Genetic hypertension in rats is accompanied by a defect in renal prostaglandin catabolism.
Noradrenaline releases prostaglandins in the kidney, and in rats these augment rather than reduce vasoconstriction produced by the amine. Homogenates of kidneys of New Zealand rats inbred for hypertension exhibit lower prostaglandin inactivation by 15-hydroxydehydrogenase than controls. At the same time, augmentation of noradrenaline vasoconstriction by the released prostaglandin is exaggerated. This biochemical defect could be the inherited abnormality primarily responsible for the development of hypertension in these animals.
D000818:Animals; D004195:Disease Models, Animal; D004357:Drug Synergism; D006911:Hydroxyprostaglandin Dehydrogenases / Q000172:deficiency; D006973:Hypertension / Q000235:genetics / Q000378:metabolism*; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011458:Prostaglandins E / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats; D014655:Vascular Resistance / Q000187:drug effects
D011448:Prostaglandin Antagonists; D011458:Prostaglandins E; D006911:Hydroxyprostaglandin Dehydrogenases; D009638:Norepinephrine; D007213:Indomethacin