RESUMO
Necrosis of the outer two-thirds of the cortex (CN) was induced with boiling water in the left kidney of rats. Two days afterward, morphological damage was shown to be limited to the superficial cortex; deep nephron population was well-preserved. Glucose reabsorption under basal and glucose loading conditions, and extraction of p-aminohippurate, used as indices of proximal tubule integrity, were normal in control and experimental kidneys 48 h after cortical necrosis. Basal fractional water and electrolyte excretion did not differ between control and experimental kidneys. Calculated mean single-nephron glomerular filtration rate (GFR) and plasma flow for superficial (SupGFR and SupNPF) and juxtamedullary nephrons (JMGFR and JMPF) were similar to those obtained by micropuncture and Hanssen's technique for SupGFR, and for JMGFR by Hanssen's. Volume expansion led to a 27% increase in calculated SupGFR, but no change in JMGFR. The JMPF increased by 81%, whereas SupNPF increased by only 23%, suggesting that, in this model, GFR of deep nephrons may be independent of plasma flow. The results indicate that deep nephrons retain their functional integrity 48 h after cortical necrosis. After volume expansion fractional excretion of sodium was greater, and fractional water reabsorption less, in CN than in control kidneys. Thus handling of sodium and water by superficial and deep nephrons under basal conditions was similar, but reabsorptive capacity for deep nephrons of CN was lower during volume expansion. The present studies suggest that deep nephrons can maintain relatively normal function in cortical necrosis.
Assuntos
Córtex Renal/patologia , Animais , Feminino , Taxa de Filtração Glomerular , Córtex Renal/fisiopatologia , Córtex Renal/ultraestrutura , Glomérulos Renais/patologia , Glomérulos Renais/fisiopatologia , Glomérulos Renais/ultraestrutura , Microscopia Eletrônica de Varredura , Necrose , Néfrons/patologia , Néfrons/fisiopatologia , Néfrons/ultraestrutura , Potássio/sangue , Potássio/urina , Ratos , Ratos Endogâmicos , Valores de Referência , Circulação Renal , Sódio/sangue , Sódio/urinaRESUMO
The involvement of the liver in the control of the renal excretion of water and sodium can be deduced from some recent investigations. Hypertonic or isotonic sodium chloride infusion into the hepatic portal vein enhanced renal sodium excretion when compared with identical infusions into a systemic vein. It has been suggested that a humoral factor produced by the liver could be a functional link between the liver and the kidney. In order to test this hypothesis, the present experiments were carried out in two groups of anesthetized dogs. Animals from group I were infused with NaCl (855 mmol/l) at a rate of 0.05 ml/min/kg b.w. during 30 min, into the portal vein. Blood samples were withdrawn from the suprahepatic vein, before (SH1) and coinciding with the maximal natriuresis after hypertonic saline infusion (SH2). Plasma from SH1 and SH2 were infused into the left renal artery (LRA) of dogs from group II. Two 20 min clearance periods were performed before and after each SH-infusion. After both SH-infusions urinary sodium excretion (UNaV) was significantly increased from preinfusion values in both kidneys, and these increases were significantly greater after SH2 than after SH1. No significant differences were found in UNaV between left and right kidney. After both plasma infusions the increases in urinary volume and osmolar clearance were higher in the infused than in the not infused kidney. These results suggest that the plasma leaving the liver contains a substance with natriuretic activity and that the infusion of hypertonic NaCl into the portal vein could induce either a higher secretion of the same substance or the presence of other different substance.
Assuntos
Fígado/fisiologia , Natriurese , Animais , Cães , Feminino , Taxa de Filtração Glomerular , Fígado/irrigação sanguínea , Masculino , Circulação Renal , Solução Salina HipertônicaRESUMO
The involvement of the liver in the control of the renal excretion of water and sodium can be deduced from some recent investigations. Hypertonic or isotonic sodium chloride infusion into the hepatic portal vein enhanced renal sodium excretion when compared with identical infusions into a systemic vein. It has been suggested that a humoral factor produced by the liver could be a functional link between the liver and the kidney. In order to test this hypothesis, the present experiments were carried out in two groups of anesthetized dogs. Animals from group I were infused with NaCl (855 mmol/l) at a rate of 0.05 ml/min/kg b.w. during 30 min, into the portal vein. Blood samples were withdrawn from the suprahepatic vein, before (SH1) and coinciding with the maximal natriuresis after hypertonic saline infusion (SH2). Plasma from SH1 and SH2 were infused into the left renal artery (LRA) of dogs from group II. Two 20 min clearance periods were performed before and after each SH-infusion. After both SH-infusions urinary sodium excretion (UNaV) was significantly increased from preinfusion values in both kidneys, and these increases were significantly greater after SH2 than after SH1. No significant differences were found in UNaV between left and right kidney. After both plasma infusions the increases in urinary volume and osmolar clearance were higher in the infused than in the not infused kidney. These results suggest that the plasma leaving the liver contains a substance with natriuretic activity and that the infusion of hypertonic NaCl into the portal vein could induce either a higher secretion of the same substance or the presence of other different substance.