Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas, United States.
Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California Davis, Davis, California, United States.
J Appl Physiol (1985). 2024 May 1;136(5):1226-1237. doi: 10.1152/japplphysiol.00879.2023. Epub 2024 Mar 28.
Cyclooxygenase (COX) products of arachidonic acid metabolism, specifically prostaglandins, play a role in evoking and transmitting the exercise pressor reflex in health and disease. Individuals with type 2 diabetes mellitus (T2DM) have an exaggerated exercise pressor reflex; however, the mechanisms for this exaggerated reflex are not fully understood. We aimed to determine the role played by COX products in the exaggerated exercise pressor reflex in T2DM rats. The exercise pressor reflex was evoked by static muscle contraction in unanesthetized, decerebrate, male, adult University of California Davis (UCD)-T2DM ( = 8) and healthy Sprague-Dawley ( = 8) rats. Changes (Δ) in peak mean arterial pressure (MAP) and heart rate (HR) during muscle contraction were compared before and after intra-arterial injection of indomethacin (1 mg/kg) into the contracting hindlimb. Data are presented as means ± SD. Inhibition of COX activity attenuated the exaggerated peak MAP (Before: Δ32 ± 13 mmHg and After: Δ18 ± 8 mmHg; = 0.004) and blood pressor index (BPi) (Before: Δ683 ± 324 mmHg·s and After: Δ361 ± 222 mmHg·s; = 0.006), but not HR (Before: Δ23 ± 8 beats/min and After Δ19 ± 10 beats/min; = 0.452) responses to muscle contraction in T2DM rats. In healthy rats, COX activity inhibition did not affect MAP, HR, or BPi responses to muscle contraction. Inhibition of COX activity significantly reduced local production of prostaglandin E in T2DM and healthy rats. We conclude that peripheral inhibition of COX activity attenuates the pressor response to muscle contraction in T2DM rats, suggesting that COX products partially contribute to the exaggerated exercise pressor reflex in those with T2DM. We compared the pressor and cardioaccelerator responses to static muscle contraction before and after inhibition of cyclooxygenase (COX) activity within the contracting hindlimb in decerebrate, unanesthetized type 2 diabetic mellitus (T2DM) and healthy rats. The pressor responses to muscle contraction were attenuated after peripheral inhibition of COX activity in T2DM but not in healthy rats. We concluded that COX products partially contribute to the exaggerated pressor reflex in those with T2DM.
环氧化酶（COX）代谢花生四烯酸的产物，特别是前列腺素，在健康和疾病中都在诱发和传递运动加压反射中发挥作用。2 型糖尿病（T2DM）患者的运动加压反射增强；然而，这种反射增强的机制尚不完全清楚。我们旨在确定 COX 产物在 T2DM 大鼠增强的运动加压反射中的作用。在未麻醉、去大脑的成年雄性加利福尼亚大学戴维斯分校（UCD）-T2DM（n=8）和健康的斯普林代尔-道利（n=8）大鼠中，通过对收缩的后肢进行静力性肌肉收缩来引发运动加压反射。比较肌肉收缩前后收缩后肢内注入消炎痛（1mg/kg）前后的峰值平均动脉压（MAP）和心率（HR）的变化（Δ）。数据表示为均值±SD。COX 活性抑制减弱了增强的峰值 MAP（之前：Δ32±13mmHg，之后：Δ18±8mmHg；n=0.004）和血压指数（BPi）（之前：Δ683±324mmHg·s，之后：Δ361±222mmHg·s；n=0.006），但对 T2DM 大鼠肌肉收缩的 HR（之前：Δ23±8 次/分钟，之后：Δ19±10 次/分钟；n=0.452）反应没有影响。在健康大鼠中，COX 活性抑制不影响 MAP、HR 或肌肉收缩时的 BPi 反应。抑制 COX 活性显著降低 T2DM 和健康大鼠局部前列腺素 E 的产生。我们得出结论，外周抑制 COX 活性可减弱 T2DM 大鼠肌肉收缩的加压反应，表明 COX 产物部分参与了 T2DM 患者运动加压反射的增强。我们在去大脑、未麻醉的 2 型糖尿病（T2DM）和健康大鼠中，在收缩的后肢内抑制环氧化酶（COX）活性前后，比较了静力性肌肉收缩的加压和心加速反应。T2DM 患者的肌肉收缩加压反应在周围 COX 活性抑制后减弱，但在健康大鼠中没有减弱。我们得出结论，COX 产物部分参与了 T2DM 患者加压反射的增强。
