Mechanically-activated ion channels (MACs) of cultured rat mesangial cells were stimulated by applying suction to patch pipets or by exposing cells to hypoosmotic media. MAC density was estimated as 1.5 +/- 0.4 per mu 2. In the absence of any stimulus, MAC open probabilities (N * P) were < 0.0001 increasing as a function of stretch or extracellular hypoosmolarity. Single channel mean open time during stretch increased with patch depolarization whereas hyperpolarization of the membrane delayed MAC inactivation. Ionic conductance of MACs, based on average slope conductances at hyperpolarized potentials, was 76 pS in high external K+ (N = 5) and 40 pS in high external Na+ (N = 8). PK+/PNa+ was estimated to be 4.7. MACs did not permeate Cl-, at least outwardly. Whole cell currents in response to voltage steps applied to resting cells in control conditions were approximately ohmic between -120 mV and 40 mV and were linearly and reversibly dependent on extracellular osmolarity. Our results demonstrate that: (1) MACs can be activated by both negative hydrostatic pressures applied to the pipet and by osmotic gradients; (2) MAC kinetic behavior is sensitive to membrane potential; (3) MACs may participate in cellular responses to physical forces.

No abstract

Studies using conventional and patch-clamp microelectrode techniques demonstrate that in a number of cell types angiotensin II (All) causes reversible changes in transmembrane ionic currents, and that these effects can be mimicked by various membrane-associated and cytosolic messengers. All modulates the current amplitude of ion channels, as well as their activation threshold and their open/closed time probability. Stimulatory and inhibitory effects on ion channel activity are a fundamental feature of the development of All actions on target organs.