Somatostatin and alpha 2-adrenergic agonists selectively inhibit vasopressin-induced cyclic AMP accumulation in MDCK cells

FEBS Lett. 1986 Mar 17;198(1):38-42. doi: 10.1016/0014-5793(86)81180-2.

Abstract

The effect of somatostatin and alpha 2-adrenergic agonists on cyclic AMP accumulation was examined in MDCK cells, grown in defined medium. These hormones inhibited vasopressin-induced cyclic AMP formation, without affecting either the basal or the glucagon- and prostaglandin E2-stimulated level. Pretreating the cells with pertussis toxin, or incubating them with MnCl2 at a low concentration reversed the effect of somatostatin and alpha 2-agonists. These results suggest that somatostatin and norepinephrine could selectively modulate the renal effect of vasopressin, via the inhibitory regulatory subunit (Ni) of adenylate cyclase.

MeSH terms

  • Adenylate Cyclase Toxin
  • Adrenergic alpha-Agonists / pharmacology*
  • Animals
  • Cells, Cultured
  • Cyclic AMP / metabolism*
  • Dinoprostone
  • Dogs
  • Glucagon / pharmacology
  • Kidney / metabolism
  • Manganese / pharmacology
  • Pertussis Toxin
  • Prostaglandins E / pharmacology
  • Somatostatin / pharmacology*
  • Vasopressins / pharmacology*
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Adenylate Cyclase Toxin
  • Adrenergic alpha-Agonists
  • Prostaglandins E
  • Virulence Factors, Bordetella
  • Vasopressins
  • Manganese
  • Somatostatin
  • Glucagon
  • Cyclic AMP
  • Pertussis Toxin
  • Dinoprostone