Na+ transport by rabbit urinary bladder, a tight epithelium.
By in vitro experiments on rabbit bladder, we reassessed the traditional view that mammalian urinary bladder lacks ion transport mechanisms. Since the ratio of actual-to-nominal membrane area in folded epithelia is variable and hard to estimate, we normalized membrane properties to apical membrane capacitance rather than to nominal area (probably 1 muF approximately 1 cm2 actual area). A new mounting technique that virtually eliminates edge damage yielded resistances up to 78,000 omega muF for rabbit bladder, and resistances for amphibian skin and bladder much higher than those usually reported. This technique made it possible to observe a transport-related conductance pathway, and a close correlation between transepithelial conductance (G) and short-circuit current (Isc) in these tight epithelia. G and Isc were increased by mucosal (Na+) [Isc approximately 0 when (Na+) approximately 0], aldosterone, serosal (HCO-3) and high mucosal (H+); were decreased by amiloride, mucosal (Ca++), ouabain, metabolic inhibitors and serosal (H+); and were unaffected by (Cl-) and little affected by antidiuretic hormone (ADH). Physiological variation in the rabbits' dietary Na+ intake caused variations in bladder G and Isc similar to those caused by the expected in vivo changes in aldosterone levels. The relation between G and Isc was the same whether defined by diet changes, natural variation among individual rabbits, or most of the above agents. A method was developed for separately resolving conductances of junctions, basolateral cell membrane, and apical cell membrane from this G--Isc relation. Net Na+ flux equalled Isc. Net Cl- flux was zero on short circuit and equalled only 25% of net Na+ flux in open circuit. Bladder membrane fragments contained a Na+-K+-activated, ouabain-inhibited ATPase. The physiological significance of Na+ absorption against steep gradients in rabbit bladder may be to maintain kidney-generated ion gradients during bladder storage of urine, especially when the animal is Na+-depleted.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000450:Aldosterone / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D001693:Biological Transport, Active; D002118:Calcium / Q000494:pharmacology; D002712:Chlorides / Q000378:metabolism; D002794:Choline / Q000494:pharmacology; D003486:Cyanides / Q000494:pharmacology; D004032:Diet; D004553:Electric Conductivity; D004848:Epithelium / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D008297:Male; D009584:Nitrogen / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000378:metabolism*; D001743:Urinary Bladder / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology
D001639:Bicarbonates; D002712:Chlorides; D003486:Cyanides; D014667:Vasopressins; D000450:Aldosterone; D010042:Ouabain; D000584:Amiloride; D012964:Sodium; D000251:Adenosine Triphosphatases; D009584:Nitrogen; D002794:Choline; D002118:Calcium