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Random Crossref JSON output of an article
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"abstract": "<jats:p>This study investigated the influence of chronic crowding stress on nitric oxide (NO) production, vascular function and oxidative status in young Wistar-Kyoto (WKY), borderline hypertensive (BHR) and spontaneously hypertensive (SHR) female rats. Five-week old rats were exposed to crowding for two weeks. Crowding elevated plasma corticosterone<mml:math xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" id=\"M1\"><mml:mo stretchy=\"false\">(</mml:mo><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.05</mml:mn><mml:mo stretchy=\"false\">)</mml:mo></mml:math>and accelerated BP (<mml:math xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" id=\"M2\"><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.01</mml:mn></mml:math>versus basal) only in BHR. NO production and superoxide concentration were significantly higher in the aortas of control BHR and SHR versus WKY. Total acetylcholine (ACh)-induced relaxation in the femoral artery was reduced in control SHR versus WKY and BHR, and stress did not affect it significantly in any genotype. The attenuation of ACh-induced relaxation in SHR versus WKY was associated with reduction of its NO-independent component. Crowding elevated NO production in all strains investigated but superoxide concentration was increased only in WKY, which resulted in reduced NO-dependent relaxation in WKY. In crowded BHR and SHR, superoxide concentration was either unchanged or reduced, respectively, but NO-dependent relaxation was unchanged in both BHR and SHR versus their respective control group. This study points to genotype-related differences in stress vulnerability in young female rats. The most pronounced negative influence of stress was observed in BHR despite preserved endothelial function.</jats:p>",
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