Vasopressin-elicited refractoriness of the response to vasopressin in toad urinary bladder

Abstract

Incubation of the urinary bladder of B. marinus with high concentrations of vasopressin produces refractoriness to subsequent stimulation of water permeability to low concentrations of vasopressin. Development of refractoriness is directly dependent on concentration of vasopressin and duration of incubation with the hormone. Refractoriness develops in the absence of transepithelial water flow, is evident following a 2-h recovery period of incubation in hormone-free Ringer solution, and is reversed after prolonged incubation in hormone-free Ringer solution. Development and reversal of refractoriness is not altered by actinomycin D or cycloheximide. The steps at which refractoriness develops have been identified partially. Under different conditions, refractoriness involves the following: reduced vasopressin-sensitive adenylate cyclase activity, reduced epithelial cell cAMP accumulation in response to vasopressin in the absence of demonstrable change in vasopressin-sensitive adenylate cyclase activity, cAMP phosphodiesterase activity, or loss of cAMP into the Ringer solution, and refractoriness of water permeability response to exogenous cAMP.