AJP - Renal Physiology, Vol 252, Issue 6 1028-F1041, Copyright © 1987 by American Physiological Society
Cytosolic calcium and the action of vasopressin in toad urinary bladder
A. Taylor, E. Eich, M. Pearl, A. S. Brem and E. Q. Peeper
The effects of experimental procedures believed to increase cytosolic
calcium on basal and vasopressin-stimulated osmotic water flow and
transepithelial sodium transport were examined in the toad urinary bladder.
Exposure of isolated toad bladders to quinidine, calcium ionophores
(A23187, X537A), or low-sodium or potassium-free serosal solutions resulted
in a dose-dependent decrease in the hydrosmotic response to vasopressin or
exogenous adenosine 3',5'-cyclic monophosphate (cAMP). The degree of
inhibition of cAMP-induced water flow induced by low-sodium or
potassium-free serosal bathing media varied, and in a similar manner, with
the serosal calcium concentration. The effects of quinidine sulfate (2 X
10-4 M), X537A (2 X 10(-5) M), and low serosal sodium (20 mM), but not that
of A23187 (10(-5) M), were readily reversible. Exposure to quinidine (4 X
10(-4) M), A23187 (10(-5) M), X537A (5 X 10(-6) M), or low serosal sodium
(2 mM) also inhibited the basal short-circuit current (SCC). Vasopressin,
4-20 mU/ml, completely overcame the inhibition of the SCC induced by
quinidine, A23187, or low serosal sodium, but a submaximal dose of hormone
(4 mU/ml) failed to fully reverse the inhibitory effect of X537A, 5 X
10(-6) M. These results are consistent with the view that 1) a Na-Ca
exchange process operates across the basolateral surface of the granular
epithelial cells of the toad urinary bladder in vivo, and 2) the level of
free calcium in the granular cell cytosol plays a modulatory role in the
control of apical membrane water and sodium permeability by vasopressin,
and in the regulation of the basal rate of transepithelial sodium
transport.
