Effects of sex hormones on genioglossal muscle contractility and SR Ca2+-ATPase activity in aged rat.
This investigation was designed to examine whether short-term administration of sex hormones could produce changes in contractile properties and the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) function in genioglossal muscle (GG) of aged male rats. Twenty-four aged male rats were randomly divided into three groups to receive an intramuscular injection of either 0.1mg/kg oestrogen (group A), 2.5 mg/kg testosterone (group B), or 0.2 ml sterile peanut oil (group C, control), twice a week, during 4 weeks. After hormone treatment, in vivo isometric contractile properties were determined using surgically prepared GG muscles with platinum electrodes for stimulation of the medial branch of the hypoglossus nerve. Sarcoplasmic reticulum Ca(2+)-ATPase activity was measured in muscle homogenates by detecting the amount of inorganic phosphorus ion released in a standard coupled enzyme assay. SERCA1 mRNA level was observed using a real-time quantitative reverse transcription-polymerase chain reaction (Q-RT-PCR). It was found that, compared with group C, testosterone treatment decreased the fatigue resistance in GG muscles (p<.05), whereas no change was observed in the isometric twitch (P(t)) and tetanic tension (P(0)) (p>.05). By contrast, in oestrogen treated GG muscles, no significant modification was found either in the contractile or in endurance properties (p>.05). The change in GG fatigue resistance of group B was associated with a marked decrease in SR Ca(2+)-ATPase activity when compared with that of the control group (p<.01). Furthermore, SERCA1 mRNA level was also down regulated in group B (p<.05). No prominent differences in SR Ca(2+)-ATPase activity and SERCA1 mRNA expression existed between group A and group C (p>.05). The present results show that exogenous testosterone produces more pronounced changes in GG muscle fatigue resistance than oestrogen does by acting at SR Ca(2+)-ATPase activity and SERCA gene expression.
Liu
Yue-Hua
YH
Department of Orthodontics, School of Stomatology, Tongji University, Shanghai, China 200072. joshua66@126.com
Qi
Juan
J
Hou
Yu-Xia
YX
Wang
Fei
F
D000818:Animals; D004967:Estrogens / Q000494:pharmacology; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D018763:Muscle Fatigue / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000033:anatomy & histology / Q000187:drug effects* / Q000201:enzymology / Q000502:physiology; D009929:Organ Size / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000096:biosynthesis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology; D014059:Tongue / Q000187:drug effects* / Q000502:physiology
D004967:Estrogens; D012739:Gonadal Steroid Hormones; D012333:RNA, Messenger; D013739:Testosterone; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases