Inhibition of pituitary bioactive prolactin secretion in the male rat by the glucocorticoid agonist decadron phosphate.

In the present studies, the soluble glucocorticoid agonist, decadron phosphate (DEC), was administered i.v. to intact adult male rats in order to evaluate the effects of glucocorticoid receptor stimulation on circulating levels of immunoreactive (ir-) and bioactive (bio-) prolactin (PRL). In light of reports that glucocorticoid-specific receptors exist within the rat brain, additional experiments investigated the effects of intracerebroventricular (i.c.v.) administration of graded doses of the same drug on pituitary ir- and bioPRL secretion. Concentrations of ir- and bioPRL in samples obtained before and after drug treatments were determined by standard PRL radioimmunoassay and the Nb2 rat node lymphoma bioassay, respectively. Rats injected i.v. with 0.5 mg DEC/kg body weight, but not those treated with a tenfold lesser dose, exhibited decreased plasma irPRL concentrations. However, both doses promoted a decline in circulating levels of bioPRL compared to vehicle-treated controls, along with an overall reduction in the plasma bio/irPRL ratio. The magnitude and duration of this drug-induced decline in biopotency of secreted hormone was dose-dependent. While the plasma bio/irPRL ratio was diminished only transiently in rats injected with 0.05 mg DEC/kg, treatment with the higher dose led to a sustained decrease in the plasma bio/irPRL ratio for the duration of the experiment. The current studies also show that intracerebral administration of DEC resulted in dose-dependent alterations in pituitary PRL release. Circulating levels of ir- and bioPRL were not altered in rats injected i.c.v. with 10 ng of DEC, the lowest dose tested.(ABSTRACT TRUNCATED AT 250 WORDS)     

Counteraction by morphine of stress-induced inhibition of growth hormone release in the rat

The purpose of this study was to determine the effect of morphine (MOR) administration on pituitary growth hormone (GH) release during stress in the male rat. Circulating GH levels were significantly decreased following a brief (2 min) exposure to either, during repetitive etherization coupled with blood withdrawal, and during continuous immobilization. Under all three stress conditions, systemic administration of MOR resulted in a significant increase in plasma GH levels compared to the vehicle-treated group. These results indicate that the pathway for opiate-induced stimulation of GH release is functional during stress, and suggest that the suppressive effect of stress does not involve a blockade of opiate receptor stimulation of GH. Thus, the present findings, taken together with reports that the overall activity of central opioid neurons is enhanced during stress, support the view that the decline in GH is due to the overriding inhibitory influence of an independent nonopioid mechanism. However, MOR can apparently increase opiate receptor stimulation sufficiently to counteract this inhibitory signal, implying that stress and the opiates may influence GH release via separate mechanisms.