Abstract
1. An increase in plasma chloride concentration (PC1) decreases renal blood flow (RBF) and glomerular filtration rate (GFR) and inhibits the intrarenal release of renin and angiotensin II (AII). Captopril was administered to indomethacin-treated dogs to assess the role of AII independent of prostaglandins (PGs) in the haemodynamic response to hyperchloraemia. Studies were performed on kidneys that were denervated by autotransplantation. 2. Anesthetized greyhounds received an intrarenal infusion of 0.616 M-sodium acetate, which was changed to 0.616 M-NaCl (hyperchloraemia). These infusions increased the plasma sodium and osmolality at the experimental kidney by 7-11% throughout but increased the PC1 during the hypertonic NaCl infusions only (122 .+-. 3 to 136 .+-. 3 mM). 3. In vehicle-treated dogs (n = 8), hyperchloraemia reduced the GFR (1.4 .+-. 0.1 to 1.0 .+-. 0.1 ml min-1 kg-1: P < 0.05) and the RBF (13.0 .+-. 1.4 to 8.3 .+-. 0.6 ml min-1 kg-1: P < 0.01): these changes were reversible on return to the 0.616 M-sodium acetate infusion. Hyperchloraemia reduced the release of AII into renal lymph (2.5 .+-. 0.9 to 1.2 .+-. 0.4 pg min-1 kg-1; P < 0.01). 4. Indomethacin (0.6 mg kg-1 and 0.2 mg kg-1 h-1 intrarenally: n = 4) blunted (P < 0.05) the Cl- induced fall in RBF (10.4 .+-. 1.1 to 8.2 .+-. 0.6 ml min-1 kg-1) without changing significantly the fall in GFR or the release of AII into renal lymph. 5. Captopril (1.5 mg kg-1 and 0.7 mg kg-1 h-1 intrarenally) given to indomethacin-treated dogs (n = 6) abolished Cl- induced changes in release of AII into lymph (0.6 .+-. 0.2 to 0.7 .+-. 0.1 pg min-1 kg-1; not significant, n.s.) without modifying the fall in RBF (14.4 .+-. 1.8 to 12.2 .+-. 1.5 ml min-1 kg-1). However, after captopril, the Cl- induced fall in GFR was abolished (1.0 .+-. 0.1 to 1.2 .+-. 0.2 ml min-1 kg-1; n.s.). 6. In conclusion, Cl- induced renal vasoconstriction is modulated by vasoconstrictor PGs but not by AII. However, the Cl- induced fall in GFR requires a fall in renal AII generation.