McIntyre A, Zhou X F, Marley P D, Livett B G
Department of Biochemistry, University of Melbourne, Parkville, Vic., Australia.
Neurosci Lett. 1990 May 4;112(2-3):269-75. doi: 10.1016/0304-3940(90)90215-u.
The interaction between hypoglycaemic stress and hypovolaemic stress in promoting adrenaline secretion from the adrenal medulla has been studied in anaesthetised and conscious rats. In anaesthetized rats, insulin (1 IU/kg, i.v.) markedly increased plasma adrenaline concentrations whereas blood sampling alone did not. The hypoglycaemic response to insulin was greatly reduced if donor blood was used instead of saline to replace the withdrawn blood. The hypoglycaemic response was abolished by captopril or saralasin. The results suggest that adrenaline secretion in response to hypoglycaemic stress in anaesthetized rats is potentiated by hypovolaemic activation of the renin-angiotensin system. In contrast, in fully conscious rats, the response to hypoglycaemia was not abolished by captopril, indicating that in the absence of barbiturate anaesthesia, the hypoglycaemic release of catecholamines is not potentiated by the renin-angiotensin system.
在麻醉和清醒的大鼠中，研究了低血糖应激和低血容量应激在促进肾上腺髓质分泌肾上腺素方面的相互作用。在麻醉大鼠中，静脉注射胰岛素（1 IU/kg）可显著提高血浆肾上腺素浓度，而仅进行采血则不会。如果用供血而非生理盐水来补充所采出的血液，对胰岛素的低血糖反应会大大降低。卡托普利或沙拉新可消除低血糖反应。结果表明，麻醉大鼠中肾素 - 血管紧张素系统的低血容量激活可增强对低血糖应激的肾上腺素分泌。相比之下，在完全清醒的大鼠中，卡托普利不会消除对低血糖的反应，这表明在没有巴比妥类麻醉的情况下，肾素 - 血管紧张素系统不会增强儿茶酚胺的低血糖释放。
