Peptidergic and adrenergic regulation of electrogenic ion transport in isolated gills of the flounder (Platichthys flesus L.)

Summary

Electrogenic potentials measured in isolated gills of seawater-adaptedPlatichthys flesus conform to the current model proposed for salt secretion by teleost chloride cells. Gills perfused and bathed with identical salines maintained a stable potential (“blood”-side positive) thought to represent the activity of a chloride pump. Furosemide added to the perfusate (1×10⁻⁴ and 5×10⁻⁴ mol l⁻¹) caused a large inhibition of the transepithelial potential. Cyclic 8-(4-chlorophenylthio) adenosine-3′:5′-monophosphate (5×10⁻⁵ mol l⁻¹) stimulated the transepithelial potential and decreased the arterial vascular resistance. The adenylate cyclase activator forskolin mimicked the effects of the cAMP derivative on branchial vascular resistance and, at low concentrations, on electrogenic ion transport. At high concentration (>5×10⁻⁷ mol l⁻¹) forskolin inhibited the transepithelial potential. These results implicate cAMP as an important intracellualr regulator of both ionoregulatory and haemodynamic functions in the teleost gill.

The β-adrenergic agonist isoprenaline administered as injected doses in the perfusate produced a stimulation of the transepithelial potential and a decrease in the arterial vascular resistance. A dose-response analysis showed that half-maximal haemodynamic effects occurred at significantly lower doses of agonist than those required for half-maximal stimulation of the potential. The pancreatic hormone glucagon also caused dose-dependent stimulation of the transepithelial potential but had no effect on arterial vascular resistance. It is suggested that regulation of the rate of branchial monovalent ion excretion may be under peptidergic as well as adrenergic control.