The endothelin system has been implicated in various renal diseases. This review focuses on the involvement of endothelin-1 in pathogenesis and pathophysiology of acute and chronic renal failure with regard to its hemodynamic and nonhemodynamic effects. Future developments concerning the use of endothelin receptor antagonists and the role of endothelin in the kidney transplantation setting are discussed.

Acute Kidney Injury↗

PubMedDate not supplied

Preferential COX-2 inhibitor, meloxicam, compromises renal perfusion in euvolemic and hypovolemic rats.

Nonsteroidal anti-inflammatory drugs can impair renal perfusion through inhibition of cyclooxygenase (COX)-mediated prostaglandin synthesis. We investigated the influence of the preferential COX-2 inhibitor, meloxicam (MELO), on renal hemodynamics in eu- and hypovolemic rats compared to the nonselective COX inhibitor indomethacin (INDO). The hypovolemic state was obtained in rats by three daily injections of furosemide (2 mg/kg i.p.) followed by a sodium-deficient diet for 7 days. In euvolemic rats (n = 6) neither INDO (5 mg/kg i.v.) nor MELO (1 or 2 mg/kg i.v.) influenced mean arterial blood pressure (MAP) or impaired renal (RBF) and cortical blood flow (CBF). Medullary blood flow (MBF) decreased after INDO (18%; p<0.05), and dose-dependently after MELO (1 mg, 10%; 2 mg, 18%; p<0.05). In hypovolemic rats (n = 6) INDO and MELO had no effect on MAP. RBF and CBF were reduced after INDO (11 or 20%; p<0. 05), but showed no changes after MELO. INDO induced a decrease in MBF (22%; p<0.05) which was less pronounced after MELO (12%; p <0.05). In conclusion the preferential COX-2 inhibitor MELO compromized renal perfusion in the outer medulla both in eu- and hypovolemic animals.

Animals↗