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Air jet stress (AJS) induces ET‐1 mediated reactive oxygen species (ROS) production that increases blood pressure in Dahl salt‐sensitive (DS) rats.
Author(s) -
Loria Analia Silvina,
D'Angelo Gerard,
Pollock David M,
Pollock Jennifer S
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.969.5
Subject(s) - medicine , endocrinology , reactive oxygen species , chemistry , blood pressure , antagonist , endothelin receptor , receptor , endothelin 1 , blockade , receptor antagonist , biology , biochemistry
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.