Relation of ADH effects to altered membrane fluidity in toad urinary bladder.

Area of Science:

• Cell Biology
• Membrane Physiology
• Renal Physiology

Background:

• Antidiuretic hormone (ADH) regulates water and urea permeability in the toad urinary bladder.
• ADH stimulation leads to intramembranous particle aggregates in granular cell luminal membranes, correlating with water permeability.
• The role of membrane fluidity in ADH-mediated transport changes is not fully understood.

Purpose of the Study:

• To investigate the relationship between ADH-stimulated changes in urea and osmotic water permeability and membrane fluidity.
• To determine if membrane fluidity changes are required for the formation of intramembranous particle aggregates.
• To elucidate the mechanisms underlying ADH-stimulated water and urea transport.

Main Methods:

• Comparison of ADH-stimulated urea and osmotic water permeability, luminal membrane aggregates, and membrane fluidity (n-butyramide permeability) at room temperature and cold.
• Assessment of membrane fluidity using n-butyramide permeability as a probe.

Main Results:

• The occurrence of luminal membrane aggregates is independent of accompanying ADH-induced changes in membrane fluidity.
• ADH-stimulated osmotic water permeability is also independent of coincident membrane fluidity changes.
• ADH-stimulated transbladder urea movement appears to involve channels, with membrane fluidity changes potentially influencing their formation.

Conclusions:

• Hormonally stimulated water permeability in toad bladder involves membrane channels and is not solely dependent on lipid solubility-diffusion.
• While a critical level of membrane fluidity is necessary, aggregate formation and water transport are not directly coupled to fluidity changes.
• ADH-induced changes in membrane fluidity may play a role in the formation of channels involved in urea transport.