Interaction of glucocorticoids in stimulation of liver tyrosine aminotransferase and tryptophan pyrrolase by estrogen in female rats.

Bilateral adrenalectomy inhibited the increase in liver tyrosine aminotransferase and tryptophan pyrrolase activity after s.c. administration of cca 50 micrograms 17-beta-estradiol (Agofollin SPOFA, Praha) per 1 kg body weight daily for 14 days. Moreover, the authors describe the restitution of the estrogen effect by peroral dexamethasone intake via the drinking saline offered to the animals during the period of Agofollin treatment. In rats substituted in this way the resulting enzyme activities even exceeded those caused by dexamethasone alone.

Plasma testosterone during bicycle ergometer exercise without and after L-dopa pretreatment.

The level of testosterone in plasma during submaximal, prolonged submaximal and maximal exercise on a bicycle ergometer was measured in healthy untrained men. To evaluate the possible involvement of prolactin in the regulation of testosterone secretion during exercise, the influence of prolactin inhibition by oral L-dopa (1 g) pretreatment was also studied. The exercise evoked a small but significant rise of testosterone concentration with peak levels immediately at the end of work performance or 10 min after that. No substantial difference between the response to submaximal and maximal exercise was noted. In these experiments the findings by others on a lack of plasma LH changes and significant increase of plasma prolactin were confirmed. Pharmacological blockade of prolactin release by L-dopa pretreatment failed to modify the response of testosterone to bicycle ergometer exercise. It may be suggested that prolactin is not involved in the induction of plasma testosterone increase during physical exercise.

Decreased plasma cortisol response to pharmacological stimuli after glucose load in man.

The influence of glucose administration on plasma cortisol level after its elevation by pharmacological and physiological interventions in healthy male volunteers was studied. The increase of plasma cortisol after 1 g of L-dihydroxyphenylalanine (L-dopa) failed to be significant. However, after a concomitant oral administration of 100 g glucose, a fall of cortisol level significant also vs. initial control values was observed. The infusion of beta adrenergic blocking agent (propranolol) enhanced the cortisol response to physical exercise. However, the glucose given before propranolol infusion abolished the enhancement of cortisol response induced by this drug. The mechanism of the inhibitory effects of glucose remains to be elucidated.

Gonadotropin receptors in rat during altered testicular function.

Specific testicular binding of 125I-HCG and plasma levels of testosterone are decreased in rats three weeks after hypophysectomy or adrenalectomy plus thyroidectomy but they are not changed after adrenalectomy or thyroidectomy. The affinity of gonadotropin receptors to HCG is not altered.

[Effect of a prolonged stay in space on the reaction of the adrenal cortical and medullary layers]. / Vliianie dlitel'nogo prebyvaniia v kosmose na reaktsiiu korkovogo i mozgovogo sloia nadpochechnikov.

Concentrations of corticosteron and catecholamines, and activities of catecholamine synthesizing enzymes, tyrosine hydroxylase, dopamine-beta-hydroxylase and phenyl ethanol amine-N-methyl-transferase, were measured in the adrenals of rats flown for 19.5 days aboard the biosatellite Cosmos-782, synchronous and vivarium control animals sacrificed on R + 0 and R + 26 days. The flown rats showed a moderate but significant increase in the adrenal weight, corticosteron concentration and tyrosine hydroxylase activity on R+0 day. These parameters returned to the normal on R+26 day. This data gives evidence that the adrenocortical and sympathoadrenal systems were not significantly stimulated by the space flight effects; therefore, weightlessness cannot be considered as a potent stressful agent, although its some stressogenic effect has been documented.

Effect of adrenergic receptor blockade on cortisol and GH response to insulin-induced hypoglycemia in man.

The effect of several drugs presumably influencing central catecholaminergic receptors on plasma cortisol and GH response to insulin-induced hypoglycemia was studied in healthy adult males. The intravenous infusion of alpha-adrenergic blocking agents tolazoline or phentolamine supressed plasma cortisol and GH response to insulin-induced hypoglycemia. After an infusion of beta-adrenergic antagonist propranolol both hypoglycemia and rise in plasma cortisol and GH were prolonged. Finally, the administration of dopaminergic blocker pimozide failed to affect the plasma cortisol response, but slightly suppressed the enhancement of GH release during hypoglycemia. Caution is recommended before making suggestions about neuroendocrine regulations from the data obtained after systemic administration of drugs. Nevertheless, it may be concluded that the hypothesis on the inhibitory role of the central alpha-adrenergic system on ACTH secretion suggested in rats and dogs was not confirmed by our results obtained in man.

Effect of glucose on the glucagon response to L-dopa in normal and diabetic subjects.

The effect of an oral dose of 1 gm. L-dopa either without or after a concomitant oral administration of 100 gm. glucose on the plasma level of pancreatic glucagon, plasma immunoreactive insulin (IRI), and plasma growth hormone (GH) was assessed in eight normal and 10 insulin-treated diabetic subjects. In the normal group the stimulatory effect o L-dopa on pancreatic glucagon release was reconfirmed. Moreover, in the diabetics essentially the same plasma glucagon increase after drug administration was found, such a response being inhibited in both groups by glucose. The increase of plasma GH after L-dopa in both healthy persons and diabetics and the inhibition of this response by glucose in healthy subjects was reconfirmed. Furthermore, the same effect of exogenous glucose on the L-dopa induced GH release was observed in diabetics. It may be concluded that glucagon may play a pathogenetic role in the worsening of parkinsonian diabetic patients during the treatment with L-dopa and that diabetic hyperglycemia per se seems to be insufficient for an inhibition of the release of both glucagon and GH AFTer L-dopa.

Effects of phentolamine and clonidine on pituitary-adrenocortical axis during stress in conscious rats.

For evaluation of the effect of several drugs on the hypothalamo-pituitary-adrenocortical axis during stress, after testing various tress stimuli (swimming, restrain) the 15 min exposure of rats to novel environment was chosen. Subcutaneous administration of clonidine hydrochloride (BOEHRINGER; Ingelheim, 60 micorgram kg-1), a drug stimulating alpha-adrenergic receptors, did not result in any any changes in plasma corticosterone level either during basal or under stress conditions. In contrast, the administration of alpha-adrenergic blocking agent--phentolamine (RegitineR CIBA; 4 mg kg-1)--produced a significant elevation of resting corticosterone level, but failed to influence the stress-induced corticosterone increase.

Plasma testosterone response to HCG in normal men without and after administration of anabolic drug.

In young, adult male volunteers Leydig cell function tests were performed consisting of i.m. administration of 1500, 3000 or 4500 IU of HCG on days 1, 2 and 3 and plasma testosterone determination by radioimmunoassay. The stimulatory effect of HCG known from the literature is reconfirmed. However, no difference between the effect of the three dosage levels was found and the first significant effect of HCG was observed 24 h after its first application. Testosterone levels on day 3 and 4 are higher but not different from each other. A depression of plasma testosterone after treatment with an anabolic steroid (1alpha, 17alpha-dimethyl-5alpha-androstan-17-ol-3-one) 20 mg daily for 14 days is described. Reactivity to HCG was sustained in these subjects, but testosterone response to HCG was diminished at all investigated time intervals.

Plasma testosterone of rats subjected to immobilization stress and/or HCG administration.

The effect of immobilization stress (IMO) on the plasma testosterone level in rats has been investigated. Plasma testosterone was not changed after 10 or 20 min IMO for 3 consecutive days as compared to nonstressed animals and the 10-min trial was without effect even if it was applied daily for 42 days. Thre days IMO for 60 min caused a significant hormone decrease, which was even more pronounced after 3 or 42 days IMO for 120 min. The administration of HCG to rrats immobilized 3 days for 120 min resulted in the increase of testosterone, however, the final level was significantly lower in comparison to nonstressed controls.