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Renal haemodynamics during hyperchloraemia in the anaesthetized dog: effects of captopril
1Department of Medicine, University of Florida College of Medicine, Gainesville.
Insights
Increased plasma chloride (hyperchloraemia) reduces kidney function and renin release. Captopril and indomethacin revealed angiotensin II
Area of Science:
- Nephrology
- Physiology
- Pharmacology
Background:
- Elevated plasma chloride concentration (PC1) is known to decrease renal blood flow (RBF) and glomerular filtration rate (GFR).
- PC1 also inhibits the intrarenal release of renin and angiotensin II (AII).
- The role of AII independent of prostaglandins (PGs) in the hemodynamic response to hyperchloraemia requires further investigation.
Purpose of the Study:
- To assess the role of angiotensin II (AII) independent of prostaglandins (PGs) in the hemodynamic response to hyperchloraemia.
- To investigate the effects of hyperchloraemia on renal hemodynamics and AII release in dogs.
- To determine the impact of indomethacin and captopril on these responses.
Main Methods:
- Studies were performed on denervated kidneys of anaesthetized greyhounds.
- Intrarenal infusion of 0.616 M-sodium acetate was switched to 0.616 M-NaCl to induce hyperchloraemia.
- Measurements included plasma chloride, RBF, GFR, and AII release into renal lymph.
- Captopril and indomethacin were administered to assess the roles of AII and PGs.
Main Results:
- Hyperchloraemia reduced GFR and RBF in vehicle-treated dogs, with reversible changes.
- Hyperchloraemia significantly reduced the release of AII into renal lymph.
- Indomethacin administration blunted the decrease in RBF during hyperchloraemia but did not significantly alter GFR or AII release.
Conclusions:
- Angiotensin II (AII) plays a role in the reduction of renal blood flow (RBF) during hyperchloraemia.
- Prostaglandins (PGs) contribute to the blunting of the RBF response to hyperchloraemia.
- Further research is needed to fully elucidate the complex interplay between AII, PGs, and renal hemodynamics in hyperchloraemia.
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. Anaesthetized 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 PCl 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 less than 0.05) and the RBF (13.0 +/- 1.4 to 8.3 +/- 0.6 ml min-1 kg-1; P less than 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 less than 0.01). 4. Indomethacin (0.6 mg kg-1 and 0.2 mg kg-1 h-1 intrarenally; n = 4) blunted (P less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)