Volume regulatory influx of electrolytes from plasma to brain during acute hyperosmolality.
Brain volume is regulated during acute hyperosmolal states based, in part, on the tissue gain of Na, Cl, and K [H. F. Cserr, M. DePasquale, and C.S. Patlak, Am. J. Physiol. 253 (Renal Fluid Electrolyte Physiol. 22): F522-F529, 1987]. This study evaluates the contribution of influx from plasma to the volume regulatory gain of electrolyte. Blood-to-brain transfer constants, K1, were measured as a function of plasma osmolality, over the range 300-385 mosmol/kg, for sodium (22Na) and potassium (42K or 86Rb) and as a marker for nonselective changes in permeability for [14C]mannitol. Osmolality was elevated by intraperitoneal injection of hypertonic NaCl, mannitol, or sucrose. K1 for Na, K, and mannitol each increased linearly with plasma osmolality. Increases in K1 for Na and mannitol were small and were proportional to their respective diffusion coefficients, consistent with the development of a small leak pathway. Increases in K1 for K were much larger, consistent with osmotic stimulation of a selective permeability pathway. Quantitative analysis of the results suggests that uptake from plasma accounts for most of the K gained by brain tissue in response to acute hyperosmolality but for only a small fraction of the Na. This provides indirect evidence for an additional source of Na, presumably from cerebrospinal fluid.
D000818:Animals; D001810:Blood Volume; D001812:Blood-Brain Barrier; D001921:Brain / Q000502:physiology*; D006955:Hypernatremia / Q000503:physiopathology; D007700:Kinetics; D008353:Mannitol / Q000008:administration & dosage; D008704:Methazolamide / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D013395:Sucrose / Q000008:administration & dosage; D014882:Water-Electrolyte Balance
D008353:Mannitol; D013395:Sucrose; D012964:Sodium; D012413:Rubidium; D011188:Potassium; D008704:Methazolamide