{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T19:03:42Z","timestamp":1777921422703,"version":"3.51.4"},"reference-count":48,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,5,24]],"date-time":"2012-05-24T00:00:00Z","timestamp":1337817600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:p>Cyclo\u2010oxygenase (COX) enzymes are responsible for the formation from arachidonic acid of prostaglandins, among other metabolites. Prior studies have suggested that inhibition of the COX pathway attenuates the responses of sympathetic nerve activity and blood pressure during static muscle contraction. Static muscle contraction activates the exercise pressor reflex, which in turn increases sympathetic nerve activity and blood pressure. Also, COX products contribute to exaggeration of the exercise pressor reflex in heart failure (HF). This dysfunction of the exercise pressor reflex has previously been shown to be mediated primarily by muscle mechanoreflex overactivity. It is well known that COX\u20101 and COX\u20102 are two isoforms of the enzyme that lead to formation of these important biological mediators involved in the muscle reflex. Thus, in the present study, we determined whether the COX\u20101 and\/or COX\u20102 pathway contribute(s) to the augmented mechanoreflex activity in HF. First, Western blot analysis was employed to examine protein expression of COX\u20101 and COX\u20102 in skeletal muscle tissue of control rats and rats with HF induced by myocardial infarction. Our data show that there is no significant difference in COX\u20101 expression in both experimental groups. However, COX\u20102 displays significant overexpression in rats with HF compared with control rats (optical density 1.06 \u00b1 0.05 in control and 1.6 \u00b1 0.05 in HF, <jats:italic>P<\/jats:italic> &lt; 0.05 <jats:italic>versus<\/jats:italic> control). Second, the mechanoreflex was evoked by passive tendon stretch, and the reflex sympathetic and pressor responses to muscle stretch were examined after COX\u20101 and COX\u20102 inhibitors (FR\u2010122047 and SC\u2010236) were individually injected into the arterial blood supply of the hindlimb muscles. The results demonstrate that the stretch\u2010evoked reflex responses in rats with HF were significantly attenuated by administration of SC\u2010236, but not by FR\u2010122047, i.e. renal sympathetic nerve activity and mean arterial pressure responses evoked by 0.5 kg of muscle tension were 52.3 \u00b1 8.9% and 19 \u00b1 1.4 mmHg, respectively, in control conditions and 26.4 \u00b1 5.6% and 5.7 \u00b1 1.6 mmHg (<jats:italic>P<\/jats:italic> &lt; 0.05 <jats:italic>versus<\/jats:italic> control group) after 0.25 mg kg<jats:sup>\u22121<\/jats:sup> of SC\u2010236. Muscle stretch\u2010evoked renal sympathetic nerve activity and mean arterial pressure responses were 51.8 \u00b1 8.2% and 18.7 \u00b1 1.2 mmHg, respectively, in control conditions and 48.3 \u00b1 5.3% and 17.5 \u00b1 1.9 mmHg (<jats:italic>P<\/jats:italic> &gt; 0.05 <jats:italic>versus<\/jats:italic> control group) after 1.0 mg kg<jats:sup>\u22121<\/jats:sup> of FR\u2010122047. Accordingly, the results obtained from this study support our hypothesis that heightened COX\u20102 expression within the hindlimb muscles contributes to the exaggerated muscle mechanoreflex in congestive HF.<\/jats:p>","DOI":"10.1113\/expphysiol.2012.065425","type":"journal-article","created":{"date-parts":[[2012,4,21]],"date-time":"2012-04-21T06:24:23Z","timestamp":1334989463000},"page":"943-954","source":"Crossref","is-referenced-by-count":22,"title":["Muscle cyclo\u2010oxygenase\u20102 pathway contributes to the exaggerated muscle mechanoreflex in rats with congestive heart 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