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1. High-Na tissues exposed to a Na-free solution with dimethyldiethanol ammonium chloride (DDA) or sucrose replacing Na, develop an increase in membrane permeability to small ions and molecules such as Na, K, sucrose and CoEDTA. 2. The increase in permeability only occurs when the Na gradient across the cell membrane is reversed, and is not due to damaging effects of the Na-free solution. It does not occur in normal or high-K tissues, and 15 mM-[Na]0 is enough to prevent the permeability change in high-Na tissues. 3. Tissues with increased permeability maintain high levels of Ca and the increased permeability does not occur in Ca-free solutions, or in solutions containing 5 mM-La3+. The rate of development of membrane leakiness depends on the level of extracellular Ca. 4. Tissues exposed to iodoacetic acid (IAA) and dinitrophenol (DNP) also develop a membrane leakiness, dependent on extracellular Ca and blocked by La3+. 5. The time taken for development of the increase in membrane permeability in metabolically inhibited tissues can be affected by the Na gradient. With no gradient, or a slightly reversed gradient the membrane break-down occurs more rapidly. 6. It is concluded that the increase in permeability is caused by an increase in internal Ca ions, and that the Na gradient as well as the levels of ATP are important in controlling Ca movements. 7. Tension recordings also support the some form of Na--Ca exchange mechanism operating in the taenia, and this mechanism is not completely blocked by La3+ ions, although they suppress the break-down in membrane permeability.