Renal kallikrein-kinin, prostaglandin E2, and dopamine systems in young normotensive subjects with a family history of essential hypertension.
Before dopamine infusion, there were no differences in urinary excretion of sodium (UNaV), fractional excretion of sodium (FENa), kinin and kallikrein quantity (KALQ), activity (A) or specific activity (Sp) between the young normotensive subjects with (FH[+]) and without a family history of essential hypertension (FH[-]), whereas urinary dopamine excretion was significantly lower and urine volume (UV) and urinary prostaglandin E2 (PGE2) were significantly higher in FH(+) subjects than in FH(-) subjects. After infusion of dopamine (3 micrograms/kg/min for 60 min), the increases in UV, UNaV, FENa, kinin, KALA, KALSp, and PGE2 were higher in FH(+) than in FH(-) subjects. From these results, it was concluded that (1) the augmented response of urinary kallikrein-kinin and PGE2 to infused dopamine in FH(+) subjects could be explained by the hereditary suppression of dopamine in the kidneys, and (2) the maintenance of a normal level of the basal kallikrein-kinin system and an increase of PGE2 in FH(+) subjects may be caused by compensatory mechanisms other than that of renal dopamine.
Shimamoto
K
K
Second Department of Internal Medicine, Sapporo Medical College, Japan.
Ura
N
N
Nishimura
M
M
Iimura
O
O
D000328:Adult; D015232:Dinoprostone / Q000652:urine*; D004298:Dopamine / Q000494:pharmacology* / Q000652:urine; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D007610:Kallikreins / Q000652:urine*; D007668:Kidney / Q000502:physiology*; D007705:Kinins / Q000652:urine*; D008297:Male; D012964:Sodium / Q000378:metabolism
D007705:Kinins; D012964:Sodium; D007610:Kallikreins; D015232:Dinoprostone; D004298:Dopamine