Parallel inactivation of alpha 2-adrenergic agonist binding and Ni by alkaline treatment

FEBS Lett. 1985 Nov 18;192(2):321-5. doi: 10.1016/0014-5793(85)80134-4.


Alpha 2-Adrenergic receptor-mediated inhibition of adenylate cyclase requires the guanine nucleotide-binding protein, Ni. This protein may also be required for stabilization of high-affinity alpha 2-adrenergic agonist binding. Human platelet membranes treated under alkaline conditions (pH 11.5) exhibited a selective loss of high-affinity agonist binding as measured by p-[3H]aminoclonidine and [3H]UK 14,304. Binding of the antagonist [3H]yohimbine was largely unaffected with retention of greater than 60% of control binding sites. Ni, determined by pertussis toxin-catalyzed [32P]ADP-ribosylation of cholate extracts from alkaline-treated membranes, was also markedly reduced. The parallel loss of alpha 2-agonist binding and Ni provides additional evidence that Ni is required for alpha 2-adrenergic agonist binding.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenylate Cyclase Toxin
  • Binding, Competitive
  • Blood Platelets / metabolism*
  • Cell Membrane / metabolism
  • GTP-Binding Proteins / metabolism*
  • Humans
  • Hydrogen-Ion Concentration
  • Kinetics
  • NAD / blood
  • Pertussis Toxin
  • Receptors, Adrenergic, alpha / metabolism*
  • Virulence Factors, Bordetella / metabolism


  • Adenylate Cyclase Toxin
  • Receptors, Adrenergic, alpha
  • Virulence Factors, Bordetella
  • NAD
  • Pertussis Toxin
  • GTP-Binding Proteins