Nitrogen excretion and the cardiorespiratory physiology of the gulf toadfish, Opsanus beta.

Abstract

Gulf toadfish, Opsanus beta, are facultatively ureotelic and can excrete the majority of their nitrogenous waste as urea. Urea excretion occurs in "pulses." The hypothesis that pulsatile urea excretion reflects sudden, transient, generalized increases in the branchial conductance was investigated by the simultaneous monitoring of cardiorespiratory variables, oxygen uptake, and whole-body urea, ammonia, and/or 3H2O effluxes. The direct monitoring of both expired branchial water and water exiting a respirometer demonstrated that urea pulses were derived from the gills. No significant changes in ventilation or cardiac frequency, oxygen uptake, or ammonia efflux were observed during natural urea pulses, refuting the hypothesis that pulsatile urea excretion reflects pulsatile increases in the generalized diffusive properties of the gill for solute transfer. An alternative model for pulsatile urea excretion postulates that the gill urea permeability is increased periodically by the insertion and/or activation of specific urea transporters into gill cell membranes. Pulsatile urea excretion was abolished by pretreatment with the cytoskeletal-disrupting agent colchicine; colchicine may block trafficking of urea transporter-containing vesicles. Exocytosis of water following the fusion of vesicles with gill cell membranes could explain the significantly elevated 3H2O efflux observed during urea pulses.