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Mechanisms of action of GH
The process of growth, which is common to all multicellular organisms, is complex and involves the interaction of a multiplicity of factors; despite this, the GH/IGF function still maintains its preminence, and, in turn, the same is true for all approaches aimed at reducing the consequences of GH/IGF excess. In this review paper, we will deal briefly with some aspects of GH/IGF mechanism of action which are instrumental to the appreciation of a novel class of a "designer" GH antagonist, for use in conditions characterized by excess GH action and elevated serum IGF-I
α2-Adrenergic stimulation enhances growth hormone secretion in the dog: a presynaptic mechanism?
ntravenous administration of clonidine (CLO), (2,4 and 8 ug/kg), a predominantly α2-adrenergic receptor agonist, induced in unanesthetized dogs clear-cut and dose -related rises in plasma GH (cGH) levels. Pretreatment with the selective antagonist of α1-adrenergic receptors prazosin (0.1 mg/Kg iv) left unaltered the cGH rise inducedby 4 ug/Kg of CLO whilst blockade of α2-adrenergic receptors by yohimbine (2.5 mg/Kg iv) completely prevented it. In dogs treated 24 h previously with reserpine (0.5 mg/Kg iv), a depletor of brain catecholamine stores, CLO was ineffective to stimulate cGH release. These data indicate that in the dog the GH-releasing effect of CLO occurs via stimulation of α2-adrenergic receptors and suggest that the latter are located presynaptically in relation to norepinephrine neurons
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