The renal prostaglandin kallikrein-kinin-system in Brattleboro rats with hereditary hypothalamic diabetes insipidus.
The results of estimation of renal prostaglandin (PG) excretion showed a significantly decreased excretion of PGE2 by 71% and that of PGF2 alpha--by 28% in rats with hereditary diabetes insipidus (DI), compared to the control Long Evans (LE) rats. The results suggested an inhibition of renal PG synthesis in DI rats due to the absence of stimulatory effect of ADN in DI rats lacking ADH. An inverse correlation between plasma renin activity and renal PG excretion was found (r = --0.36). The renal kallikrein excretion of DI rats was not significantly different compared to that of LE rats. An attempt for explanation of these results was made.
D000818:Animals; D003919:Diabetes Insipidus / Q000235:genetics / Q000378:metabolism*; D015237:Dinoprost; D015232:Dinoprostone; D007610:Kallikreins / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D007705:Kinins / Q000378:metabolism; D008297:Male; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D051381:Rats; D011910:Rats, Brattleboro; D012084:Renin-Angiotensin System
D007705:Kinins; D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D015237:Dinoprost; D007610:Kallikreins; D015232:Dinoprostone