β-Adrenergic Stimulation of Adenosine-3’,5’-Monophosphate (c-AMP) Accumulation and of Prolactin and Growth Hormone Secretion in Rat Anterior Pituitary Cell Cultures

Abstract

The .beta.-adrenergic agonist L-isoproterenol (ISO) (10-9-10-7 M) provoked a prompt and profound increase of intracellular cAMP accumulation in monolayer cultures of rat anterior pituitary. In superfused reaggregate cell cultures ISO also stimulated cAMP outflow. The effect was blocked by propranolol and the highly selective .beta.2-receptor blocker ICI 118.551 [erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol]. Epinephrine (E), norepinephrine (NE) and the highly selective .beta.2-agonist zinterol (ZIN) also stimulated cAMP accumulation. The order of potency ZIN .gtoreq. ISO > E .mchgt. NE together with the high potency of ICI 118.551 suggests the .beta.-effect is mainly through the .beta.2-receptor subtype. The same concentration of ISO strongly stimulated growth hormone (GH) release and, as previously shown, prolactin (PRL) release from superfused reaggregate cell cultures, but not luteinizing hormone or TSH release. Stimulation of PRL and GH release from these cultures was also induced by the adenylate cyclase activator forskolin. Some interference of .beta.-adrenergic effects on contaminating fibroblasts or endothelial cells could be reasonably excluded. .beta.-Adrenergic stimulation of cAMP accumulation in anterior pituitary cells apparently elicits GH and PRL release.