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At least 991 records · Page 55Linked to original sources
PubMed1989

Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis.

Renal acidification in renal proximal tubule is thought to be mediated by luminal Na-H antiporter and the HCO3- generated by this antiporter is removed from the cell by a basolateral Na-HCO3 cotransporter. To study the effect of respiratory acid-base disorders on these transport systems, we have measured the Na-HCO3 cotransport in basolateral membranes and Na-H antiporter in luminal membranes in control rabbits, rabbits exposed to 10% CO2 (chronic hypercapnia), and rabbits exposed to 10% O2-90% N2 (chronic hypocapnia). The Vmax of HCO3(-)-dependent 22Na uptake was significantly higher in chronic hypercapnia than controls (2.54 +/- 0.03 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.001). Likewise, the Vmax of the Na-H antiporter was also increased compared with controls (924.9 +/- 42.1 vs. 549.1 +/- 62.8 fluorescence units (FU).300 micrograms protein-1.min-1). In chronic hypocapnia, the Vmax of Na-HCO3 cotransport was lower than controls (0.72 +/- 0.11 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.05). There was no difference, however, in the Vmax of the Na-H antiporter between hypocapnia and control (524.2 +/- 24.3 vs. 549.1 +/- 62.8, FU.300 micrograms protein-1.min-1). The Vmaxs of the Na-HCO3 cotransport and of the Na-H antiporter in hypocapnic, control, and hypercapnic rabbits were linearly related (r = 0.81), suggesting a simultaneous adaptation of the two systems in respiratory acid-base disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1990

Na(+)-H+ exchange in choroid plexus and CSF in acute metabolic acidosis or alkalosis.

Basolateral Na(+)-H+ exchange was analyzed with an in vivo model of choroid plexus (CP) epithelium in nephrectomized adult rats anesthetized with ketamine. Acid-base balance in blood was altered for 1 h over a pH continuum of 7.19 to 7.53 by equimolar intraperitoneal injections of HCl, NH4Cl, NaCl, or NaHCO3. Compartmental analysis enabled determination of CP intracellular pH (pHi) [dimethadione (DMO) method] and the choroid cellular concentration of 23Na (stable) and 22Na (tracer). HCl acidosis reduced the outwardly directed transmembrane basolateral H+ gradient, lowered the [23Na]i by 25%, and decreased the influx coefficient (Kin) for 22Na from blood into CP parenchyma (by 45% from 0.211 to 0.117 ml.g-1.h-1) and into cerebrospinal fluid (CSF) (by 43%, from 0.897 to 0.516). Compared with acid-loaded rats (HCl or NH4Cl), the NaHCO3-alkalotic animals had significantly enhanced uptake of 22Na into the CP-CSF system. This pH-dependent transport of Na+ from blood to CP was abolished by pretreatment with amiloride, an inhibitor of Na(+)-H+ exchange. Except in severe acidosis (HCl), the choroid cell pHi (7.05 +/- 0.02 in NaCl controls) and [HCO3-] (11-12 mM) remained stable in the face of acidemic and alkalemic challenges. With respect to reaction of the blood-CSF barrier to plasma acid-base perturbations, the responses of the fourth ventricle plexus pHi, [Na+]i, and 22Na uptake were similar to corresponding ones in lateral plexuses. We conclude that in the choroidal epithelium there is a Na(+)-H+ exchange activity capable of modulating Na+ flux into the CSF by approximately 50% as arterial pH is varied from 7.2 to 7.5.

Acid-Base Equilibrium↗
PubMed1990

Ion concentrations in the rat CCD: differences between cell types and effect of alkalosis.

We have previously shown that the isolated perfused cortical collecting duct (CCD) from chloride-depleted alkalotic (CDA) rats continues to secrete HCO3 for up to 3 h. To determine whether the sustained alteration in transport was associated with changes in intracellular ion concentrations, we performed energy-dispersive X-ray microanalysis in microdissected tubule bundles obtained from CDA rats and rats with normal acid-base status (CON). Before analysis, the bundles from both groups were incubated for 1 h in vitro in a modified Ringer solution (pH 7.4, 105 mM Cl). Principal (PC) and intercalated cells (IC) of the CCD from CON animals differed in the nuclear concentration of Na (17.0 vs. 24.7 mmol/l cell water), K (192.5 vs. 177.0 mmol/l cell water), and Cl (17.8 vs. 47.8 mmol/l cell water). Cells of the cortical thick ascending limb of Henle (CTAL) had the lowest Na and Cl values (11.5 and 14.8 mmol/l cell water, respectively). CDA resulted in no systematic Cl changes. In the IC the nuclear Na concentration was significantly increased (32.0 vs. 24.7 mmol/l cell water) and in all cells a small reduction in K concentration was detectable. These findings suggest that 1) the different transport functions of IC, PC, and CTAL are associated with differences in the intracellular ion composition, and 2) the sustained HCO3 secretion seen in CCD from CDA rats cannot be explained as the result of intracellular Cl depletion.

Alkalosis↗