Alpha-2-adrenergic pathways release growth hormone via a non-GRF-dependent mechanism in normal human subjects

Clin Endocrinol (Oxf). 1988 Sep;29(3):309-16. doi: 10.1111/j.1365-2265.1988.tb01229.x.

Abstract

Administration of a supramaximal dose of GRF 1-44 (200 micrograms, i.v.) to normal human volunteers increased GH levels while a further bolus of GRF (200 micrograms i.v.) given 2 hours later failed to increase plasma GH levels. In contrast, alpha-adrenergic receptor agonism with either propranolol-adrenaline infusion or clonidine increased plasma GH levels at a time when GH responses to this supramaximal dose of GRF were absent. This indicates that alpha-adrenergic pathways stimulate GH secretion through a non-GRF-dependent mechanism in normal human subjects.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Adult
  • Clonidine / pharmacology
  • Epinephrine / pharmacology
  • Growth Hormone / blood
  • Growth Hormone / metabolism*
  • Growth Hormone-Releasing Hormone / pharmacology*
  • Humans
  • Pituitary Gland, Anterior / drug effects
  • Pituitary Gland, Anterior / metabolism*
  • Propranolol / pharmacology
  • Receptors, Adrenergic, alpha / drug effects*

Substances

  • Receptors, Adrenergic, alpha
  • Growth Hormone
  • Growth Hormone-Releasing Hormone
  • Propranolol
  • Clonidine
  • Epinephrine