Eicosanoid-dependence of responses of pre- but not postglomerular vessels to noradrenaline in rat isolated kidneys.

1. We investigated the role of nitric oxide (NO) and of vasoactive eicosanoids in the control of renal vascular resistance (RVR) and glomerular filtration rate (GFR) and of their responses to noradrenaline (NA). This study was conducted in single-pass perfused, isolated kidney preparations of the rat. 2. NA (63, 110 and 160 nM) dose-dependently increased RVR and to a lesser degree GFR. 3. In baseline conditions, N omega-nitro-L-arginine methylester (L-NAME, 100 microM) increased GFR more than RVR, thus demonstrating a basal release of NO which predominates in postglomerular vessels. 4. In kidneys stimulated with NA, L-NAME potentiated the increases in RVR but not in GFR. Indomethacin (1.5, 150 nM and 15 microM) did not alter GFR but markedly and dose-dependently reduced the NA-induced increase in RVR. Similar results were obtained with GR 32191B (10 and 100 microM), a prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist. 5. Indomethacin (15 microM) suppressed the enhancing effects of L-NAME on RVR responses to NA but did not affect those on GFR. 6. It is concluded that the mechanisms of the response to NA differ among pre- and postglomerular vessels. In preglomerular vessels the vasoconstrictor action and the NO release depend upon the activation of PGH2/TxA2 receptors, while both are eicosanoid-independent in the postglomerular vessels.