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In this study we tested the hypothesis that shear-stress-dependent endothelium-derived nitric oxide (EDNO) release acts as a physiological blood pressure buffer. EDNO was blocked by the false substrate for EDNO-synthesis (NG-nitro-L-arginine (L-NNA), 16.5 ± 2 mg/kg body weight i.v.) over 24 hours. Blood pressure and heart rate (HR) were examined over this period in freely moving conscious dogs (N = 6). After L-NNA, mean arterial pressure (MAP) increased from 116±5 mmHg to 134±5 mmHg (P < 0.01), heart rate decreased from 97 ± 6 to 68 ± 3 beats/min (P < 0.01). The power spectrum revealed a 2.1 fold increase of power in the frequency range between 0.01-0.5 Hz (P < 0.05) in response to L-NNA. These data suggest, that blockade of EDNO provides sustained hypertension over a 24 hour recordings and that EDNO is important as a physiological blood pressure buffer in the frequency range below 0.5 Hz. Thus, the endothelium participates in the control blood pressure variability together with arterial baroreceptors
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