Natriuresis induced by intracarotid infusion of hypertonic NaCl.
The intracarotid infusion of hypertonic sodium chloride in anesthetized dogs pretreated with vasopressin and mineralocorticoid resulted in an increase in sodium excretion as well as an increase in the percent of the filtered load of sodium excreted. This increase was not due to changes in renal hemodynamics or arterial blood pressure. The change in fractional sodium excretion was approximately 1%. Intracarotid infusion of isotonic sodium chloride did not result in a natriuretic response. The intracarotid infusion of hyperosmotic glucose did not evoke an increase in sodium excretion. Femoral vein infusions of hypertonic sodium chloride failed to evoke any natriuretic response. These data indicate that a sodium-sensing mechanism may exist in the brain that can alter the renal handling of sodium. The efferent mechanism of the response is discussed.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries; D004285:Dogs; D005260:Female; D005268:Femoral Vein; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology; D007263:Infusions, Parenteral; D007668:Kidney / Q000098:blood supply; D011188:Potassium / Q000652:urine; D012039:Regional Blood Flow / Q000187:drug effects; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000008:administration & dosage*
D012965:Sodium Chloride; D012964:Sodium; D005947:Glucose; D011188:Potassium