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Temporal changes in eicosanoid excretion in Angiotensin (A) II‐induced hypertension
Author(s) -
Liclican Elvira L,
Li Jing,
Pedraza Paulina L,
Chen YuJung,
Ferreri Nicholas R,
Quilley John,
McGiff John C,
Carroll Mairead A
Publication year - 2006
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.20.4.a765-c
Subject(s) - eicosanoid , angiotensin ii , medicine , endocrinology , excretion , renin–angiotensin system , chemistry , blood pressure , biochemistry , arachidonic acid , enzyme
The 10‐day AII infusion model of hypertension alters arachidonic acid metabolism involving 1) adenosine‐stimulated epoxyeicosatrienoic acid (EETs) synthesis and 2) tumor necrosis factor (TNF)‐activated COX‐2‐PGE 2 mechanisms. Male Sprague‐Dawley rats (age 8‐10 weeks) were infused with AII (125 ng/min); sham control rats received 0.01 N acetic acid. Day 3 values: systolic blood pressure (SBP): AII 195±11 vs. Sham 123±4 mmHg; urinary excretion of EETs increased to AII 8.9±3.7 vs. Sham 1.7±0.3 ng/d (p<0.05). Peak EET excretion coincided with increased adenosine excretion: AII 3.86±1.0 vs. Sham 0.79±0.2 adenosine/internal standard ratio (p<0.05). Urinary TNF excretion: AII 466±106 vs. Sham 80±26 pg/d (p<0.05); PGE 2 excretion: AII 389±94 vs. Sham 140±20 ng/d. Day 10 values: SBP: AII 184±5 vs. Sham 120±5 mmHg; EETs excretion fell to levels not different from those of Sham. TNF and PGE 2 excretion remain elevated: AII 457±12 vs. Sham 41±11 pg/d; AII 645±143 vs. Sham 237±44 ng/d, respectively (p<0.05). The role of heme oxygenase‐1 (HO‐1) in producing a decline in EET production in rats receiving AII was examined. Rats were infused with subpressor concentrations of AII (40 ng/min) for 3 days with and without concurrent SnCl 2 treatment to induce HO‐1. SnCl 2 treatment produced diminished release of EETs from isolated kidneys (AII 8.3±3.8 vs. AII + SnCl 2 0.29±0.27 ng/min). Features of the 10‐day AII infusion model of hypertension are: 1) initial rise and late decline in EET production; the latter possibly via activation of HO‐1 and 2) sustained increased PGE 2 excretion.