plasma adrenaline and caused a very marked increase in noradrenaline, beginning at 15 min of the infusion and reaching a maximum (10-fold increase) at the end of the infusion. The heart, but not the vascular tissue, showed an increase in adrenaline content. Propranolol (0.5 + 0.5 mg . kg-1) or cocaine (0.5 + 0.5 mg . kg-1) prevented the increase in plasma noradrenaline caused by adrenaline. Isoprenaline (10 ng . kg-1 . min-1) infused during 30 min caused a smaller (2.7-fold) increase in noradrenaline levels, and those effects were also prevented by propranolol or cocaine. From these results, it is concluded that in vivo the increase in noradrenaline plasma levels is due to an activation of beta-adrenoceptors and that this plasma noradrenaline appears to be of neuronal origin. The results also suggest that adrenaline or isoprenaline, after being taken up into nerve terminals, when released activate presynaptic beta-receptors and facilitate the release of neuronal noradrenaline.
静脉注射肾上腺素（100纳克·千克⁻¹·分钟⁻¹）30分钟导致犬血浆肾上腺素增加，并使去甲肾上腺素显著增加，从注射15分钟开始，在注射结束时达到最大值（增加10倍）。心脏而非血管组织的肾上腺素含量增加。普萘洛尔（0.5 + 0.5毫克·千克⁻¹）或可卡因（0.5 + 0.5毫克·千克⁻¹）可防止肾上腺素引起的血浆去甲肾上腺素增加。静脉注射异丙肾上腺素（10纳克·千克⁻¹·分钟⁻¹）30分钟使去甲肾上腺素水平升高幅度较小（2.7倍），普萘洛尔或可卡因也可阻止这些效应。从这些结果可以得出结论，在体内，血浆去甲肾上腺素水平的升高是由于β-肾上腺素能受体激活，且这种血浆去甲肾上腺素似乎起源于神经元。结果还表明，肾上腺素或异丙肾上腺素被摄取到神经末梢后，释放时会激活突触前β受体并促进神经元去甲肾上腺素的释放。
