The influence of acute ethanol exposure on growth hormone release in female rats.

This study investigates the site (hypothalamic or pituitary) at which ethanol (ETOH) alters GH release in female rats. Both the hypothalamic response to clonidine (CLON), an alpha 2-adrenergic agonist, and the pituitary response to growth-hormone releasing hormone (GRH) were tested. Jugular cannulae were inserted for drug administration and undisturbed blood sampling. ETOH was injected IP 24 and 1 h before experimentation. In animals receiving saline or ETOH (1, 2, or 3 g/kg), there was no response to CLON and no difference in GH levels between groups. On the other hand, there was a significant surge in GH release in response to a high dose of GRH (1000 ng/kg) in both saline controls and in ETOH (3 g/kg) animals. Although there was no difference in the height of the surge between groups, baseline GH levels were higher in animals that received ETOH. In response to a low dose of GRH (250 ng/kg) the GH surge was only significant in the ETOH animals. In animals receiving somatostatin antiserum (anti-SRIF; 0.5 ml) in combination with the low GRH dose, the surge in GH levels was significant in both saline and ETOH animals, however, the surge was higher in saline compared to ETOH animals. The results of this study suggest that: 1) ETOH alters the SRIF system (release of reception) in female rats and that this interaction is evident when GRH concentration is low, and 2) ETOH may also inhibit GH release by interfering with the GRH system, however, the site of this influence most likely does not involve an alpha 2-GRH component.