Antidiuretic hormone-dependent membrane capacitance and water permeability in the toad urinary bladder

Abstract

Antidiuretic hormone (ADH) increased the electrical capacitance of apical membrane of the toad bladder; this effect was modulated by the osmotic gradient across the tissue. Capacitance was measured from the transepithelial voltage response to constant-current pulses using bladders depolarized with KCl-sucrose serosal solution to reduce basolateral resistance and with Na-free mucosal solution to increase apical membrane resistance. Addition of ADH (20 mU/ml) increased capacitance by 28 +/- 9% (mean +/- SD) in the absence and by 8 +/- 3% in the presence of an osmotic gradient (200 mosM, mucosal side hypotonic). With bladders stimulated in the absence of an osmotic gradient, rapidly imposing a gradient resulted in a peak rate of water flow that declined to 40% of the peak value after 15-20 min. ADH-dependent capacitance also decreased with a similar time course. Removal of ADH reversed the capacitance change (t1/2 = 10-15 min), but the reversal was slower than the decline in water flow to basal levels (t1/2 less than 5 min). Colchicine and cytochalasin B also inhibited the ADH-induced capacitance increase. The capacitance change was also inhibited when the mucosal solution was made hypertonic with raffinose. The results are interpreted within the framework of a previously proposed model of ADH-stimulated water transport in which cytoplasmic vesicular structures fuse with the apical plasma membrane.

Non-coordinate Regulation of Endogenous Epithelial Sodium Channel (ENaC) Subunit Expression at the Apical Membrane of A6 Cells in Response to Various Transporting Conditions

“…We found that both ADH and long term aldosterone increased apical membrane ␤-xENaC. In both of these conditions, estimates of channel activity by electrophysi-ologic techniques or biochemical methods suggest an increase in the number of active apical membrane holochannels (20,21,67,68,73). This suggests that ␤-xENaC delivered from intracellular compartments may assemble with ␣␥ heterodimers already present at the cell surface.…”

Cytoskeleton-dependent endocytosis is required for apical type 1 angiotensin II receptor-mediated phospholipase C activation in cultured rat proximal tubule cells.

“…In the case ofglucose transport, microfilament disruption with cytochalasin B resulted in impaired glucose transporter trafficking and diminished glucose uptake (50-53). Toad bladder studies have revealed that water transport is dependent upon water channel movement through the cytoskeleton, since water transport was inhibited after disruption of either microfilaments (54)(55)(56)(57) or microtubules (54,55,57). Although endocytosis through cytoskeletal domains appears to be required for a number of AP functions, there is little information about the role of the cytoskeleton in receptor-mediated signal transduction.…”

Identification of specific apical membrane polypeptides associated with the antidiuretic hormone-elicited water permeability increase in the toad urinary bladder.

“…ADH stimulation without net osmotic water flow (no osmotic gradient) produces aggrephore fusion without apical membrane retrieval (9,10,26 (27 (Fig. 1B).…”