Abstract
Neuropeptide Y (NPY) is a unique modulator of renal function that enhances urine flow and sodium excretion despite marked reductions in renal blood flow. We investigated whether the cyclooxygenase inhibitor indomethacin alters the renal NPY effects in anesthetized rats. Treatment with 5 mg/kg indomethacin i.p. lowered urinary prostaglandin excretion by ≈85%. Systemic infusion of NPY elevated mean arterial pressure by ≈15 mm Hg and renovascular resistance by ≈8.0 mm Hg/ml/min, whereas the related peptide YY3–36(PYY3–36) did not. Nevertheless, both peptides enhanced urine flow rate by ≈250 and ≈100 μl/15 min, respectively, and sodium excretion by ≈15 μmol/15 min. Treatment with indomethacin did not affect NPY- and PYY3–36-induced alterations of systemic and renovascular hemodynamics but completely abolished NPY- and PYY3–36-induced diuresis and natriuresis. Endogenous creatinine clearance was not affected by any treatment. We conclude that cyclooxygenase-derived arachidonic acid metabolites are not involved in the systemic or renal hemodynamic effects of NPY and PYY3–36 but mediate NPY- and PYY3–36-induced diuresis and natriuresis.
Footnotes
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Send reprint requests to: Dr. Martin C. Michel, Nephrology Laboratory IG 1, Klinikum, 45122 Essen, Germany. E-mail:martin.michel{at}uni-essen.de
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↵1 This work was supported in part by the Deutsche Forschungsgemeinschaft (Mi 294/5–2).
- Abbreviations:
- MAP
- mean arterial pressure
- NPY
- neuropeptide Y
- PYY3–36
- peptide YY3–36
- RBF
- renal blood flow
- RVR
- renovascular resistance
- i.p.
- intraperitoneal
- ANOVA
- analysis of variance
- Received August 4, 1997.
- Accepted April 28, 1998.
- The American Society for Pharmacology and Experimental Therapeutics
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