Evidence for alpha-adrenergic regulation of episodic growth hormone and prolactin secretion in the undisturbed male rat.

The present experiments were designed to study the effect of the centrally active alpha-adrenergic receptor agonist, clonidine, on episodic GH and PRL secretion in male rats after selective blockade of norepinephrine (NE) and epinephrine (EP) synthesis with the dopamine-beta-hydroxylase inhibitor, FLA-63. Freely behaving, chronically cannulated rats were maintained on a constant light-dark cycle in isolation test chambers. Beginning at 1000 h, blood samples were removed every 20 min for 5-h periods without disturbing the animal. FLA-63 was administered (10 or 20 mg/kg ip) at 0845 h. Clonidine (15 or 150 microgram/kg iv) was given at times that coincided with the spontaneous occurrence of episodic GH peaks or troughs observed in control animals. Results of the present study are summarized as follows: 1) selective blockade of NE and EP synthesis with FLA-63 (20 mg/kg) caused complete suppression of episodic GH but had no significant effect on PRL release; 2) clonidine (150 microgram/kg) restored the pulsatile pattern of GH secretion in FLA-63-treated rats, and 3) clonidine (15 and 150 microgram/kg) stimulated PRL release in a dose-dependent manner. These findings suggest a major stimulatory role of alpha-adrenergic receptors in episodic GH and PRL secretion.