Efferent role of ADH in CNS-induced natriuresis.
Ventriculocisternal perfusion (VCP) of artificial cerebrospinal fluid (CSF) was performed in pentobarbital-anesthetized dogs. Renal function was studied in protocols consisting of a 1-h experimental period in which the animals received either CSF with an elevated sodium concentration (300 mM, high Na) via VCP or antidiuretic hormone (ADH) intravenously, bracketed by 1-h control and recovery periods. High Na VCP caused an increase in plasma ADH measured by radioimmunoassay (to 176% of control) that coincided with a natriuresis (to 180% of control). In a second set of experiments, these changes in endogenous ADH were mimicked experimentally with intravenous infusions of synthetic ADH in animals receiving continuous VCP with normal sodium artificial CSF. The dose-response relationship between log ADH and urinary sodium excretion for the intravenous ADH experiments was not different from the relationship for those experiments in which ADH was elevated as a consequence of high Na VCP. These results suggest that ADH causes part, if not all, the natriuresis induced by high Na VCP.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001834:Body Water / Q000378:metabolism; D001921:Brain / Q000502:physiology*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005919:Glomerular Filtration Rate / Q000187:drug effects; D009318:Natriuresis / Q000187:drug effects*; D009476:Neurons, Efferent / Q000502:physiology*; D010477:Perfusion; D011188:Potassium / Q000652:urine; D012964:Sodium / Q000134:cerebrospinal fluid / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology*
D014667:Vasopressins; D012964:Sodium; D011188:Potassium