AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 6 917-R921, Copyright © 1987 by American Physiological Society
Calcium transport in turtle bladder
S. Sabatini and N. A. Kurtzman
Department of Internal Medicine, School of Medicine, Texas Tech University Health Sciences Center, Lubbock 79430.
Unidirectional 45Ca fluxes were measured in the turtle bladder under
open-circuit and short-circuit conditions. In the open-circuited state net
calcium flux (JnetCa) was secretory (serosa to mucosa) and was 388.3 +/-
84.5 pmol.mg-1.h-1 (n = 20, P less than 0.001). Ouabain (5 X 10(-4) M)
reversed JnetCa to an absorptive flux (serosal minus mucosal flux = -195.8
+/- 41.3 pmol.mg-1.h-1; n = 20, P less than 0.001). Amiloride (1 X 10(-5)
M) reduced both fluxes such that JnetCa was not significantly different
from zero. Removal of mucosal sodium caused net calcium absorption; removal
of serosal sodium caused calcium secretion. When bladders were short
circuited, JnetCa decreased to approximately one-third of control value but
remained secretory (138.4 +/- 54.3 pmol.mg-1.h-1; n = 9, P less than
0.025). When ouabain was added under short-circuit conditions, JnetCa was
similar in magnitude and direction to ouabain under open-circuited
conditions (i.e., absorptive). Tissue 45Ca content was approximately equal
to 30-fold lower when the isotope was placed in the mucosal bath,
suggesting that the apical membrane is the resistance barrier to calcium
transport. The results obtained in this study are best explained by
postulating a Ca2+-ATPase on the serosa of the turtle bladder epithelium
and a sodium-calcium antiporter on the mucosa. In this model, the energy
for calcium movement would be supplied, in large part, by the
Na+-K+-ATPase. By increasing cell sodium, ouabain would decrease the
activity of the mucosal sodium-calcium exchanger (or reverse it),
uncovering active calcium transport across the serosa.
