PMID: 8938670Nov 1, 1996Paper

Effect of urodilatin on platelet-activating factor-induced bronchoconstriction, vasoconstriction and edema formation in isolated rat lung

Naunyn-Schmiedeberg's Archives of Pharmacology
S UhligA Wendel

Abstract

In the isolated perfused rat lung, perfusion with platelet-activating factor causes bronchoconstriction, vasoconstriction and edema formation. The bronchoconstriction and vasoconstriction are largely mediated by thromboxane, whereas the edema formation is due to enhanced vascular permeability unrelated to eicosanoids. Since natriuretic peptides are known to relax smooth muscle and were suggested to attenuate enhanced vascular permeability, we investigated the effect of urodilatin on the PAF-induced alterations in lung function. Pretreatment with urodilatin (0.25 microM or 0.75 microM) reduced the PAF-induced increase in airway and vascular resistance by approximately 50%. Urodilatin pretreatment, however, was completely ineffective against the PAF-induced increase in weight gain and in vascular permeability, as assessed by the vascular filtration coefficient. Furthermore, urodilatin failed to affect the release of thromboxane into the perfusate in PAF-exposed lungs. Thus, urodilatin relaxes airway and vascular smooth muscle, but fails to reduce edema formation in PAF-perfused rat lungs.

Citations

Sep 3, 2002·American Journal of Respiratory and Critical Care Medicine·Rolf GöggelStefan Uhlig
Dec 16, 2004·Critical Care Medicine·Henning D StubbeFrank Hinder
Apr 6, 2004·American Journal of Physiology. Lung Cellular and Molecular Physiology·C MartinS Uhlig
Sep 8, 2007·Canadian Journal of Physiology and Pharmacology·Shyam S Mohapatra

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