Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

摘要: Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower prekallikrein, compared with those normal the same strain. Systolic blood pressure, determined by tail-cuff method, 5-week-old (106 +/- 0.4 mm Hg, n = 7) rate systolic pressure increase age were not different from in rats. Weekly injections deoxycorticosterone acetate (5 mg/kg s.c.) 1% sodium chloride solution drinking water after uninephrectomy at 7 weeks caused a gradual rats, reaching plateau 18 age, whereas that deficient rose rapidly to 158 6 Hg 2 start treatment continued slightly, becoming significantly higher than 8, 9, 10, 11, 12 (p less 0.05 or 0.01). The urinary prokallikrein active kallikrein slightly before acetate-salt but increased this treatment, these 3.6- 4.7-fold treatment. Urinary free kinin, collected ureter untreated was below detection limit. level molecular weight kininogen, substrate glandular kallikrein, decreased during Continuous subcutaneous injection aprotinin an osmotic pump induced significant pressure. These results indicate may play suppressive role hypertension.