Calcium channel blockers inhibit amiloride-stimulated short-circuit current in frog tadpole skin
Cox, T.C.
American Journal of Physiology 263(4 Pt 2): R827-R833
1992
ISSN/ISBN: 0002-9513 PMID: 1415795 Document Number: 390982
The larval frog skin has a very high electrical resistance and a correspoinding low rate of transepithelial ion transport. Amiloride, a blocker of sodium transport in adult skin, transiently stimulates rather than inhibits short-circuit current (I-sc) across larval skin. The time course and concentration response to amiloride and the effects of calcium channel blockers on I-sc were studied with larval frog skin mounted in modified Ussing chambers. The amiloride (1 mM) transient was markedly blunted if the skin was previously exposed to low amiloride (0.01-0.1 mM) concentrations. The calcium channel blockers verapamil, nitrendipine, diltiazem, W-7, and lanthanum all blunted the amiloride transient. Diltiazem itself caused a rapid transient in I-sc, indicating that it may be a partial agonist. These data suggest that the amiloride-stimulated cation channels rapidly desensitize in a manner similar to the acetylcholine receptor. The decline in I-sc after amiloride stimulation could be caused by amiloride block of the open channel. Blockade of amiloride stimulation by well-known calcium channel blockers suggests that these larval cation channels may have some characteristics in common with calcium channels.