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. 2000 Apr 1;105(7):925–933. doi: 10.1172/JCI8609

Figure 5.

Figure 5

Circulating ET-1 levels and blood pressure response to ETA blockade in DBH-ETB;ETB+/+ and DBH-ETB;ETBsl/sl rats. DBH-ETB;ETBsl/sl rats exhibited increased circulating ET-1 levels as measured by sandwich-type enzyme immunoassay (a). The level of dietary sodium did not significantly affect circulating ET-1 levels in DBH-ETB;ETB+/+ rats. However, ETB genotype significantly affected plasma ET-1 levels. a shows a significant increase in plasma ET-1 in DBH-ETB;ETBsl/sl rats (13.2 ± 2.8 pg/mL) compared with DBH-ETB;ETB+/+ rats (2.1 ± 1.8 pg/mL; P < 0.02) on a sodium-deficient deficient diet. On a high-sodium diet, the plasma ET-1 level in DBH-ETB;ETBsl/sl rats (23.9 ± 4.2 pg/mL) was also significantly increased compared with DBH-ETB;ETB+/+ rats (4.4 ± 1.4 pg/ml; P < 0.001). DBH-ETB;ETBsl/sl rats on a high-sodium diet exhibited a significantly increased plasma ET-1 level compared with DBH-ETB;ETBsl/sl rats on a sodium-deficient diet, although diet was not an independent variable affecting plasma ET-1 concentration by 2-way ANOVA. (b) DBH-ETB;ETBsl/sl rats exhibit an increased acute depressor response to ETA blockade with FR139317 (10 mg/kg, intra-arterially) compared with ETB+/+ rats on a high-sodium diet. DBH-ETB;ETBsl/sl rats are significantly hypertensive compared with DBH-ETB;ETB+/+ rats before and after treatment with FR139317. However, the change in MAP in DBH-ETB;ETBsl/sl rats in response to FR139317 (–15 ± 5 mmHg) is significantly greater than in DBH-ETB;ETB+/+ rats (–3 ± 2 mmHg; AP = 0.01).