5-HYDROXYTRYPTAMINERGIC RECEPTOR-MEDIATED REGULATION OF GROWTH-HORMONE SECRETION IN HOLSTEIN STEERS OCCURS VIA ALPHA(2)-ADRENERGIC-DEPENDENT AND ALPHA(2)-ADRENERGIC-INDEPENDENT MECHANISMS

In vitro and in vivo experiments were used to determine the relationsh ip between 5-hydroxytryptaminergic and alpha(2)-adrenergic receptors i n regulation of growth hormone secretion in cattle. Activation of 5-hy droxytryptaminergic receptors (10(-8), 10(-5), 10(-4) M quipazine) or alpha(2)-adrenergic receptors (10(-8), 10(-6), 10(-4) M clonidine) had no effect on secretion of growth hormone from perifused anterior pitu itary cells. In vivo, quipazine (0.2 mg/kg body wt, iv) and clonidine (8 mu g/kg body wt, iv), when injected separately, each maximized secr etion of growth hormone in Holstein steers. However, concurrent admini stration of quipazine and clonidine at these doses additively increase d secretion of growth hormone (mean areas under curves=439, 914, 1425, and 2359 +/- a pooled SEM of 246 ng . ml(-1). min for vehicle, clonid ine, quipazine, and quipazine plus clonidine treatments, respectively) . Blockade of 5-hydroxytryptaminergic receptors with cyproheptadine (0 .2 or 1.0 mg/kg body wt, sc, 0740 hr) decreased basal concentrations o f growth hormone but had no effect on the ability of clonidine (8 mu g /kg body wt, iv, 0840 hr) to increase secretion of growth hormone (mea n areas under curves=591, 1218, 363, 1087, and 1002 +/- a pooled SEM o f 177 ng . ml(-1). min for vehicle-vehicle, vehicle-clonidine, 0.2 mg cyproheptadine-vehicle, 0.2 mg cyproheptadine-clonidine and 1.0 mg cyp roheptadine-clonidine treatments, respectively). Blockade of alpha(2)- adrenergic receptors with either yohimbine (5 mg/kg body wt, sc, 0740 hr) or idazoxan (20 mg/kg body wt, sc, 0740 hr) suppressed both basal and 5-hydroxytryptaminergic receptor-stimulated (0.2 mg quipazine/kg b ody wt, iv, 0840 hr) secretion of growth hormone (mean areas under cur ves=568, 1252, 410, and 558 +/- a pooled SEM of 108 ng . ml(-1). min f or vehicle-vehicle, vehicle-quipazine, yohimbine-vehicle, and yohimbin e-quipazine treatments, respectively, and means of 553, 1468, 194, and 686 +/- a pooled SEM of 221 ng . ml(-1). min for vehicle-vehicle, veh icle-quipazine, idazoxan-vehicle, and idazoxan-quipazine treatments, r espectively). We conclude that two mechanisms in the central nervous s ystem mediate 5-hydroxytryptaminergic receptor-stimulated secretion of growth hormone in cattle; one independent and another dependent on al pha(2)-adrenergic receptors, possibly via regulation of basal growth h ormone secretion. In contrast, alpha(2)-adrenergic receptor-induced se cretion of growth hormone occurs independently of 5-hydroxytryptaminer gic receptors.