title: Role played by interleukin-6 in evoking the exercise pressor reflex in decerebrate rats: effect of femoral artery ligation.
abstract: IL-6 signaling via the soluble IL-6 receptor (sIL-6r) has been shown to increase primary afferent responsiveness to noxious stimuli. This finding prompted us to test the hypothesis that IL-6 and sIL-6r would increase the exercise pressor reflex in decerebrate rats with freely perfused femoral arteries. We also tested the hypothesis that soluble glycoprotein (sgp)130, an inhibitor of IL-6/sIL-6r signaling, would decrease the exaggerated exercise pressor reflex that is found in decerebrate rats with ligated femoral arteries. In rats with freely perfused femoral arteries, coinjection of 50 ng of IL-6 and sIL-6r into the arterial supply of the hindlimb significantly increased the peak pressor response to static (control: 14 ± 3 mmHg and IL-6/sIL-6r: 17 ± 2 mmHg, P = 0.03) and intermittent isometric (control: 10 ± 2 mmHg and IL-6/sIL-6r: 15 ± 4 mmHg, P = 0.03) hindlimb muscle contraction. In rats with ligated femoral arteries, injection of 50 ng of sgp130 into the arterial supply of the hindlimb reduced the peak pressor response to static (control: 24 ± 2 mmHg and sgp130: 16 ± 3 mmHg, P = 0.01) and intermittent isometric (control: 16 ± 2 mmHg and sgp130: 13 ± 2 mmHg, P = 0.04) hindlimb muscle contraction, whereas there was no effect of sgp130 on the exercise pressor reflex in rats with freely perfused femoral arteries. We conclude that coinjection of exogenous IL-6 and sIL-6r increased the exercise pressor reflex in rats with freely perfused femoral arteries. More importantly, we also conclude that IL-6 and sIL-6r play an endogenous role in evoking the exercise pressor reflex in rats with ligated femoral arteries but not in rats with freely perfused femoral arteries.
authors.affiliation: Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania scopp@hmc.psu.edu.
authors.forename: Steven W
authors.initials: SW
authors.lastname: Copp
authors.affiliation: Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania.
authors.forename: Audrey J
authors.initials: AJ
authors.lastname: Stone
authors.affiliation: Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania.
authors.forename: Jianhua
authors.initials: J
authors.lastname: Li
authors.affiliation: Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania.
authors.forename: Marc P
authors.initials: MP
authors.lastname: Kaufman
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D050822:Cytokine Receptor gp130 / Q000494:pharmacology; D003655:Decerebrate State / Q000503:physiopathology*; D005263:Femoral Artery / Q000601:surgery; D006614:Hindlimb / Q000098:blood supply / Q000187:drug effects*; D015850:Interleukin-6 / Q000378:metabolism / Q000494:pharmacology*; D008026:Ligation; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D005082:Physical Exertion / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D019947:Receptors, Interleukin-6 / Q000378:metabolism; D012018:Reflex / Q000187:drug effects* / Q000502:physiology; D012021:Reflex, Abnormal / Q000187:drug effects*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D015850:Interleukin-6; D019947:Receptors, Interleukin-6; D050822:Cytokine Receptor gp130
keywords: cytokines; skeletal muscle afferents; sympathetic nervous system