The effect of catecholamines on ion transport in the toad bladder

Abstract

Noradrenalin (8 · 10 −6 M) and adrenalin (6 · 10 −6 and 6 · 10 −7 M) were found to cause marked stimulation of short-circuit current (S.C.C.) in isolated toad bladder, but isoprenalin (8 · 10 −7 M) was found to be without effect. The percentage rise in S.C.C. due to noradrenalin was found to be inversely proportional to the initial S.C.C. or total conductance of the bladder. Again in the case of noradrenalin the rise in S.C.C. was almost completely abolished by α-adrenergic blockade but not by β-blockade. This rise in S.C.C. was found not to be significantly different from the rise in net Na + flux. Bidirectional Cl − fluxes were estimated using 82Br as a companion radionuclide to 36Cl. No significant net Cl − flux was apparent, either before or after addition of any of the three catecholamines tested. However, in some cases the unidirectional Cl − fluxes rose markedly following addition of noradrenalin or of adrenalin and this change was not reflected in a change in total conductance. This anomaly was noted to occur in bladders whose initial conductance was of the order of 0.5 kΩ −1 · cm −2 or greater. The evidence presented suggests that two actions of catecholamines on ion transport in toad bladder are (a) to increase Na + transport via stimulation of α-adrenergic sites and (b) at the concentrations tested to cause an increase in passive Cl permeability in bladders whose initial conductance is high.