Skeletal Muscle Stretch‐Induced PGE 2 Formation does not Impact the Muscle Mechanoreflex in Decerebrate Rats

Mechanical and metabolic signals associated with skeletal muscle contraction stimulate thin fiber muscle afferents and produce reflex increases in blood pressure (i.e., the exercise pressor reflex). There is an interplay between those signals as metabolites may sensitize afferent responsiveness to mechanical signals. A common strategy used to study the mechanical component of the exercise pressor reflex (i.e., the mechanoreflex) in isolation from the metabolic component is to measure the reflex increase in blood pressure during passive hindlimb muscle stretch in an experimental animal preparation. Passive muscle stretch has been presumed to impart a purely mechanical stimulus. However, intermittent but not static mechanical stimulation of cultured skeletal muscle cells was found to increase PGE 2 production and PGE 2 has been shown to sensitize the muscle mechanoreflex. Based on those findings, the purpose of this investigation was to test the hypothesis that in decerebrate, unanesthetized rats, dynamic but not static hindlimb skeletal muscle stretch would increase interstitial PGE 2 concentration. Moreover, we tested the hypothesis that COX inhibition with indomethacin would attenuate the stretch‐induced increase in PGE 2 concentration and the increase in blood pressure during mechanoreflex activation. Experiments were performed on 28 young adult male Sprague‐Dawley rats. The microdialysis technique was used to collect triceps surae muscle interstitial fluid at rest and during 4 minutes of 1 Hz dynamic muscle stretch and 4 minutes of static muscle stretch (performed in random order and separated by 10 minutes). Muscle stretch was performed by manually turning the rack and pinion. We found that triceps surae muscle interstitial PGE 2 concentration was significantly increased during both static (↑38%, p=0.01) and dynamic (↑56%, p<0.01) stretch above their respective baseline concentrations (n=9). Indomethacin (1μg/kg) significantly reduced baseline PGE 2 concentration and prevented the increase in PGE 2 during static (n=4) and dynamic (n=5) stretch. Importantly, indomethacin had no effect on the peak pressor response during static (control: 15±4, indomethacin: 16±4 mmHg; p=0.82) and dynamic (control: 17±2, indomethacin: 18±4 mmHg; p=0.68) stretch (n=7). Collectively, these data indicate that static and dynamic hindlimb muscle stretch in decerebrate, unanaesthetized rats increased muscle interstitial PGE 2 concentration. The magnitude of increase in PGE 2 , however, was not sufficient to impact the muscle mechanoreflex. Support or Funding Information 1R01HL142877 to SWC This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .