Stimulation of alpha-adrenoceptors inhibits cholesterol synthesis in freshly isolated human mononuclear leukocytes

Life Sci. 1995;57(17):1613-20. doi: 10.1016/0024-3205(95)02137-8.

Abstract

Specific agonists and antagonists for alpha 1- and alpha 2-adrenoceptors were used to determine an alpha-adrenoceptor-mediated action of adrenaline on the rate of sterol synthesis from [14C]acetate in freshly isolated human mononuclear leukocytes. In the presence of the beta-adrenergic blocker propranolol (1 microM), adrenaline (100 microM) and noradrenaline (100 microM) suppressed sterol synthesis by 36% and 38%, respectively, suggesting an action via alpha-adrenoceptors. The catecholamine effect could be mimicked by alpha 2-selective beta-phenethylamines including alpha-methylnoradrenaline, but not by imidazolines. alpha 1-Selective agonists like phenylephrine and methoxamine had no effect on the pathway. Accordingly, the effects of adrenaline and the alpha 2-selective agonist alpha-methylnoradrenaline on sterol synthesis were attenuated by the unselective alpha-antagonist phentolamine and the selective alpha 2-antagonist yohimbine, but not by the alpha 1-antagonist prazosin. The results provide evidence that catecholamines can affect sterol synthesis in human mononuclear leukocytes by stimulating alpha-adrenoceptors of the alpha 2-subtype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cholesterol / biosynthesis*
  • Clonidine / pharmacology
  • Dopamine / pharmacology
  • Dose-Response Relationship, Drug
  • Epinephrine / pharmacology
  • Humans
  • Leukocytes, Mononuclear / metabolism*
  • Norepinephrine / pharmacology
  • Phentolamine / pharmacology
  • Propranolol / pharmacology
  • Receptors, Adrenergic, alpha / drug effects*
  • Receptors, Adrenergic, alpha / physiology*
  • Sterols / metabolism

Substances

  • Receptors, Adrenergic, alpha
  • Sterols
  • Cholesterol
  • Propranolol
  • Clonidine
  • Dopamine
  • Norepinephrine
  • Epinephrine
  • Phentolamine