Plasma kinin concentration in @entity8147 -salt XXXX .

@entity1811 @entity101 @entity1219 @entity3371 @entity8147 @entity1812 @entity35 @entity4420
We investigated the status of circulating kinins in @entity35 with severe @entity101 caused by drinking 1% @entity1219 (saline) and treatment with @entity8147 ( @entity4420 , 25 mg/kg/wk s.c.) for 5 weeks. Saline-drinking @entity35 treated with @entity4420 had a higher systolic blood pressure (210 +/- 4 mm Hg) than did @entity35 without @entity4420 treatment drinking water (138 +/- 3 mm Hg) or saline (141 +/- 3 mm Hg). The concentration of kinins in the inferior vena cava plasma of @entity4420 -salt @entity101 @entity35 did not differ from the venous plasma kinin concentration in normotensive @entity35 drinking water or saline. In contrast, the arterial plasma kinin concentration in @entity4420 -salt @entity101 @entity35 (7.0 +/- 0.8 pg/ml) was lower (p less than 0.002) than that in water-drinking controls (14.0 +/- 2.2 pg/ml); it also was lower (p less than 0.005) in saline-drinking @entity35 (8.1 +/- 0.9 pg/ml) than in water-drinking controls. Infusion of @entity1812 (20 micrograms/kg/min i.v.) increased arterial plasma kinins in all the groups. Nonetheless, the arterial plasma kinin concentration achieved during @entity1812 infusion in @entity4420 -salt @entity101 (1590 +/- 130 pg/ml) and in saline-drinking @entity35 (1540 +/- 100 pg/ml) was lower than that in water-drinking @entity35 (2140 +/- 210 pg/ml). On the other hand, during infusion of the @entity1811 inhibitor @entity3371 (80 micrograms/hr i.p.) for 3 days, neither @entity4420 -salt @entity101 @entity35 nor saline-drinking normotensive @entity35 exhibited significant reduction of arterial plasma kinins relative to the level in water-drinking controls. These data indicate that high salt intake, irrespective of the level of blood pressure, causes the arterial plasma concentration of kinins to fall.(ABSTRACT TRUNCATED AT 250 WORDS)
