The paradox of alpha 2 adrenergic regulation of prolactin (PRL) secretion. I. The PRL-releasing action of the alpha 2 receptor agonists

Abstract

Systemic (IV) administration of the alpha 2 receptor agonist clonidine is known to stimulate secretion of PRL and growth hormone (GH) suggesting a stimulatory role of the central alpha 2 receptors in the regulation of the two hormones. The present work confirms this notion for GH but indicates that the alpha 2 agonists stimulate PRL release by a peripheral action not involving central alpha 2 receptors. This conclusion is based on the following findings: 1) The minimum effective IV dose of clonidine or UK 14304 was four times larger for activation of PRL than GH secretion and had already manifest extracentral effects (elevation of arterial BP). 2) Subcutaneous injection of UK 14304 (220 micrograms/kg) elevated plasma GH but not PRL levels indicating that an effective activation of the central alpha 2 receptors does not stimulate PRL release. 3) Peripherally acting alpha 2 agonists (p-aminoclonidine, oxymetazoline) had no effect on GH secretion but stimulated PRL release in a manner identical with the effect of clonidine or UK 14304. 4) The peripherally acting alpha 2 antagonist DG-5128 blocked only the PRL secretory response to UK 14304 whereas the peripherally and centrally active yohimbine blocked the PRL and GH responses.