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- W1036175246 abstract "Introduction Urotensin-II (U-II) is a vasoconstrictor peptide and its potency can be up to 100 fold greater than that of endothelin-1 (ET-1). ET-1 plays a major role in the vascular changes associated with salt-sensitive hypertension, but the effects of U-II in arteries from these animals have not yet been defined. Objective We hypothesized that DOCA-salt rats have increased vascular reactivity to U-II. Methods and Results Wistar rats were unilaterally nephrectomyzed and deoxycorticosterone-acetate (DOCA) (200mg/Kg) pellets were implanted. DOCA rats received water containing 1% NaCl/0.2% KCl, for 5 weeks. Aortic rings were mounted in myograph chambers and functional studies were performed. DOCA rats displayed increased systolic pressure (Control: 117±1 vs DOCA: 179±3; mmHg). Maximal contractions (mN) to U-II were decreased in endothelium-intact (Control: 16.6±1 vs DOCA: 8.8±1) and endothelium-denuded (Control: 21.3±1.1 vs DOCA: 10.4±0.9) aortas from DOCA rats. This difference was abolished in endothelium-intact vessels incubated with 10−5M urantide (U-II antagonist) (Control: 13.5±0.9 vs DOCA: 12.7±0.9). Conclusion Our results suggest that U-II production/release is augmented in mineralocorticoid hypertension and that decreased vascular reactivity to the peptide may represent counter-regulatory mechanisms that limit additional vascular damage to this potent vasoconstrictor." @default.
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- W1036175246 date "2009-04-01" @default.
- W1036175246 modified "2023-09-25" @default.
- W1036175246 title "DOCA‐salt hypertensive rats display decreased vascular reactivity to urotensin‐II" @default.
- W1036175246 doi "https://doi.org/10.1096/fasebj.23.1_supplement.1017.35" @default.
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