Regulation of apical K channels in rat cortical collecting tubule during changes in dietary K intake.
Long-term adaptation to a high-K diet is known to increase the density of conducting secretory K (SK) channels in the luminal membrane of the rat cortical collecting tubule (CCT). To examine whether these channels are involved in the short-term, day-to-day regulation of K secretion, we examined the density of K channels in animals fed a high-K diet for 6 or 48 h. CCTs were isolated and split open to provide access to the luminal membrane. Cell-attached patches were formed on principal cells with 140 mM KCl in the patch-clamp pipette. SK channels were recognized from their characteristic single-channel conductance (40-50 pS) and gating patterns. Animals fed a control diet had SK channel densities of 0.40 channels/micrometer(2). When the diet was changed for one containing 10% KCl for 6 h, the channel density increased to 1.51 channels/micrometer(2). Maintaining the animals on a high-K diet for 48 h resulted in a further increase in SK channels to 2.29 channels/micrometer(2). Animals fed a low-K diet for 5 days or longer had SK densities of 0.53 channels/micrometer(2), not significantly different from control values. The presence of conducting Na channels in the luminal membrane will also affect K secretion by the CCT by altering the electrical driving force through the K channels. The density of Na channels, measured with LiCl in the pipette, was 0. 08 for controls and 1.00 and 1.08 channels/micrometer(2) after 6 h and 48 h on a high-K diet. Plasma aldosterone increased from 15 +/- 4 ng/dl (controls ) to 36 +/- 8 and 98 +/- 23 ng/dl after 6 and 48 h of K loading, respectively. The increase in K channel density could not be reproduced by infusion of the animals with aldosterone. We conclude that regulation of the density of conducting Na and K channels may contribute to day-to-day variation in the rate of renal K secretion and to the short-term maintenance of K balance.
Palmer
L G
LG
Department of Physiology, Weill Medical College of Cornell University, New York, New York 10021, USA.
Frindt
G
G
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D004553:Electric Conductivity; D005260:Female; D015640:Ion Channel Gating; D007672:Kidney Cortex; D007685:Kidney Tubules, Collecting / Q000378:metabolism*; D008297:Male; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism* / Q000502:physiology; D017419:Potassium, Dietary / Q000008:administration & dosage* / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015222:Sodium Channels / Q000378:metabolism / Q000502:physiology
D015221:Potassium Channels; D017419:Potassium, Dietary; D015222:Sodium Channels