<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Silen, W</style></author><author><style face="normal" font="default" size="100%">Machen, T E</style></author><author><style face="normal" font="default" size="100%">Forte, J G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Acid-base balance in amphibian gastric mucosa.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acid-Base Equilibrium</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Anura</style></keyword><keyword><style  face="normal" font="default" size="100%">Bicarbonates</style></keyword><keyword><style  face="normal" font="default" size="100%">Carbon Dioxide</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrophysiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastric Mucosa</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrogen-Ion Concentration</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphates</style></keyword><keyword><style  face="normal" font="default" size="100%">Potassium</style></keyword><keyword><style  face="normal" font="default" size="100%">Rana catesbeiana</style></keyword><keyword><style  face="normal" font="default" size="100%">Solutions</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1975</style></year><pub-dates><date><style  face="normal" font="default" size="100%">1975 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">229</style></volume><pages><style face="normal" font="default" size="100%">721-30</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;It has been established that H+ secretion can be maintained in frog stomach in the absence of exogenous CO2 by using a nutrient bathing fluid containing 25 mM H2PO4 (pH approximately equal to 4.5) or by lowering the pH of a nonbuffered nutrient solution to about 3.0-3.6. Exogenous CO2 in the presence of these nutrient solutions uniformly caused a marked decrease in H+ secretion, PD, adn short-circuit current (Isc) and an increase in transmucosal resistance (R). Elevation of nutrient [k+] to 83 mM reduced R significantly but transiently without change in H+ when nutrient pH less than 5.0, whereas R returned to base line and H+ increased when nutrient pH greater than 5.0. Acidification of the nutrient medium in the presence of exogenous CO2 results in inhibition of the secretory pump, probably by decreasing intracellular pH, and also interferes with conductance at the nutrient membrane. Removal of exogenous CO2 from standard bicarbonate nutrient solution reduced by 50% the H+, PD, and Isc without change in R; K+-free nutrient solutions reverse these changes in Isc and PD but not in H+. The dropping PD and rising R induced by K+-free nutrient solutions in 5% CO2 - 95% O2 are returned toward normal by 100% O2. Our findings support an important role for exogenous CO2 in maintaining normal acid-base balance in frog mucosa by acting as an acidifying agent.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/2015?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kahn, T</style></author><author><style face="normal" font="default" size="100%">Bosch, J</style></author><author><style face="normal" font="default" size="100%">Levitt, M F</style></author><author><style face="normal" font="default" size="100%">Goldstein, M H</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effect of sodium nitrate loading on electrolyte transport by the renal tubule.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Bicarbonates</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Transport</style></keyword><keyword><style  face="normal" font="default" size="100%">Chlorides</style></keyword><keyword><style  face="normal" font="default" size="100%">Chlorothiazide</style></keyword><keyword><style  face="normal" font="default" size="100%">Diuresis</style></keyword><keyword><style  face="normal" font="default" size="100%">Dogs</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrolytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Ethacrynic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Glomerular Filtration Rate</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrogen-Ion Concentration</style></keyword><keyword><style  face="normal" font="default" size="100%">Kidney Tubules</style></keyword><keyword><style  face="normal" font="default" size="100%">Nitrates</style></keyword><keyword><style  face="normal" font="default" size="100%">Potassium</style></keyword><keyword><style  face="normal" font="default" size="100%">Sodium</style></keyword><keyword><style  face="normal" font="default" size="100%">Sodium Chloride</style></keyword><keyword><style  face="normal" font="default" size="100%">Urine</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1975</style></year><pub-dates><date><style  face="normal" font="default" size="100%">1975 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">229</style></volume><pages><style face="normal" font="default" size="100%">746-53</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Effects of sodium nitrate were compared with sodium chloride loading on transport of electrolytes by the nephron. Maximal levels of free water clearance/clomerular filtration rate (CH2O/GFR) averaged 8.4% with nitrate loading and 14.4% with saline loading. Since ethacrynic acid and chlorothiazide exert their major natriuretic effect in the distal nephron, the increment in Na ad Cl reabsorbed beyond the proximal tubule. The administration of these agents resulted in an increase in fractional sodium excretion (CNa/GFR) of 21.1%, urinary sodium excretion (UNaV) of 1,126 mueq/min, and urinary chloride excretion (UClV) of 848 mueq/min during nitrate loading compared with an increase in CNa/GFR of 37.6%, UNaV of 2,362 mueq/min, and UClV of 2,397 mueq/min during saline loading. The smaller diuretic-induced increment in Na and Cl excretion in the nitrate studies suggests, as do the hydrated studies, that less Cl and Na are reabsorbed in the distal nephron during nitrate than saline loading. At every level of UNaV, fractional bicarbonate reabsorption was higher, urine pH was lower, and urinary potassium excretion (UKV) was higher in the nitrate studies. Thus, compared with saline loading, sodium nitrate decreases chloride and sodium reabsorption in the distal nephron. The higher hydrogen and potassium secretion in the nitrate studies may be consequent to the decreased ability of the distal nephron to reabsorb chloride.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/2016?dopt=Abstract</style></custom1></record></records></xml>