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- W98644608 abstract "We have previously reported that AJS elicits increases in plasma endothelin-1 (ET-1) and blood pressure. Because ET-1 increases ROS in vascular and neuronal tissue, we tested the hypothesis that the AJS-induced increase in blood pressure is influenced by ET-1-dependent ROS production. AJS was induced in male DS rats (9–10 weeks old on a normal salt diet) once per week over 2 weeks by administration of air jet pulses (3 min). Animals were untreated (C) (week 1), or given either tempol (1 mM in drinking water) or a non-selective ETA/B receptor antagonist (A-182086, 30 mg/Kg/day in food) (week 2). In telemetry-instrumented rats, the AJS-induced pressor response was significantly reduced in tempol treated rats vs. Co (15.9 ± 2.5 vs. 27.2 ± 3.8 mmHg × 3 min, p < 0.05). In addition, tempol enhanced the blood pressure recovery vs. C (p< 0.05). Pre-treatment with A-182086 blocked the AJS-induced pressor response vs. C (6.9 ± 6.7 vs. 43.8 ± 12.2 mmHg × 3 min, p<0.05) and enhanced the post-stress recovery vs. C (p < 0.05). ETA/B receptor blockade abolished the AJS-mediated rise in plasma 8-isoprostane (43 ± 5 to 41 ± 4 pg/ml) compared with C (37 ± 3 to 63 ± 8 pg/ml, p <0.05). These findings suggest that AJS stimulates the ET-1 pathway that activates ROS production. Activation of ROS contributes to the AJS-induced increase in pressor response and blunting of the blood pressure recovery in DS rats." @default.
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- W98644608 date "2008-03-01" @default.
- W98644608 modified "2023-09-25" @default.
- W98644608 title "Air jet stress (AJS) induces ET‐1 mediated reactive oxygen species (ROS) production that increases blood pressure in Dahl salt‐sensitive (DS) rats." @default.
- W98644608 doi "https://doi.org/10.1096/fasebj.22.1_supplement.969.5" @default.
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