Interactions between nitric oxide and prostanoids in isolated perfused kidneys of the rat.

1. The present study was aimed to assess the interaction between nitric oxide (NO) and thromboxane (Tx) A2-prostaglandin (PG) H2 in single-pass perfused isolated kidneys of the rat. 2. Noradrenaline (NA, 63 and 110 nM) dose-dependently elevated the renal vascular resistance (RVR), the glomerular filtration rate (GFR) and the urinary excretion of sodium (UNa V). Infusion of N omega-nitro-L-arginine methyl ester (L-NAME, 100 microM), an inhibitor of NO synthesis, enhanced the effects of NA on RVR and on UNa V, but decreased those on GFR. The TxA2-PGH2 (TP) receptor blockade by GR32191B (10 microM) attenuated this potentiating effect of L-NAME. 3. When renal perfusion pressure was stepwise increased from 90 to 150 mmHg, L-NAME similarly decreased renal perfusion flow rate and GFR. 4. The venous excretion of TxB2 and 6-keto-PGF1 alpha was increased by L-NAME in baseline conditions as well as after NA or increasing renal perfusion pressure (RPP). 5. These results suggest that: (1) TxA2 and PGH2 play an important role in the overall effect of the renal prostanoids, (2) NO strongly interacts with the cyclo-oxygenase pathway and reduces the prostanoid synthesis in the kidney, and (3) the pressor effect of L-NAME partly relies upon the vasoconstrictor effect of TxA2 and PGH2.