Vascular Kallikrein in Deoxycorticosterone Acetate–Salt Hypertensive Rats

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We determined the status of vascular kallikrein in rats with severe hypertension caused by treatment with deoxycorticosterone acetate (DOCA) and drinking of 1% Nad for 6 weeks. We assayed active and total kininogenase (kallikrein) activity in the perfusate and in arterial and venous tissue. DOCA-salt rats had higher systolic blood pressure at 6 weeks (214±5 mm Hg) than rats drinking tap water (135±4 mm Hg) or saline (145±8 mm Hg). Kininogenase in the perfusate (nanograms bradykinin per minute per kilogram body weight) increased significantly at 2 weeks, from 5.8±2.1 to 8.9±1.4 for active kallikrein and from 28.7±0.4 to 48.7±2.9 for total kallikrein. Total kallikrein returned to control values at 4 weeks, whereas it was significantly reduced at 6 weeks (20.9±0.7). Active kallikrein was significantly depressed at 4 and 6 weeks (1.08±0.1 and 0.85±0.1, respectively [P<.05]). Active kallikrein in arterial tissue (picograms bradykinin per milligram per minute) showed a small but significant increase at 2 weeks, from 156±7 to 201 ±10 (P<.05), finally decreasing significantly by 6 weeks to 64±3; however, total kallikrein showed a significant decrease only at 6 weeks, from 844±17 to All±21. Both active and total kallikrein in the veins were higher than control values at 2 weeks, changing from 437±7 to 541±19 and from 1619±17 to 2062±86, respectively. Venous kallikrein remained elevated until the end of the experiment. These findings suggest that mineralocorticoids increase vascular kallikrein and that established hypertension lowers both arterial kallikrein and kallikrein released by the vasculature, whereas venous kallikrein is under a different regulatory control. The vascular kallikrein-kinin system may help counteract the elevation of vascular resistance in the earliest stages of DOCA-salt hypertension.

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