Intracerebroventricular infusion of sodium chloride-rich artificial cerebrospinal fluid in rats induces natriuresis and releases an inhibitor of prostaglandin synthesis.
Urinary sodium excretion in anaesthetized rats subjected to high-sodium artificial cerebrospinal fluid (CSF) infusion into the lateral brain ventricle, was significantly higher than in rats infused with normal-sodium CSF. Urinary immunoreactive 6-ketoprostaglandin F1 alpha, the stable derivative of prostacyclin, was significantly reduced in the high-sodium CSF group, as compared with the normal-sodium CSF group. When dog aortic endothelium was incubated in the presence of plasma, endothelial prostacyclin production was found to be inhibited by plasma from rats infused with high-sodium CSF compared with the effect of plasma from the rats infused with normal-sodium CSF. Our results indicate that intracerebroventricular infusion of high-sodium CSF induces a natriuretic response and is associated with the appearance of a humoral factor which blocks prostacyclin biosynthesis.
D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000818:Animals; D001681:Biological Assay; D002552:Cerebral Ventricles; D002555:Cerebrospinal Fluid / Q000502:physiology*; D003864:Depression, Chemical; D011464:Epoprostenol / Q000096:biosynthesis*; D007263:Infusions, Parenteral; D008297:Male; D009318:Natriuresis / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology*
D012965:Sodium Chloride; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol