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Resveratrol reverses both thromboxane A2 receptor and non‐receptor (K+) mediated pulmonary vasoconstriction
Author(s) -
Natale Elizabeth Kathleen,
Slutzky Jessica L,
Chicoine Louis G
Publication year - 2009
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.23.1_supplement.770.10
Subject(s) - resveratrol , hypoxic pulmonary vasoconstriction , vasoconstriction , thromboxane , chemistry , pharmacology , lung , thromboxane a2 , receptor , medicine , endocrinology , anesthesia , platelet , biochemistry
Resveratrol (3,5,4′‐trihydroxystilbene) is an antioxidant found in red wine. Recent studies have demonstrated that resveratrol attenuates platelet activation/aggregation via increased NO/cyclic GMP formation. We tested the hypothesis that resveratrol reverses Thomboxane A2 receptor mediated pulmonary vasoconstriction. The lungs of adult male Spague‐Dawley rats (weight 225‐300 g) were isolated, ventilated (5% CO2, balance RA) and perfused with a physiological salt solution (PSS) at constant flow rate (30 mL/kg/min). U46619 , a thromboxane A 2 mimetic, was added to the perfusate to induce a stable pulmonary arterial pressure increase of 8‐10 mmHg (n=3). Increasing doses of resveratrol (3‐300 ug/mL) were added to the perfusate. The addition of resveratrol resulted in a dose dependent decrease in pulmonary arterial pressures. We then tested the hypothesis that resveratrol reverses non‐recptor mediated pulmonary vasoconstriction using KCl. We preconstricted the lungs with K + (20‐30 mM), which resulted in an arterial pressure increase of 8‐10 mmHg (n=3). Increasing doses of resveratrol (3‐300 ug/mL) were added to the perfusate. The addition of resveratrol resulted in a dose dependent decrease in pulmonary arterial pressure, such that resveratrol reversed K + constriction at concentrations >100 ug/mL. These results demonstrate that resveratrol reverses both, receptor‐mediated as well as non‐receptor mediated pulmonary vasoconstriction.