C S Wilcox1, W J Welch. 1. Department of Medicine, University of Florida College of Medicine, Gainesville.
Abstract
UNLABELLED: In experiments in anesthetized rats, the hypothesis that angiotensin II (Ang II) infusion released thromboxane (TxA2) which modulated the systemic and renal vasoconstriction was tested. Intravenous Ang II (500 ng.kg-1.min-1) increased MAP by 35 +/- 3 mm Hg and the excretion of TxB2 (P less than 0.03), whereas a similar pressor infusion of phenylephrine did not increase TxB2 excretion. A TxA2 receptor antagonist (TxRA) SQ-29,548 (8 mg.kg-1.hr-1) or pretreatment with a thromboxane synthesis inhibitor (TSI), UK-38,485 (50 mg.kg-1.day-1 x 3) blunted (P less than 0.005) the pressor response to 12 +/- 2 and 11 +/- 2 mm Hg, respectively, whereas TxRA did not modify the pressor response to phenylephrine. Infusion of Ang II at a dose of 50 ng.kg-1.min-1 reduced the GFR and increased the filtration fraction and renal vascular resistance. TxRA blunted (P less than 0.01) these effects of Ang II. IN CONCLUSION: 1.) Ang II releases TxA2 within the kidney independent of hypertension; 2.) TxA2 can mediate much of the pressor and renal hemodynamic responses to Ang II.
UNLABELLED: In experiments in anesthetized rats, the hypothesis that angiotensin II (Ang II) infusion released thromboxane (TxA2) which modulated the systemic and renal vasoconstriction was tested. Intravenous Ang II (500 ng.kg-1.min-1) increased MAP by 35 +/- 3 mm Hg and the excretion of TxB2 (P less than 0.03), whereas a similar pressor infusion of phenylephrine did not increase TxB2 excretion. A TxA2 receptor antagonist (TxRA) SQ-29,548 (8 mg.kg-1.hr-1) or pretreatment with a thromboxane synthesis inhibitor (TSI), UK-38,485 (50 mg.kg-1.day-1 x 3) blunted (P less than 0.005) the pressor response to 12 +/- 2 and 11 +/- 2 mm Hg, respectively, whereas TxRA did not modify the pressor response to phenylephrine. Infusion of Ang II at a dose of 50 ng.kg-1.min-1 reduced the GFR and increased the filtration fraction and renal vascular resistance. TxRA blunted (P less than 0.01) these effects of Ang II. IN CONCLUSION: 1.) Ang II releases TxA2 within the kidney independent of hypertension; 2.) TxA2 can mediate much of the pressor and renal hemodynamic responses to Ang II.