CO2-stimulated NaCl absorption in the mouse renal cortical thick ascending limb of Henle. Evidence for synchronous Na +/H+ and Cl-/HCO3- exchange in apical plasma membranes.

Abstract

These experiments evaluated salt transport processes in isolated cortical thick limbs of Henle (cTALH) obtained from mouse kidney. When the external solutions consisted of Krebs-Ringer bicarbonate (KRB), pH 7 .4, and a 95% 02-5% C0 2 gas phase, the spontaneous transepithelial voltage (Ve , mV, lumen-to-bath) was^-8 mV ; the net rate of Cl -absorption (Jcit) was^-3,600 pmol s -1 cm-2 ; the net rate of osmotic solute absorption f,~, was twicejn cit ; and the net rate of total C02 transport to t ) was indistinguishable from zero . Thus, net Cl -absorption was accompanied by the net absorption of a monovalent cation, presumably Na', and net HC03 absorption was negligible . This salt transport process was stimulated by (C02 + HC03) : omission of C02 from the gas phase and HC03 from external solutions reducedflit ,,J"m, and VQ by 50% . Furthermore, 10-4 M luminal furosemide abolished jn6i`and Ve entirely. The lipophilic carbonic anhydrase inhibitor ethoxzolamide (10-4 M, either luminal or peritubular) inhibited (C0 2 + HC03)-stimulated .3J311', j ,,,n, and V. by -50% ; however, when the combination (C02 + HC03) was absent, ethoxzolamide had no detectable effect on salt transport . Ve was reduced or abolished entirely by omission ofeither Na+ or Cl -from external solutions, by peritubular K + removal, by 10 -3 M peritubular ouabain, and by 10 -4 M luminal SITS . However, Ve was unaffected by 10-3 M peritubular SITS, or by the hydrophilic carbonic anhydrase inhibitor acetazolamide (2.2 X 10 -4 M, lumen plus bath) . We interpret these data to indicate that (C02 + HC03)-stimulated NaCl absorption in the cTALH involved two synchronous apical membrane antiport processes : one exchanging luminal Na' for cellular H + ; and the other exchanging Address reprint requests to Dr.

Potentiation of tubuloglomerular feedback in the rat by thromboxane mimetic. Role of macula densa.

“…U-46,619 promotes net Cl secretion in the stomach and ileum (25) while infusions of a TXA2 synthase inhibitor can increase renal Cl excretion (8). Studies in isolated tubules from mouse (26) and rabbit (27) (28). Juxtaglomerular cells contain a major calciumactivated chloride conductance (14,29 where it could interact with a basolateral Cl channel.…”

The plasma membrane sodium-hydrogen exchanger and its role in physiological and pathophysiological processes.

“…Similarly, studies on the intact proximal tubule of the rabbit have failed to demonstrate measurable C1~-OH~ exchange across the luminal membrane (Schwartz, 1983;Sasaki et al, 1984 (Reuss 1984), but there is dispute as to whether these exchangers contribute the major fraction of NaCl entry under basal conditions (Reuss 1984) or only during cell volume regulation . Simultaneous Na + -H + and Cl~-HCO 3~ exchange probably also occurs across the apical membrane of the mouse renal cortical thick ascending limb of Henle, although this has not yet been directly demonstrated (Friedman and Andreoli, 1982).…”

“…It is interesting to note that in many of the epithelia in which this mechanism is found, such as the gall bladder, ileum, and renal cortical thick ascending limb, Na + -coupled Cl~ transport is stimulated by CO 2 and is sensitive to inhibitors of carbonic anhydrase (Fisher et al, 1981;Heintze et al, 1981;Nellans et al, 1975;Friedman and Andreoli, 1982). These characteristics probably arise from the fact that at physiological pH values, Cl~ exchanges with HCO 3~ much more rapidly than with OH~ Knicklebein et al, 1984).…”

Renal bicarbonate reabsorption in the rat. I. Effects of hypokalemia and carbonic anhydrase.

“…Na/H exchange in the apical brush border membrane takes place along the proximal convoluted tubule and is also present in the thick ascending limb of Henle's loop of the rat and mouse, but not the rabbit (1)(2)(3)(4)(5). In addition, a directly electrogenic, ATP-driven H-ion pump has been detected in the cortical and medullary collecting duct (6)(7)(8).…”