Catecholamine excretion and beta-adrenergic responsiveness in estrogen-treated rats

Chronic treatment with an estrogenic agent is known to reduce the responsiveness to beta-adrenergic stimulation in rats. To assess the possibility that endogenously produced catecholamines may play a role in this phenomenon, female rats were treated either with implanted Silastic tubes containing estradiol benzoate (26 micrograms/kg/day) or with empty tubes. After 12 weeks of treatment, the dipsogenic, colonic temperature and tail skin temperature responses to acute administration of the beta-adrenoceptor agonist, isoproterenol, were blunted compared to controls. Each of these responses was negatively correlated with serum estradiol concentration measured by radioimmunoassay. Urinary norepinephrine output was elevated significantly in treated rats during a 24-hour basal period. During a 2-hour exposure to air at 4 degrees C, urinary outputs of norepinephrine, epinephrine, and dopamine were elevated significantly above those of controls. There were significant positive correlations between plasma estradiol concentration and the outputs of each of the above catecholamines during the 24-hour basal period and during cold exposure, with norepinephrine being the most strongly correlated. Dipsogenic and metabolic (tail skin and colonic temperature) responses to administration of isoproterenol were negatively correlated with catecholamine excretion during both the basal 24-hour period and during cold exposure. These results suggest that reduced beta-adrenergic responsiveness in estrogen-treated rats may have resulted from down-regulation of beta-adrenoceptors associated with increased secretion of catecholamines induced by chronic estrogen treatment.