Endocrine Abstracts

Background: The activation of the GHS-R1a receptor by acylated ghrelin (AG) or by synthetic GH secretagogues (GHS), potently stimulates GH release and mediates other neuroendocrine/metabolic effects. Beta-adrenergic receptor agonists negatively influence GH secretion and other metabolic functions. The GH response to AG and GHS is refractory to the inhibitory effect of β2-adrenoceptors activation but no other report has evaluated the interactions between AG and salbutamol ...