Possible involvement of prostaglandins in increases in rat plasma adrenocorticotropic hormone and corticosterone levels induced by radiation and interleukin-1 alpha alone or combined.

Exposing rats to 1-10 Gy of ionizing radiation increased plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels. In both irradiated and nonirradiated rats, recombinant human interleukin-1 alpha (rhIL-1 alpha; 1 hr before radiation/sham exposure) enhanced plasma ACTH and CORT levels. Indomethacin, a cyclooxygenase inhibitor, attenuated plasma ACTH and CORT levels induced by radiation. Indomethacin also attenuated ACTH and CORT levels induced by radiation and interleukin-1 alpha alone or combined. These results suggest that prostaglandins are involved in the increase in plasma ACTH and CORT levels induced by radiation and rhIL-1 alpha alone or combined.

Single-dose ethanol administration activates the hypothalamic-pituitary-adrenal axis: exploration of the mechanism of action.

Activation of the hypothalamic-pituitary-adrenal axis (HPAA) by single-dose ethanol administration, which achieved moderately high blood ethanol levels, was explored in naive rats in order to determine the mechanism of ethanol's activation of the stress axis. Adult male rats received a single dose (3.2 g/kg body weight-1 of a 12% solution of ethanol in physiological saline. The plasma concentration of immunoreactive (ir) adrenocorticotropic hormone (ACTH), beta-endorphin (BE) and corticosterone (CS) was determined by radioimmunoassay, whereas, plasma concentrations of epinephrine (E) and norepinephrine (NE) were quantified following reverse-phase liquid chromatographic separation and amperometric detection. Ethanol induced maximal plasma ACTH levels within minutes, which declined toward basal levels by 60 min, whereas, plasma concentration of CS rose rapidly and remained elevated at 60 min. Plasma ACTH and CS levels in saline-treated control animals did not vary significantly at any time point. Consistent with co-release of ACTH from corticotrophs, the plasma concentration of ir-BE increased 5-fold at 15 min and declined towards basal levels at 60 min after-ethanol challenge. Plasma E increased 10- to 20-fold as compared to saline controls or preinjection levels and returned to preinjection levels by 90 min, in a manner similar to ethanol-induced changes in proopiomelanocortin-derived peptides and CS. Removal of the adrenal medulla and thus the source of E prior to ethanol administration, did not attenuate activation of the HPAA. Passive immunoneutralization of arginine vasopressin (AVP), using a high-titer AVP antiserum and a protocol which was found to block ether-induced ACTH secretion by 40% in adult male rats, failed to even partially block ethanol-induced ACTH or CS secretion. The results of this study indicate that neither adrenal medulla-derived E nor AVP are significant regulators or coregulators of corticotroph secretions following a moderately high, single-dose, intragastric administration of ethanol.

Effect of single and repeated electroconvulsive shock on the hypothalamic-pituitary-adrenal axis and plasma catecholamines in rats.

The effects of single and repeated electroconvulsive shock (ECS) on the hypothalamic-pituitary-adrenal (HPA) axis and plasma catecholamines were studied. Rats were divided into three groups and each group received sham treatment, single ECS, or ten once-daily ECS. Jugular venous blood samples were obtained immediately before treatment and at 10, 30, 60, and 90 min following sham treatment, a single ECS or following the last of ten ECS. Plasma concentrations of corticosterone (CS), ACTH, immunoreactive beta-endorphin (ir-BE), epinephrine (E) and norepinephrine (NE) were determined. Following the single ECS plasma CS was significantly elevated at 10 and 30 min, ACTH was significantly elevated at 10, 30, and 60 min, whereas ir-BE and E peaked at 10 min and returned to basal concentration by 30 min. The concentration of plasma NE did not significantly vary at any time point. Following the tenth ECS the concentration of plasma CS revealed a significant attenuation of the increase at 10 and 30 min when compared with the CS changes observed following a single ECS. Plasma ACTH following chronic ECS was also significantly decreased in magnitude at 10, 30, and 60 min when compared with plasma ACTH levels following a single ECS. Ir-BE in plasma following ten ECS mirrored the changes following single ECS. In contrast to the attenuation of CS and ACTH following chronic ECS, the increase in peripheral catecholamines was markedly elevated after the last of ten ECS. Compared with single ECS, ten ECS produced significant increases in plasma E at 10, 30, and 60 min and at 10, 30, 60, and at 90 min for NE.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effect of intragastric ethanol administration on plasma levels of stress hormones.

We have previously demonstrated that single-dose ethanol administration enhanced plasma levels of ACTH, beta-endorphin, corticosterone (CS) and catecholamines. Since the secretion of proopiomelanocortin-derived peptides (e.g., ACTH, beta-endorphin) can be influenced by catecholamines and vasopressin in addition to the primary physiological regulator, corticotrophin-releasing hormone, we have attempted to determine whether or not the ethanol-induced activation of the hypothalamic-pituitary-adrenal axis (HPAA) could in part be mediated via either epinephrine or vasopressin (AVP) secretion. The selective neutralization of AVP through the administration of AVP antiserum failed to block the ethanol-induced secretion of either ACTH or CS. In addition, adrenal demedullation did not significantly attenuate the ethanol-induced increase of ACTH and CS. It would appear that neither adrenal medulla-derived epinephrine nor median eminence-derived AVP mediates ethanol's activation of the HPAA.