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1 Departments of Medicine (Cardiology) and Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, PA, USA
* To whom correspondence should be addressed. E-mail: kmonahan{at}psu.edu.
Animal studies suggest that prostanoids (i.e., such as prostacyclin) may sensitize or impair baroreceptor/baroreflex responsiveness depending on the site of administration/inhibition. We tested the hypothesis that acute inhibition of cyclooxygenase (COX), the rate-limiting enzyme in prostanoid synthesis, impairs baroreflex regulation of cardiac period (R-R interval) and muscle sympathetic nerve activity (MSNA) in humans and augments pressor reactivity. Baroreflex sensitivity (BRS) was determined at baseline (pre) and 60 min after (post) intravenous infusion of a COX antagonist (ketorolac; 45 mg) (24±1 yr; n=12) or saline (25±1 yr; n=12). BRS was assessed using the modified Oxford technique (bolus intravenous infusion of nitroprusside followed by phenylephrine). BRS was quantified as the slope of the linear portion of the: 1) R-R intervalsystolic
blood pressure relation (cardiovagal BRS) and 2) MSNA-diastolic blood pressure relation (sympathetic BRS) during pharmacological changes in arterial blood pressure. Ketorolac did not alter cardiovagal (19.4±2.1 vs. 18.4±2.4 ms/mmHg pre and post, respectively) or sympathetic BRS (-2.9±0.7 vs. -2.6±0.4 au/beat/mmHg), but significantly decreased a plasma biomarker of prostanoid generation (plasma thromboxane B2) by 53±11%. Cardiovagal BRS (21.3±3.8 vs. 21.2±3.0 ms/mmHg), sympathetic BRS (-3.4±0.3 vs. -3.2±0.2 au/beat/mmHg), and thromboxane B2 (
-1±12%) were unchanged in the control (saline infusion) group. Pressor responses to steady state incremental (0.5, 1.0, and 1.5 µg/kg/min) infusion (5 min/dose) of phenylephrine were not altered by ketorolac (n=8). Collectively, these data indicate that acute pharmacological antagonism of the COX enzyme does not impair BRS (cardiovagal or sympathetic) or augment pressor reactivity in healthy young adults.
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