In order to determine the effect of acid lumen pH on renal tubular potassium transport, cortical collecting tubules were dissected from rabbit kidneys and perfused in vitro. When the pH of the perfusate was lowered from 7.4 to 6.8, potassium secretion into the tubule lumen decreased by an average of 47%. The transepithelial voltage increased from a mean value of -32 mV (lumen negative) at pH 7.4 to -51 mV at PH 6.8. Net sodium absorption from the tubule lumen was essentially unchanged (5% mean decrease). Transepithelial voltage and potassium secretion returned to control values when the pH of the perfusate was raised to 7.4. Alterations in pH of the bath had no comparable effect on the transepithelial voltage, whether the bath pH was increased or decreased. We conclude that a decrease in the pH of the tubule fluid of itself inhibits active potassium secretion in this tubule segment, providing an additional explanation for the decrease in potassium excretion found in acidosis. The negative voltage (presumably caused by sodium absorption out of the lumen) is increased under these conditions, possibly because of reduction of a smaller counterbalancing positive voltage caused by potassium secretion into the lumen.
Patch clamp methods were used to characterize the channels on the apical membrane of initial collecting ducts from Ambystoma tigrinum. Apical membranes were exposed by everting and perfusing fragments of the renal tubule in vitro. Tubules were dissected from two groups of animals; one maintained in tap water, and the other kept in a solution of 50 mM KCl from seven to nineteen days. Patches of apical membranes on tubules taken from animals exposed to tap water expressed low-conductance amiloride sensitive sodium channels (ENaC) in 22 of 49 patches. Only three maxi K channels were observed in this group. In animals exposed to KCl, low-conductance amiloride sensitive sodium channels, 3.7 +/- 0.2 pS (36 of 45 patches) and high-conductance 98.3 +/- 5.0 pS (19 of 45 patches) potassium channels were observed. The estimated density of apical maxi K channels increased dramatically from 0.08 to 0.76 channels/mu 2 in tubules taken from animals exposed to KCl. All but four of nineteen patches which contained maxi K channels also expressed the low conductance sodium channels. Therefore, at least 85% of the maxi K channels studied were in principal cells. We speculate that the increase in maxi K channel activity may represent a mechanism for enhancing the potassium secretory capacity of the initial collecting duct. As expected, exposure of the animals to 50 mM KCl prior to dissection of the initial collecting ducts also increased the estimated density of ENaC from 0.99 to 3.89 channels/mu 2. This upregulation of sodium channel activity is presumably related to the widely recognized effect of potassium loading to increase the plasma aldosterone level.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.