Role of nitric oxide and cyclooxygenase-2 in regulating the renal hemodynamic response to norepinephrine

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2003-02, Vol.284 (2), p.488-R493
• Main Authors: Lopez, Ruth, Llinas, Maria T, Roig, Francisco, Salazar, F. Javier
• Format: Article
• Language: English
• Subjects: Animals; Blood Pressure - drug effects; Cyclooxygenase 2; Dinoprostone - metabolism; Dogs; Female; Glomerular Filtration Rate - drug effects; Hemodynamics - drug effects; Isoenzymes - metabolism; Kidney - blood supply; Kidney - drug effects; Kidney - enzymology; Kidney - metabolism; Male; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - metabolism; Norepinephrine - pharmacology; Prostaglandin-Endoperoxide Synthases - metabolism; Renal Circulation - drug effects; Sulfonamides - pharmacology; Vasoconstriction - drug effects
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00449.2002

Department of Physiology, School of Medicine, University of Murcia, 30100 Murcia, Spain We have reported that the renal hemodynamic effects of norepinephrine (NE) are modulated by cyclooxygenase-2 (COX-2)-derived metabolites. Our main objective was to examine whether there is an interaction between nitric oxide (NO) and COX-2 in modulating the renal hemodynamic effects of NE. NE was infused at three doses to anesthetized dogs pretreated with vehicle ( n  = 8), a selective COX-2 inhibitor (nimesulide) ( n  = 6), an NO synthesis inhibitor [ N G -nitro- L -arginine methyl ester; L -NAME] ( n  = 8), or with nimesulide and L -NAME ( n  = 5). During NE infusion, PGE 2 excretion increased (125%) in the control group and did not change in the L -NAME-treated dogs. The simultaneous inhibition of NO and COX-2 potentiated to a greater extent the NE-induced renal vasoconstriction than inhibition of either NO or COX-2. The NE-induced renal vasoconstriction during NO and COX-2 inhibition was reduced ( P