Prostaglandin E1 inhibits the pulmonary vascular pressor response to hypoxia and prostaglandin F2α

E. K. Weir, J. T. Reeves, R. F. Grover

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14 Scopus citations

Abstract

In the anesthetised dog an infusion of exogenous prostaglandin E1 (100μG/min) inhibits the pulmonary vascular pressor response to hypoxia. Both 25 and 100 μG/min PGE1 can reduce the transient pulmonary hypertension caused by a bolus of prostaglandin F. This suggests that hypoxia and PGF2α may share a final common pathway in producing pulmonary vasoconstriction. These results may help to explain the mechanism by which endotoxin inhibits the pulmonary vascular response to hypoxia. This effect is probably achieved by stimulating the production of an endogenous dilator prostaglandin. Exogenous PGE1 can mimic this effect.

Original languageEnglish (US)
Pages (from-to)623-631
Number of pages9
JournalProstaglandins
Volume10
Issue number6
DOIs
StatePublished - 1975

Bibliographical note

Funding Information:
This work was supported by grants #HL 14985 and HL 05973 from the National Institutes of Health. Dr. Weir is the recipient of a Fulbright Scholarship. Dr. Grover is the recipient of an NIH Research Career Development Award #HL 29237. We are grateful for the assistance of R. Glas, B. Kaplan, M. Munroe, D. Smith, E. Toyos, S. Hofmeister and D. Jackson. Prostaglandins E 1 and F2~ were kindly provided by the Upjohn Company.

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