Acute cyclooxygenase inhibition does not alter muscle sympathetic nerve activity or forearm vasodilator responsiveness in lean and obese adults

Abstract

Obesity is often characterized by chronic inflammation that may contribute to increased cardiovascular risk via sympathoexcitation and decreased vasodilator responsiveness. We hypothesized that obese individuals would have greater indices of inflammation compared with lean controls, and that cyclooxygenase inhibition using ibuprofen would reduce muscle sympathetic nerve activity (MSNA) and increase forearm blood flow in these subjects. We measured MSNA, inflammatory biomarkers (C-reactive protein [CRP] and Interleukin-6 [IL-6]), and forearm vasodilator responses to brachial artery acetylcholine and sodium nitroprusside in 13 men and women (7 lean; 6 obese) on two separate study days: control (CON) and after 800 mg ibuprofen (IBU). CRP (1.7 ± 0.4 vs. 0.6 ± 0.3 mg/L; P < 0.05) and IL-6 (4.1 ± 1.5 vs. 1.0 ± 0.1pg/mL; P < 0.05) were higher in the obese group during CON and tended to decrease with IBU (IL-6: P < 0.05; CRP: P = 0.14). MSNA was not different between groups during CON (26 ± 4 bursts/100 heart beats (lean) versus 26 ± 4 bursts/100 heart beats (obese); P = 0.50) or IBU (25 ± 4 bursts/100 heart beats (lean) versus 30 ± 5 bursts/100 heart beats (obese); P = 0.25), and was not altered by IBU. Forearm vasodilator responses were unaffected by IBU in both groups. In summary, an acute dose of ibuprofen did not alter sympathetic nerve activity or forearm blood flow responses in healthy obese individuals, suggesting that the cyclooxygenase pathway is not a major contributor to these variables in this group.

Keywords: Autonomic nervous system; blood pressure; forearm blood flow; inflammation.

Figure 1.

C‐reactive protein (A) and interleukin‐6 (B) in lean and obese adults during control (CON) (black bars) and ibuprofen (IBU) (grey bars). Data are mean ± SE, *P < 0.05 compared to lean adults, ^†P < 0.05 compared to CON.

Figure 2.

Muscle sympathetic nerve activity (MSNA) burst frequency (A) and MSNA burst incidence (B) in lean and obese adults during control (CON) (black bars) and ibuprofen (IBU) (grey bars). Data are mean ± SE.

Figure 3.

The association between muscle sympathetic nerve activity (MSNA) burst incidence and circulating concentrations of interleukin‐6 (IL‐6) during control (CON). The positive association between MSNA and IL‐6 was significant only during the CON trial.

Figure 4.

Endothelium‐dependent vasodilation was measured using forearm vascular conductance (FVC) at baseline, and in response to three doses of acetylcholine. There were no differences between lean (solid lines) and obese (dotted lines) during control (CON) (black) or ibuprofen (IBU) (grey). There were also no differences in FVC during nitroprusside infusion (data not shown).