Vasodilator effect of urotensin II, one of the most potent vasoconstricting factors, on rat coronary arteries

Eur J Pharmacol. 2000 Aug 18;402(1-2):R5-7. doi: 10.1016/s0014-2999(00)00506-9.


The effects of human urotensin II on coronary flow were studied in the perfused rat heart. Urotensin II transiently decreased coronary flow, then induced sustained vasodilatation. In the presence of a cyclooxygenase inhibitor, diclofenac, coronary vasodilatation was significantly inhibited. A nitric oxide synthase inhibitor, N(G)-nitro-L-arginine (L-NNA), attenuated the urotensin-induced vasodilatation. These data suggest that urotensin II modulates coronary flow through factors such as cyclooxygenase products and nitric oxide to elicit coronary vasodilatation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Coronary Vessels / drug effects*
  • Diclofenac / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Humans
  • In Vitro Techniques
  • Male
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitric Oxide Synthase Type III
  • Nitroarginine / pharmacology
  • Rats
  • Rats, Inbred F344
  • Urotensins / antagonists & inhibitors
  • Urotensins / pharmacology*
  • Vasoconstrictor Agents / pharmacology*
  • Vasodilator Agents / pharmacology*


  • Anti-Inflammatory Agents, Non-Steroidal
  • Enzyme Inhibitors
  • Urotensins
  • Vasoconstrictor Agents
  • Vasodilator Agents
  • Diclofenac
  • Nitroarginine
  • urotensin II
  • NOS3 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type III
  • Nos3 protein, rat