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Eicosanoid gene expression in the brain during the onset of angiotensin II‐salt hypertension in the rat
Author(s) -
Jeyaraj Ninitha A.,
Dorrance Ann,
Subramanian Madhan,
Mohankumar Sheba,
Mohankumar P.S,
Fink Gregory
Publication year - 2011
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.25.1_supplement.828.8
Pretreatment of rats with the cyclooxygenase inhibitor ketoprofen inhibits development of elevated sympathetic activity and blood pressure in the angiotensin II (AngII)‐salt model of hypertension (HT). However, ketoprofen treatment has no effect in established AngII‐salt HT. To explore the mechanism of HT prevention by ketoprofen, brain and cerebrovascular expression of 21 genes in the eicosanoid pathway were assessed in Sprague Dawley rats. Animals were fed a high salt diet (2%) and infused vehicle alone (n=5) or AngII (n=5) at 150ng/min s.c. for 4 days. Mean arterial pressure was significantly greater in AngII‐salt rats (124.9±5 mmHg) versus control rats (104.6±2.4mmHg, p<0.05). Rostral ventrolateral medulla (RVLM) of AngII‐salt rats showed a significant upregulation of PGE2‐synthase (1.18‐fold), PGE3‐synthase (1.37‐fold), PGD2‐synthase (1.56‐fold), thromboxane A2 receptor (1.15‐fold) and arachidonate 5‐lipoxygenase (2.02‐fold). In the subfornical organ (SFO), PGI2‐synthase (1.95‐fold) and PGD2‐synthase (1.82‐fold) expression were increased. Eicosanoid gene expression was unaffected in the middle cerebral artery and paraventricular nucleus. We conclude that early increases in eicosanoid synthesis in the SFO and/or RVLM may be critical to the development of AngII‐salt hypertension. Funded by: NIH grant RO1 HL076312 to the Neurogenic Cardiovascular Diseases Consortium.