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Possible role of Ca2+‐binding sites in the regulation of Na+ transport in toad urinary bladder
Author(s) -
Hardy M. A.
Publication year - 1985
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/j.1768-322x.1985.tb00434.x
Subject(s) - amiloride , toad , cyclase , biology , ouabain , adenylate kinase , stimulation , medicine , receptor , endocrinology , intracellular , biophysics , sodium , biochemistry , chemistry , organic chemistry
La3+ was used to assess the role of membrane‐bound Ca2+ in the regulation of basal and antidiuretic hormone (ADH)‐induced Na+ transport by the isolated toad urinary bladder. Na+ transport was monitored by means of a short‐circuit current (Isc) device. Mucosal La3+ (0.5‐5 mM) increased Isc, while serosal La3+ (5 mM) produced a biphasic response (stimulation followed by inhibition). The stimulatory effects of La3+ were additive when present on both sides and were suppressed by mucosal amiloride or serosal ouabain. The action of mucosal La+ was reversible but the inhibition produced by serosal La3+ was not. In the presence of serosal La3+ the natriferic effect of ADH was abolished, but Theophylline, dibutyryl‐cAMP, Amphotericin B, mucosal La3+, mucosal low pH, and phospho(enol) pyruvate, were able to increase Isc. These results suggest that Ca2+ binding sites in apical and basolateral membranes may play a key role in the modulation of both basal and ADH‐induced Na+ transport. Serosal La3+ apparently inactivates the hormone‐receptor interaction and/or the link between the ADH‐receptor complex and the activation of adenylate cyclase, but does not interfere with the operation of the Na+ “pump”, the basal activity of adenylate cyclase or any of the intracellular events that mediate the effect of ADH on Na+ transport.