Dual actions of dephostatin on the nitric oxide/cGMP-signalling pathway in porcine iliac arteries

Eur J Pharmacol. 2005 Oct 3;521(1-3):124-32. doi: 10.1016/j.ejphar.2005.08.023. Epub 2005 Sep 22.

Abstract

We examined the effects of the nitrosoamine dephostatin on the nitric oxide (NO)/cyclic guanosine 3',5'-monophosphate (cGMP)-signalling in porcine iliac arteries. Dephostatin has been characterised as a tyrosine phosphatase inhibitor, but Western blot analyses showed that dephostatin did not augment tyrosine phosphorylation of arterial proteins. However, dephostatin relaxed pre-contracted arteries, and this effect was antagonised by the soluble guanylyl cyclase inhibitor 1H[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Furthermore, dephostatin increased the cGMP content and the serine phosphorylation of vasodilator-stimulated phosphoprotein. Dephostatin also inhibited the relaxation induced by acetylcholine and the NO-donor S-nitroso-N-acetyl-penicillamine (SNAP). In contrast, dephostatin did not affect the NO-dependent actions of 1,2,3,4-Oxatriazolium, 3-(3-chloro-2-metylphenyl)-5-[[(4methylphenyl)sulfonyl]amino]-hydroxide inner salt (GEA 3175). Measurement of NO revealed that dephostatin accelerated the consumption of NO. In conclusion, dephostatin exerts dual effects on the NO/cGMP-signalling pathway in iliac arteries. The drug actions included scavenging of NO, but also stimulation of cGMP production. These effects were not related to inhibition of tyrosine phosphatases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / pharmacology
  • Acetylcholine / pharmacology
  • Animals
  • Blotting, Western
  • Cyclic GMP / metabolism
  • Cyclic GMP / physiology*
  • Enzyme Inhibitors / pharmacology
  • Guanylate Cyclase / antagonists & inhibitors
  • Hydroquinones / pharmacology*
  • Iliac Artery / drug effects*
  • Iliac Artery / metabolism
  • Iliac Artery / physiology
  • In Vitro Techniques
  • Nitric Oxide / metabolism
  • Nitric Oxide / physiology*
  • Nitric Oxide Donors / pharmacology
  • Oxadiazoles / pharmacology
  • Penicillamine / analogs & derivatives
  • Penicillamine / metabolism
  • Penicillamine / pharmacology
  • Phenylephrine / pharmacology
  • Phosphoproteins / metabolism
  • Phosphorylation / drug effects
  • Protein Tyrosine Phosphatases / antagonists & inhibitors
  • Protein Tyrosine Phosphatases / metabolism
  • Quinoxalines / pharmacology
  • Serine / metabolism
  • Signal Transduction / drug effects*
  • Swine
  • Triazoles / pharmacology
  • Tyrosine / metabolism
  • Vasoconstrictor Agents / pharmacology
  • Vasodilation / drug effects
  • Vasodilator Agents / pharmacology

Substances

  • 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one
  • Enzyme Inhibitors
  • GEA 3175
  • Hydroquinones
  • Nitric Oxide Donors
  • Oxadiazoles
  • Phosphoproteins
  • Quinoxalines
  • S-nitro-N-acetylpenicillamine
  • Triazoles
  • Vasoconstrictor Agents
  • Vasodilator Agents
  • dephostatin
  • Phenylephrine
  • Nitric Oxide
  • Tyrosine
  • Serine
  • 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
  • Protein Tyrosine Phosphatases
  • Guanylate Cyclase
  • Penicillamine
  • Cyclic GMP
  • Acetylcholine