Hypovolaemia can potentiate hypoglycaemic stress-induced adrenaline release in the anaesthetized rat.

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 The hypoglycaemic response to insulin was greatly reduced if donor blood was used instead of saline to replace the withdrawn blood.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.