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 β-adrenergic agonist 1-isoproterenol (ISO) (10^–9–10^–7M) provoked a prompt and profound increase of intracellular c-AMP accumulation in monolayer cultures of rat anterior pituitary. In superfused reaggregate cell cultures ISO also stimulated c-AMP outflow. The effect was blocked by propranolol and the highly selective β2-receptor blocker ICI 118.551. Epinephrine (E), norepinephrine (NE) and the highly selective β2-agonist zinterol (ZIN) also stimulated c-AMP accumulation. The order of potency ZIN ≧ ISO > E > NE together with the high potency of ICI 118.551 suggests the β-effect is mainly through the β2-receptor subtype. The same concentrations 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 thyroid stimulating hormone release. Stimulation of PRL and GH release from these cultures was also induced by the adenylyl cyclase activator forskolin. Since interference of β-adrenergic effects on contaminating fibro-blasts or endothelial cells could be reasonably excluded, the present data suggest that β-adrenergic stimulation of c-AMP accumulation in anterior pituitary cells elicits GH and PRL release.

Mechanisms for gonadotropin-releasing hormone potentiation of growth hormone rebound following norepinephrine inhibition in goldfish pituitary cells

“…Since norepinephrine (NE) (50) and epinephrine (EP) (23) can be detected in hypophyseal portal blood at concentrations higher than that of peripheral blood, adrenergic input acting directly at the pituitary level has been suggested. This idea has been confirmed by the findings that ␤-adrenoreceptors are expressed in somatotrophs (1) and ␤ 2 -agonists can induce GH release and cAMP production in rat pituitary cells (49). Apparently, ␣ 2 -adrenoreceptors are not involved in GH release at the pituitary level (33).…”

Atenolol Enhances Growth Hormone Release to Exogenous Growth Hormone-Releasing Hormone but Fails to Alter Spontaneous Nocturnal Growth Hormone Secretion in Boys with Constitutional Delay of Growth

“…First, these agents lack the inherent ability to stimulate G H secretion, although they increase the potency of other G H secretagogues (7,8,(10)(11)(12)(13). Second, (3-adrenergic agonists have a direct stimulatory effect on G H secretion from rat anterior pituitary cells in vitro (26)(27)(28)(29), but do not affect subsequent GHRH-stimulated G H release (Krieg RJ, personal communication). In contrast, isoproterenol infusion to intact rats predominately inhibits subsequent GHRH stimulation, an effect abolished by prior administration of an antiserum to SRIH (Krieg RJ, personal communication).…”

Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells

“…In the same animal model, norepinephrine (NE) and epinephrine (Ep) can be detected in the hypophyseal portal blood (24,54), suggesting that adrenergic input may have direct effects at the pituitary level. This idea is supported by the findings that ␤-adrenoreceptors are expressed in somatotrophs (1) and ␤ 2 -agonists (e.g., zinterol) can induce GH secretion in rat pituitary cells (51). The GH-releasing effect caused by ␤ 2 stimulation at the pituitary level is mediated through cAMP production (16) and elevation in intracellular Ca 2ϩ levels (41).…”