Abstract
Abstract only Cyclooxygenase (COX) catalyzes the formation of prostaglandins and influences blood flow regulation. Previous studies have shown that COX inhibition reduces cerebral blood flow velocity and cerebrovascular reactivity to CO 2 (CVR), however, the effects of COX inhibition on neurovascular regulation is unknown. Sympathetic nerve activity is an important modulator of blood pressure and blood flow. The purpose of this study was to determine the effect of COX inhibition on the muscle sympathetic nerve activity (MSNA) response to hypercapnia during CVR testing. Methods Fifteen healthy adults were evaluated (M/F = 7/8; age = 40 ± 21 years; BMI = 24 ± 2 kg/m 2 ) before (Pre) and 90 minutes after oral administration of the COX inhibitor indomethacin (Indo), given at 1.2mg/kg. Mean arterial pressure (MAP), heart rate (HR) and MSNA were measured continuously throughout the protocol. After baseline measurements were recorded, participants were evaluated breathing 6% CO 2 . Results are reported as mean ± SE. Results At baseline, HR was 54 ± 2 bpm, MAP was 100 ± 4 mmHg, MSNA burst frequency was 24 ± 2 bursts/min and MSNA burst incidence was 45 ± 4 bursts/100hb. The change in HR when exposed to hypercapnia was not different after Indo (Pre: 6 ± 2 bpm vs. Indo: 4 ± 1 bpm; p>0.05). The change in MAP (Pre: 0 ± 2 mmHg vs. Indo: 6 ± 1 mmHg; p<0.05), MSNA burst frequency (Pre: 1 ± 1 bursts/min vs. Indo: 4 ± 1 bursts/min; p<0.05), and MSNA burst incidence (Pre: −3 ± 2 bursts/100hb vs. Indo: 4 ± 2 bursts/100hb; p<0.05) was greater after Indo administration. Conclusion The sympathetic response to hypercapnia was greater following the administration of Indo. Taken together, these results suggest that hypercapnia‐induced sympathoexcitation may be altered following COX inhibition. Future studies could evaluate if the sympathetic responses to hypercapnia vary with age or sex. Support or Funding Information NIH HL118154