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EETs oppositely regulate pulmonary and systemic pressure in hypoxia
Author(s) -
Kandhi Sharath,
Qin Jun,
Froogh Ghezal,
Alruwaili Norah,
Wolin Michael S.,
Huang An,
Sun Dong
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.758.1
Subject(s) - epoxide hydrolase 2 , hypoxia (environmental) , ventricular pressure , medicine , pulmonary hypertension , chemistry , pharmacology , blood pressure , endocrinology , oxygen , enzyme , biochemistry , organic chemistry
Aim To study the effects of epoxyeicosatrienoic acids (EETs) on the pulmonary and systemic circulations in response to hypoxia. Methods Male wild type (WT) and soluble epoxide hydrolase knockout (sEH‐KO) mice, and WT mice fed with a sEH inhibitor ( t ‐TUCB; 1mg/kg/day) via oral gavage for 4 weeks, were used. Right ventricular systolic pressure (RVSP) and systemic arterial pressures (MABP) were recorded via catheterizations, in response to breathing 100% and 10% oxygen (hypoxia). Results Baseline of RVSP was comparable among the three groups of mice, whereas, MABP was significantly lower in sEH‐KO and TUCB‐treated groups compared to WT mice. Exposure of mice to hypoxia elicited significant increases in RVSP with more predominant increases in TUCB‐treated and sEH‐KO than WT mice. 14,15‐EEZE that had no effects on responses of WT mice, prevented hypoxia‐induced elevation of RVSP in other two groups. Hypoxia decreased MABP, which was reversed by EEZE in sEH‐KO and TUCB‐treated mice. Conclusions Hypoxia elicited the elevation of RVSP but reduction of MABP, responses that were potentiated, as a function of the deletion of sEH gene and inhibition of sEH activity. Support or Funding Information (This work was supported by NIH HL070653 and HL115124)