Role of neuropeptide Y and its receptor subtypes in neurogenic pulmonary edema

Eur J Pharmacol. 1996 Feb 5;296(3):297-305. doi: 10.1016/0014-2999(95)00705-9.


The effect of neuropeptide Y on the number of perivascular carbon deposits, assessed as a measure of lung vascular permeability, was examined in isolated perfused lung preparations of rats. The number of carbon particle deposits after bronchial application of neuropeptide Y was increased in a dose-dependent manner. In the presence of a beta-adrenoceptor antagonist, norepinephrine augmented the effects of neuropeptide Y. Peptide YY, an analog of neuropeptide Y, demonstrated a much lower potency for increasing the number of carbon deposits, and neuropeptide Y-(18-36), which elicits a weak antagonist action on the neuropeptide Y Y3 receptor, significantly decreased the neuropeptide Y-induced increase. Furthermore, examination of the influence of neuropeptide Y-(18-36) pretreatment on fibrin-induced neurogenic pulmonary edema, in rats, revealed a reduction of the protein concentration ratio of tracheal fluid to serum. Therefore, we conclude that neuropeptide Y may elevate vascular permeability in the pulmonary circulation, conceivably through the neuropeptide Y Y3 receptor, and that neuropeptide Y may in fact play a physiological role even in the in-situ pulmonary circulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Capillary Permeability
  • Carbon / metabolism
  • Male
  • Neuropeptide Y / pharmacology*
  • Norepinephrine / pharmacology
  • Propranolol / pharmacology
  • Pulmonary Edema / etiology*
  • Pyrilamine / pharmacology
  • Rats
  • Rats, Wistar
  • Receptors, Neuropeptide Y / classification
  • Receptors, Neuropeptide Y / physiology*


  • Neuropeptide Y
  • Receptors, Neuropeptide Y
  • Carbon
  • Propranolol
  • Pyrilamine
  • Norepinephrine