Response of tissues of the rat to anisosmolality in vivo

Rats were exposed to osmotic stress either acutely, over periods of 1 or 4 h, or chronically, over several days. In acute experiments, hyposmolality was induced by intraperitoneal infusion of dilute glucose or mannitol solutions, whereas hyperosmolality was induced by use of sodium chloride, concentrated glucose or mannitol solutions, or urea. Chronic hypernatremia was induced by daily administration of sodium chloride to water-deprived animals; chronic hyponatremia was induced by daily injection of antidiuretic hormone supplemented with glucose. Animals were made hyperglycemic using streptozotocin or uremic by ureteral ligation. Where appropriate, animals were anesthetized with thiobutabarbital (Inaktin) or ether. In acute experiments, analysis of the composition of the cardiac ventricle, diaphragm, liver, and renal cortex showed no evidence of cell volume regulatory processes involving transmembrane movement of potassium ions. There was a small but significant increase in free amino acids [measured as ninhydrin-positive substance (NPS)] in cardiac muscle exposed to hypertonic solutions of sodium chloride and glucose but not when plasma osmolality was raised using mannitol. In cerebral cortical tissue, after 4 h of exposure to acute hypertonicity by infusion of sodium chloride or glucose, there was a significant increase in tissue potassium content and a slight increase in NPS content. In chronic experiments, tissue analysis revealed good evidence for cellular volume readjustment only in cerebral cortex and heart. In the cortex, levels of free amino acids, principally taurine and glutamate (plus glutamine), showed large increases during hypernatremia and hyperglycemia and corresponding decreases during hyposmolality. In heart the principal amino acid present was taurine, and it, together with aspartate and glutamate (plus glutamine), showed large changes under osmotic stress. Other tissues analyzed showed only small changes in composition.