A variety of lesions of the central nervous system may be associated with disturbances of renal function characterized by either the increased urinary loss of sodium and chloride (1-3) or the retention of salt (3-8). It has also been postulated that changes in the excretion of salt, secondary to alterations in the volume of blood or extracellular fluid, are mediated by a "volume receptor" located in the cranial cavity (9-12). The following experiments were therefore undertaken in order to investigate the influence of alterations in intracranial venous volume and pressure, and cerebrospinal fluid (CSF) volume and pressure on renal function.
METHODSFemale dogs were anesthetized with sodium pentobarbital (30 mg. per Kg.) except for two experiments in which chloralose (75 mg. per Kg.) was used. Urine was collected through an indwelling catheter. The bladder was washed out with distilled water after each collection and emptied completely by blowing out with air. Glomerular filtration rate was measured by the clearance of exogenous creatinine (Ccr) (13) and renal plasma flow was estimated from the clearance of paraminohippurate
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