• 1 January 1982
    • journal article
    • research article
    • Vol. 221  (3) , 577-583
Abstract
The effect of acute stresses on plasma norepinephrine, epinephrine and dopamine-.beta.-hydroxylase (DBH) were evaluated in control and 6-hydroxydopamine-treated, awake cannulated guinea pigs. Forced immobilization for 1 h caused a 3- and 5-fold increase in plasma DBH and norepinephrine, respectively. Pretreatment with 6-hydroxydopamine (23 mg/kg body wt i.a., [intraarterially] 72 and 48 h before stress) reduced by 70% the increase in plasma DBH and totally prevented the rise in plasma catecholamines evoked by the restraining stress. Injection of insulin (5 U/kg body wt. i.a.) induced a 60% decrease in blood glucose, a 1-fold increase in plasma DBH and a selective 4-fold increase in plasma epinephrine; these effects were not modified by chemical sympathectomy. Forced immobilization and hypoglycemia produce a preferential activation of the sympathetic postganglionic nerves and of the adrenal medulla, respectively, and in guinea pigs both stresses increase plasma DBH. The kinetics of disappearance of plasma DBH were studied after subjecting the guinea pigs for 1 h to forced immobilization. Although 7 of 12 animals showed a biphasic rate of fall of plasma DBH, in each case there was a rapid initial fall possibly due to the distribution of the enzyme with a half-time of 1.65 h. Similar findings were observed in 6-hydroxydopamine-treated guinea pigs. The distribution of DBH is the most important process in reducing the augmented plasma DBH levels elicited by a short-term stress and this process is not dependent on the integrity of the sympathetic nerves nor on the adrenal or sympathetic origin of the enzyme. The ratio, content of releasable DBH present in sympathetic nerves and adrenal glands/total circulating pool of DBH apparently is the factor that determines whether an increase in plasma DBH would occur in animals exposed to an acute stress.