This study was designed to elucidate the acid-base balance local to the collecting duct urine (CD) and vasa recta blood (VR) in the rat renal papilla in diuresis. The pH changes were measured in both a furosemide-induced and a volume-load-induced diuresis, whereas the PCO2 (i.e., CO2 tension) and HCO3- concentration were measured only in a furosemide-induced diuresis. In an antidiuresis, the pH of the VR was more acidic than that of the systemic arterial blood (DeltapH = 0.44-0.73). Additionally, the pH of the ascending VR was significantly lower than that of the descending VR (DeltapH = 0.14-0. 16). In diuresis, the pH of the CD decreased (DeltapH = 0.81-0.97), while the pH of the descending and the ascending VR increased; however, the increase was only significant in the ascending VR (DeltapH = 0.23-0.30). Consequently, the significant difference in the pH gradient between the descending and the ascending VR was eliminated. The PCO2 values in the CD and the ascending VR were not different from those in antidiuresis, while the HCO3- concentration in the CD and the ascending VR, respectively, decreased and increased significantly. Thus, in diuresis, the decrease in the pH of the CD and the increase in the pH of the ascending VR result, respectively, from the decrease and the increase in the HCO3- concentration, with no changes in the PCO2 values.

No abstract

This study was designed to elucidate the effects of ochratoxin A (OTA) on pH homeostasis in the kidney. We measured pH in the proximal (PT) and the distal (DT) tubular fluid, the collecting duct urine (CD), the descending and the ascending vasa recta blood (VR), and the renal arterial blood (RA). OTA increased pH significantly in PT, DT, CD as well as in the descending and ascending VR, whereas pH in RA remained unchanged. We further determined CO2 tension (pCO2) and HCO3- in PT, CD as well as in the descending and ascending VR. OTA significantly increased HCO3- in PT, CD and the descending and ascending VR, with no changes in pCO2. Therefore, the increases in pH in PT, CD and the descending and ascending VR result from the increase in HCO3-. Our results suggest that OTA inhibits HCO3- reabsorption in the tubules, leading to the impairment of urinary acidification, and that OTA further leads to the disturbance of the acid-base state (alkalinization) in the interstitium in renal papilla. The impairment of urinary acidification may contribute to the disturbance of pH homeostasis in the renal papilla. The disturbance of pH homeostasis by OTA could be related to its nephrotoxicity.

We tried to study in depth the recovery process in the cortical and the medullary oxygen (O2) consumption of normal and streptozotocin diabetic rat kidneys after ischemia. It was found that the cortical and the medullary O2 consumption decreased after ischemia, reaching their lowest levels at 1 day after every ischemic duration in normal and diabetic kidneys. In the period prior to ischemia to 1 day after ischemia, no significant difference was seen in the decrease in O2 consumption between the cortex and the medulla in normal kidney, whereas the medullary O2 consumption significantly decreased compared with the cortical O2 consumption in diabetic kidney. From 1 day to 4 weeks after ischemia, the increase in the cortical O2 consumption was significantly higher than that in the medulla of normal kidney. In contrast, the increase in the medullary O2 consumption was significantly higher than that in the cortex of diabetic kidney. Consequently, up to 4 weeks after ischemia, the decrease in the cortical O2 consumption was significantly lower than in the medulla of normal kidney, while there was no significant difference regarding the decrease in O2 consumption between the cortex and the medulla in diabetic kidney. These results suggest that there is a clear difference in the postischemic recovery process of O2 consumption between the cortex and the medulla, and also between normal and diabetic rat kidneys.

No abstract