Effect of aldosterone on electrical resistance of toad bladder

Abstract

The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

Energetics of sodium transport in the urinary bladder of the toad. Effect of aldosterone and sodium cyanide.

“…AIP may increase the permeability of the mucosal membrane to sodium, thereby indirectly facilitating the extrusion of sodium at the serosal surface of the epithelial cell (permease hypothesis) (6)(7)(8). The observed rise in intracellular sodium concentration (6,7) and the fall in transepithelial electrical resistance (8) are consistent with the permease hypothesis. However, Lipton and Edelman (9) showed no change in intracellular sodium concentration in response to aldosterone.…”

Sodium transport inhibitor from bovine hypothalamus.

“…The bioassay used for routine checking of sodium transport inhibition is the toad bladder preparation, as described by Leaf et al (14). Transepithelial sodium transport is measured as the short-circuit current (SCC), and conductance measurements are made at 10-sec intervals throughout the study (15) with adequate controls for comparison. For an experiment to be considered positive, the SCC must return to basal levels after the membrane is bathed with fresh buffer.…”

Correlates of aldosterone-induced increases in Cai2+ and Isc suggest that Cai2+ is the second messenger for stimulation of apical membrane conductance.

“…This expression of hormone action is initiated only after a latent period of 60-90 min, and is dependent on mRNA (4) and protein synthesis (5). Experiments in intact tissue and cultured amphibian cells suggest that the aldosterone-induced increase in electrogenic sodium transport can be viewed as involving an early phase lasting [6][7][8][9][10][11][12] h, and a delayed or chronic phase, that persists as long as agonist is present. The early phase is characterized by a gradual increase in apical membrane conductance for sodium, due to activation of amiloride-sensitive sodium This work has previously been reported in preliminary form.…”

“…Address correspondence to John P. Hayslett Receivedfor publication 06 February 1991 and in revisedform 22 July 1991. channels located in the apical membrane or insertion of preformed channels into the cell membrane (6,7). During the chronic phase, hormone action stimulates the production of a and ,B subunits ofNa-K-ATPase (8).…”