Ionic requirements of proximal tubular fluid reabsorption: Flow dependence of fluid transport

Studies on microvillus membrane from rabbit kidney cortex suggest that chloride absorption may occur by chloride/formate exchange with recycling of formic acid by nonionic diffusion. We tested whether this transport mechanism participates in active NaCI reabsorption in the rabbit proximal tubule.In proximal tubule S2 segments perfused with low HCO3 solutions, the addition of formate (0.25-0.5 mM) to the lumen and the bath increased volume reabsorption (Jv) by 60%; the transepithelial potential difference remained unchanged. The effect of formate on Jv was completely reversible and was inhibited both by ouabain and by luminal 4,4'-diisothiocyanostilbene-2,2'-disulfonate.Formate (0.5 mM) failed to stimulate Jv in early proximal convoluted tubules perfused with high HCO3 solutions. As measured by miniature glass pH microelectrodes, this lack of formate effect on Jv was related to a less extensive acidification of the tubule fluid when high HCO3 solutions were used as perfusate. These data suggest that chloride/formate exchange with recycling of formic acid by nonionic diffusion represents a mechanism for active, electroneutral NaCI reabsorption in the proximal tubule.

Section: Methodsmentioning

confidence: 87%

Effect of formate on volume reabsorption in the rabbit proximal tubule.

Schild¹,

Giebisch²,

Karniski³

et al. 1987

“…In this study reductions in APR were closely and directly correlated with concurrent declines in SNGFR. Of note is the recent evidence obtained from several isolated tubule microperfusion studies (36,37), indicating that an alteration in proximal tubule luminal flow rate is capable of modifying transepithelial fluid transport. The possibility therefore exists that the Kf-induced reduction in SNGFR in PAN-perfused kidneys brings about a concurrent fall in APR by virtue of a luminal influence on transepithelial fluid transport.…”

Section: Discussionmentioning

confidence: 99%

Role for intrarenal mechanisms in the impaired salt excretion of experimental nephrotic syndrome.

Ichikawa¹,

Rennke²,

Hoyer³

et al. 1983

250

175

A B S T R A C T A unilateral model of puromycin aminonucleoside (PAN)-induced albuminuria was produced in Munich-Wistar rats to examine the mechanisms responsible for renal salt retention. 2 wk after selective perfusion of left kidneys with PAN (n = 8 rats) or isotonic saline (control, n = 7 rats), increases in albumin excretion and decreases in sodium excretion were demonstrated in PAN-perfused but not in nonperfused kidneys of PAN-treated rats although systemic plasma protein concentration remained at control level. Total kidney glomerular filtration rate (GFR) and superficial single nephron (SN) GFR were also reduced selectively in PAN-perfused kidneys, on average by -30%, due primarily to a marked decline in the glomerular capillary ultrafiltration coefficient (Kf), which was also confined to PAN-perfused kidneys. Values for absolute proximal reabsorption (APR) were also selectively depressed in PAN-perfused kidneys, in keeping with a similarly selective decline in peritubular capillary oncotic pressure measured in these kidneys, the latter also a consequence of the fall in Kf. In a separate group of seven PAN-treated rats, however, no differences were detected between PANperfused and nonperfused kidneys in the absolute amount of sodium reaching the early (0. In two additional groups of PAN-treated rats, infusion of saralasin (0.3 mg/kg per h, iv.) led to substantial increases in total kidney GFR and SNGFR in PAN-perfused but not in nonperfused kidneys. Despite these increases in total and SNGFR, urinary sodium excretion by PAN-perfused kidneys remained at a level far below that for nonperfused kidneys, again indicating that the antinatriuresis characterizing the PAN-perfused kidney is due to alterations in sodium handling by the tubules rather than changes in GFR. These results therefore indicate (a) that reductions in Kf and depressed sodium reabsorption by proximal tubules and Henle's loop segments in this model are brought about by intrarenal rather than circulating or systemic factors, and (b) assuming that superficial nephrons are representative of the entire nephron population, renal salt retention in this model is due primarily to intrarenal factor(s) acting beyond the distal convolution.77±0

“…Paracellular chloride transport is governed by the magnitudes of the junctional chloride permeability and the transepithelial electrochemical gradient, principally the chloride concentration gradient (9,11). Contradictory microperfusion evidence has been presented on whether active chloride transport in the late PCT is (12)(13)(14) or is not (14)(15)(16) Chloride transport in the early PCT differed from that in the late PCT both quantitatively and qualitatively. First, there was a marked augmentation in chloride transport in transition from the low filtered chloride loads of groups 1 and 5 to the normal level of group 2 (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…Another issue that has not yet been addressed is whether chloride transport in the early PCT can increase when flow rises (1 1). Flow dependence of chloride transport has been found to occur in some (12)(13)(14), but not other (14)(15)(16), microperfusion studies of the late PCT in vivo. In addition to the quantitative and possible kinetic differences with regard to luminal determinants of anion transport in the early versus late PCT, there may also be axial differences in control oftransport by peritubular factors. It has been proposed, for instance, that alkalemia suppresses late, but not early, acidification (17,18).…”

Section: Introductionmentioning

confidence: 93%

Axial heterogeneity of bicarbonate, chloride, and water transport in the rat proximal convoluted tubule. Effects of change in luminal flow rate and of alkalemia.

Liu¹,

Cogan²

1986

These studies examined regulation of superficial proximal convoluted tubule (PCIT) transport as a function of length. When single nephron glomerular filtration rate (SNGFR) increased from 28.7±0.7 nl/min in hydropenia to 41.5±0.4 nl/min in euvolemia, bicarbonate, chloride, and water reabsorption in the early (1st mm) PCI' increased proportionally: from 354±21 peaJ mm * min, 206±55 peq/mni * min, and 5.9±0.4 nl/mm * min to 520±12 peq/mm. min, 585±21 peq/mm * min, and 10.1 ±0.4 nl/ mm* min, respectively. These high transport rates did not increase further, however, when SNGFR went to 51.2±0.7 or 50.7±0.6 nl/min after atrial natriuretic factor or glucagon administration. Anion and water transport rates in the late PCI were lower and exhibited less flow dependence. During chronic metabolic alkalosis, acidification was inhibited in the late but not early PCT. In conclusion, the early PCI is distinguished from the late PCI by having high-capacity, flow-responsive but saturable, anion-and water-reabsorptive processes relatively unaffected by alkalemia.