Cytosolic calcium and the action of vasopressin in toad urinary bladder

Abstract

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.

Na Transport in Rat Gastric Mucosa: An Electron Microprobe Analysis

“…Since, however, the amiloridesensitive component of the short-circuit cur rent was diminished, only Na absorption seems to be affected under these conditions. Such inhibition of Na transport, found also in other Na transporting epithclia, might be caused by enhanced cellular Ca and/or H con centrations due to inhibition of Ca/Na and H/ Na antiporters [10,11],…”

Effects of [Ca2+]i and pH on epithelial Na+ channel activity of cultured mouse cortical collecting ducts

“…Ca 2+ as an important second messenger, has been implicated to inhibit ENaCs (Wang and Chan, 2000). In particular, increase in cytoplasmic Ca 2+ results in decrease of apical Na + permeability in the frog skin (Grinstein and Erlij, 1978), toad urinary bladder (Brem et al, 1985;Palmer, 1985;Taylor et al, 1987) and the rabbit cortical collecting tubule (Frindt et al, 1993;Frindt and Windhager, 1990;Windhager et al, 1986). However, it is still unclear whether this inhibition is due to a direct effect.…”

Transepithelial water movement in response to carbamazepine, chlorpropamide and demeclocycline in toad urinary bladder

“…basolateral cell membrane and activates adenylate cyclase, resulting in the generation of cyclic AMP which serves as an intracellular messenger for both the hydrosmotic and natriferic action of the hormone. The mechanism of the events that follow cyclic AMP generation is not clear but cytoskeletal organelles, such as microtubules and actin-containing microfilaments, are thought to be involved in producing specific changes in the surface architecture (Taylor et al, 1987). We have confirmed that toad hemibladder tissue is highly sensitive to the hydrosmotic effect of AVP and that the preparation can be used to relate the antidiuretic activity of other pharmacological agents to AVP.…”