Bicarbonate reabsorption in the papillary collecting duct of rats

Abstract

Using the technique of capillary perfusion and simultaneous luminal stop flow microperfusion the reabsorption of bicarbonate and glycodiazine from the papillary collecting duct was evaluated. Starting with equal H14CO3- and 3H-glycodiazine concentrations in the luminal and peritubular perfusates, the decrease in the luminal concentration at 10 and 45 s contact time was measured. In control rats with 25 mmol/l HCO3- in the perfusates the rate of HCO3- reabsorption calculated from the 10 s values was 0.34 nmol cm-2 s-1. In acute metabolic acidosis, the rate of bicarbonate reabsorption was 2,3 times higher. In metabolic alkalosis, the rate of bicarbonate absorption dropped to 13% of the control values. Also the 45 s values of acidotic and alkalotic animals differed significantly from each other. With 25 mmol/l glycodiazine in both perfusates the rate of buffer reabsorption as calculated from the 10 s values was 0.76 nmol cm-2 s-1 in control rats and did not deviate significantly from this value in acidotic and alkalotic animals. In control rats the bicarbonate reabsorption in % was the same, no matter whether both luminal and capillary perfusate contained 25 mmol/l bicarbonate or 10 mmol/l. In acidotic rats the rate of HCO3- reabsorption did not change significantly if all Na+ in the perfusates was replaced by choline (0.88 versus 0.79 nmol cm-2 s-1 at 25 mmol/l HCO3-). When in acidotic rats. 0.1 mmol/l acetazolamide or 1 mmol/l SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid) was added to both perfusates the rate of HCO3- reabsorption dropped by 75 and 58%, respectively. A potassium deficient diet for one week and DOCa administration had no influence on the bicarbonate reabsorption of rats which were on standard diet. The data indicate that (1) the buffer reabsorption from the papillary collecting duct is rather due to H+ ion secretion than to buffer anion reabsorption. (2) The adaptation to metabolic acidosis and alkalosis is specific for bicarbonate and not seen with glycodiazine. (3) Within the concentration range tested the HCO3- reabsorption rises linearly with the HCO3- concentration. (4) The HCO3- reabsorption in the papillary collecting duct is Na+-independent, it can be inhibited by acetazolamide and SITS, but is not influenced by K+-deficient diet plus DOCA.

Hormonal regulation of proton secretion in rabbit medullary collecting duct.

“…Acidification ofthe urine occurs in several distinct distal nephron segments including the distal convoluted tubule, cortical collecting tubule, medullary and papillary collecting ducts (5)(6)(7)(8)(9)(10). The capacity for collecting duct proton secretion (or bicarbonate reabsorption) shows segmental differences.…”

Dual regulatory mechanisms of proton transport in rat papillary collecting duct cells in culture.

“…In the rat, in vivo experiments using the techniques of capillary microperfusion and simultaneous luminal stop-flow microperfusion of the inner medullary collecting duct had led to conflicting results, suggesting that there is either tight linkage between Na+ and H+ transfers amounting to 20% of total Na + reabsorption (ULLRICH and PAPARASSILOU, 1979), or no linkage between the two ion transfers (ULLRICH and PAPARASSILOU, 1981). On the other hand, recent data from cell suspensions suggests that H + is actively secreted into the lumen via primary H+ pump in the rabbit papillary collecting ducts (PRIGENT et al, 1985).…”

Adaptive changes of H+ and/or bicarbonate transport in chronic metabolic acidosis: Its quantitative evaluation by using isolated perfused kidney.

“…The adaptation to the chronic acid-base change was noted in the proximal convoluted tubules of the rat and the rabbit (Cogan et al 1979;Tsai et al 1984), the rat distal convoluted tubules (Lucci et al 1982), the rabbit cortical and medullary collecting ducts (McKinney and Burg 1977; Laski and Kurtzman 1983;Lombard et al 1983) and the rat papillary collecting ducts (Ulrich and Papavassiliou 1981), in addition to the rat distal nephron (Terao and Tannen 1981; Kornandakieti et al 1983). The present results do not provide any insight into the localizations of the adaptation in the nephron and the relative contribu- Lions of those segments to it.…”