Key Points
- To determine the electrophysiological mechanisms and specific ionic conductances responsible for cell volume regulation following osmotic swelling in proximal renal tubules.
- Simultaneously measured tubule volume via video-optical imaging and basolateral membrane potential (Vbl) and ionic conductances using conventional microelectrodes in nonperfused rabbit S2 proximal tubules.
- Challenged tubules with hypoosmotic bathing solution (lowered from 290 to 150 mosmol/kg) in the presence or absence of bicarbonate buffer and the potassium channel blocker barium (2 mM Ba).
- Hypoosmotic exposure caused tubules to swell 72% above baseline within 1 minute before regulating back to 20 ± 3% over 4–6 minutes, accompanied by transient Vbl hyperpolarization (-14.3 ± 2.0 mV with HCO3; -10.0 ± 0.7 mV without HCO3).
- Relative basolateral potassium conductance increased from 0.16 to 0.34 at peak swelling and was abolished by 2 mM barium in bicarbonate-free solution.
- Relative basolateral chloride conductance increased from 0.08 to 0.20, evidenced by bath chloride dilution steps shifting Vbl from 5.3 ± 1.0 mV to 11.3 ± 2.1 mV (P ≤ 0.05) during peak swelling.
Structured PICO
PPopulationNonperfused rabbit proximal tubule (S2 segment)
IInterventionReduction of bathing medium osmolality to 150 mosmol/kg to induce cell swelling
CComparatorControl isotonic Ringer solution (290 mosmol/kg)
OOutcomeBasolateral membrane voltage (Vbl) and relative ionic conductance (Cl and K)surrogate
Cell swelling in rabbit proximal tubules activates basolateral membrane chloride and potassium conductances, which may underlie cell volume regulation.