Analysis of responses to serotonin in the pulmonary vascular bed of the cat.

Journal Article (Journal Article)

Pulmonary vascular responses to serotonin (5-hydroxytryptamine; 5-HT) were investigated in the intact-chest cat under constant-flow conditions. Injections of 5-HT into the perfused lobar artery in doses of 1-30 micrograms caused dose-related increases in lobar arterial pressure and, at doses of 3-30 micrograms, decreases in systemic arterial pressure. Left atrial pressure was not changed, and responses to 5-HT were not altered by a thromboxane receptor blocking agent. Responses to 5-HT were blocked by ketanserin in doses that did not alter responses to agonists that increase pulmonary vascular resistance by various mechanisms. The ketanserin-induced blockade was not surmountable and at a dose of 0.5 mg/kg iv persisted for > 4 h. Prazosin and yohimbine, selective alpha 1- and alpha 2-adrenoceptor antagonists, were without effect on the pressor response to 5-HT, and ketanserin did not reduce responses to norepinephrine or the alpha 1-agonists, phenylephrine and methoxamine. 5-HT and the thromboxane mimic, U-46619, produced large increases in pulmonary vascular resistance; however, U-46619 was 300 times more potent than 5-HT. 5-HT increased lobar arterial pressure when the lung was perfused with dextran, and increases in lobar arterial pressure in response to 5-HT were not diminished when lobar ventilation was interrupted but were enhanced by N omega-nitro-L-arginine methyl ester and to a small extent by meclofenamate. The present data suggest that increases in pulmonary vascular resistance in the cat in response to 5-HT are due to activation of an S2 receptor in undefined "resistance vessel elements." These data suggest that pulmonary vasoconstrictor responses to 5-HT may be modulated to a small extent by release of a vasodilator prostaglandin and endothelium-derived nitric oxide but are not dependent on activation of thromboxane receptors, changes in bronchomotor tone, and interaction with alpha 1-receptors or with formed elements in blood.

Full Text

Duke Authors

Cited Authors

  • McMahon, TJ; Hood, JS; Nossaman, BD; Kadowitz, PJ

Published Date

  • July 1993

Published In

Volume / Issue

  • 75 / 1

Start / End Page

  • 93 - 102

PubMed ID

  • 8104177

International Standard Serial Number (ISSN)

  • 8750-7587

Digital Object Identifier (DOI)

  • 10.1152/jappl.1993.75.1.93


  • eng

Conference Location

  • United States