THE ROLE OF ACTIVE-TRANSPORT IN POTASSIUM REABSORPTION IN THE PROXIMAL CONVOLUTED TUBULE OF THE ANESTHETIZED RAT

Citation
Rw. Wilson et al., THE ROLE OF ACTIVE-TRANSPORT IN POTASSIUM REABSORPTION IN THE PROXIMAL CONVOLUTED TUBULE OF THE ANESTHETIZED RAT, Journal of physiology, 500(1), 1997, pp. 155-164
Citations number
37
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
500
Issue
1
Year of publication
1997
Pages
155 - 164
Database
ISI
SICI code
0022-3751(1997)500:1<155:TROAIP>2.0.ZU;2-U
Abstract
1. We have previously assessed the contributions of diffusion and conv ection to net potassium reabsorption in the rat proximal convoluted tu bule (PCT). The present study was conducted to evaluate the role of ac tive transport in convective potassium reabsorption by measuring the t ransepithelial potassium reflection coefficient (sigma(K)) in the pres ence and absence of cyanide in anaesthetized rats previously prepared for in vivo microperfusion. 2. Osmotic water permeability (P-f) was me asured in double-perfused tubules (lumen and peritubular capillaries) by manipulating the applied transepithelial osmotic gradient between - 30 and +40 mosmol (kg H2O)(-1) using raffinose added to or subtracted from luminal perfusates. P-f was unaffected by the presence of cyanide when the estimated dissipation of osmotic gradients along each tubule were taken into account. 3. The proportion of K+ (and Na+) convective ly transported with water fluxes (i.e. sigma(K)) was not affected by c yanide. In the absence of active transport and following correction fo r any diffusive component, sigma(K) was 0.56 +/- 0.13, indicating subs tantial solvent drag which probably occurs via the paracellular pathwa y. 4. However, cyanide caused a reduction in net potassium flux over t he entire range of fluid fluxes used in double-perfusion experiments. Subsequent single-perfusion experiments (tubule lumen only) using the specific K+-H+-ATPase inhibitor, SCH28080, failed to reveal any direct evidence for a primary active K+ transporting mechanism involved in K + reabsorption in the PCT.