The effect of prolonged hypoxia, transient and prolonged hypotension, and of acidosis on rat kidney and muscle water, sodium, potassium, magnesium, and phosphate composition was investigated. A significant increase in kidney tissue water was found in all experimental groups. Prolonged hypotension produced a decrease in kidney potassium and magnesium content and an increase in sodium content. Hypoxia produced an increase in magnesium content. No significant changes in the kidney solutes measured resulted from transient hypotension or respiratory acidosis. Skeletal muscle water was increased in all but the hypoxic group and potassium content in all but the prolonged hypotension group. It is suggested that prolonged hypotension results in renal depletion of normal intra-cellular cations and replacement by sodium. These changes probably indicate loss of functional integrity of renal cells and may relate to the clinical syndrome of acute tubular necrosis and to delayed function of homografted cadaver kidneys.