Cyclic GMP stimulation by vasopressin in LLC-PK1 kidney epithelial cells is l-arginine-dependent

Henning Schröder, Karsten Schror

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

The l-arginine antagonist NG-monomethyl-l-arginine has been shown to inhibit nitric oxide formation from l-arginine in endothelial cells. In the present study NG-monomethyl-l-arginine was used to assess the role of l-arginine for cyclic GMP stimulation by vasopressin in a kidney epithelial cell line (LLC-PK1). Preincubation of cells with 1 μmol/l, 10 μmol/l and 100 μmol/l NG-monomethyl-l-arginine decreased cyclic GMP stimulation at 1 μmol/l vasopressin by 25%, 71% and 90%, respectively. This inhibition by NG-monomethyl- l-arginine was markedly reduced by l-arginine (2 mmol/1) but not d-arginine (2 mmol/1). Cyclic GMP stimulation by the calcium ionophore A23187 was also inhibited by NG-monomethyl-l-arginine and enantioselectively restored by l-arginine. However, NG-monomethyl-l-arginine did not affect cyclic GMP stimulation by sodium nitroprusside that spontaneously releases nitric oxide. These results suggest that, in kidney epithelial cells, vasopressin induces nitric oxide formation from l-arginine leading to activation of soluble guanylate cyclase. It is concluded that nitric oxide formation from l-arginine is not only responsible for endothelium-dependent relaxation but may be a more general pathway with regulatory function for intracellular guanylate cyclase activity.

Original languageEnglish (US)
Pages (from-to)475-477
Number of pages3
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Volume340
Issue number4
DOIs
StatePublished - Oct 1989

Keywords

  • Arginine
  • Cyclic GMP
  • Kidney epithelial cells
  • Nitric oxide
  • Vasopressin

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