"Mechanosensitive channels release tension in cell membranes by opening 'pressure relief' pores…Faced with a sudden decrease in osmotic pressure, as might be caused by a spring downpour, free-living cells are subjected to a rapid influx of water. This sharply increases the pressure of the cell contents against the membrane, potentially compromising the integrity of the cell. Most prokaryotes (bacteria and archaea) have therefore evolved a 'pressure-release valve' mechanism in which changes in membrane tension open up channels to form large, aqueous pores in the membrane. Once formed, the short-lived pores allow the passage of both solute and solvent at very high rates, quickly equilibrating hypo-osmotic imbalances across the cell wall." (Vásquez and Perozo 2009:47)

"[H]elices lining the inside of the pore tilt towards the plane of the membrane as the channel moves from the closed to the pre-expanded state, and that the whole channel structure becomes flatter. The helices maintain this orientation as the cross-section of the channel expands to reach the open state...MscL is nonselective for the ions and small molecules it transports and is activated at membrane tensions close to the breaking point of the membrane bilayer. It is thus usually thought of as a bacterium’s last line of defence against hypo-osmotic shock...a domain of MscL [mechanosensitive channel of large conductance] known as the cytoplasmic bundle acts as a sieve that limits the passage of large molecules through the pore...the first physical transition generates a 'pre-expanded' state in which the cross-sectional area of the channel is slightly larger than in the closed state. This is likely to be the most tension-dependent state of the mechanism, as the probability that the channel will open should be proportional to −γΔA, where γ is the lateral tension in the membrane." (Vásquez and Perozo 2009:48)