A Karimi, S Joukar, H Najafipour, Y Masoumi-Ardakani, B Shahouzehi
Vast adverse effects of anabolic-androgenic steroids (AASs) on athletes' cardiovascular systems have been reported. However, there is still a lack of adequate information regarding the pathways and mechanisms involved. We tested the hypothesis that adiponectin and its receptors in the heart may be affected by long-term use of AASs alongside exercising. Male Wistar rats were randomized into the control (CTL), exercise (EX), nandrolone (Nan), arachis (Arach) group which treated with arachis as vehicle, trained vehicle (EX+Arach) and trained nandrolone (EX+Nan) groups that were treated for 8 weeks. One day after the end of the protocol, animals were sacrificed and their hearts were frozen. TNF-α and adiponectin proteins of hearts were evaluated quantitatively by ELISA kits, and Western blot analysis was used for measuring adiponectin receptor protein expression. TNF-α protein increased significantly in the EX+Nan group (P<.05 vs CTL group). The AdipoR1 protein was significantly higher in the presence of nandrolone alongside exercise (P<.05 vs Nan and EX+Arach groups, P<.01 vs CTL and Arach groups). In addition, AdipoR2 protein enhanced in the EX+Nan group when compared with the other groups (P<.05 vs EX and EX+Arach groups, P<.01 vs CTL, Arach and Nan groups). Chronic nandrolone plus mild endurance exercise may be associated with imbalance in pro-/anti-inflammatory cytokines and may induce a positive modulatory effect on cardiac adiporeceptors in rat. Further studies are required before these findings can be generalized to humans.
{"title":"Low-intensity endurance exercise plus nandrolone decanoate modulates cardiac adiponectin and its receptors.","authors":"A Karimi, S Joukar, H Najafipour, Y Masoumi-Ardakani, B Shahouzehi","doi":"10.1111/aap.12056","DOIUrl":"https://doi.org/10.1111/aap.12056","url":null,"abstract":"<p><p>Vast adverse effects of anabolic-androgenic steroids (AASs) on athletes' cardiovascular systems have been reported. However, there is still a lack of adequate information regarding the pathways and mechanisms involved. We tested the hypothesis that adiponectin and its receptors in the heart may be affected by long-term use of AASs alongside exercising. Male Wistar rats were randomized into the control (CTL), exercise (EX), nandrolone (Nan), arachis (Arach) group which treated with arachis as vehicle, trained vehicle (EX+Arach) and trained nandrolone (EX+Nan) groups that were treated for 8 weeks. One day after the end of the protocol, animals were sacrificed and their hearts were frozen. TNF-α and adiponectin proteins of hearts were evaluated quantitatively by ELISA kits, and Western blot analysis was used for measuring adiponectin receptor protein expression. TNF-α protein increased significantly in the EX+Nan group (P<.05 vs CTL group). The AdipoR1 protein was significantly higher in the presence of nandrolone alongside exercise (P<.05 vs Nan and EX+Arach groups, P<.01 vs CTL and Arach groups). In addition, AdipoR2 protein enhanced in the EX+Nan group when compared with the other groups (P<.05 vs EX and EX+Arach groups, P<.01 vs CTL, Arach and Nan groups). Chronic nandrolone plus mild endurance exercise may be associated with imbalance in pro-/anti-inflammatory cytokines and may induce a positive modulatory effect on cardiac adiporeceptors in rat. Further studies are required before these findings can be generalized to humans.</p>","PeriodicalId":8872,"journal":{"name":"Autonomic & autacoid pharmacology","volume":"37 2","pages":"29-33"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35027388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neuropeptide Y (NPY) causes various central and peripheral actions through activation of G-protein-coupled NPY receptors. Although a species-dependent difference in cardiac actions of NPY has been reported, the responses to NPY have not been examined in mice, widely used experimental animals. This study aimed to clarify the responses to NPY and the receptor subtype involved in the responses in mouse atrium. Neuropeptide Y caused negative inotropic and negative chronotropic actions in spontaneous beating right atria. Negative inotropic actions were more marked than negative chronotropic actions. Therefore, negative inotropic actions were studied in detail for evaluation of the NPY-induced cardiac actions in mouse atrium. Neuropeptide Y-induced negative inotropic actions were not affected by atropine but were abolished in the atria from pertussis toxin-treated mice. In isolated atrial preparations from reserpine-treated mice, NPY-induced negative inotropic actions were significantly attenuated. [Leu31, Pro34]-NPY, but not peptide YY, was effective in decreasing spontaneous contraction in atrial preparations. Although Y1 , Y2 , Y4 and Y5 receptor mRNAs were expressed almost equally in the brain, NPY1 receptor mRNA was dominantly expressed in the atrium. In conclusion, NPY caused negative inotropic and chronotropic actions through activation of the Y1 receptor in the mouse atrium. A high expression level of Y1 mRNA in the atrium suggests a functional role of NPY in the regulation of mouse cardiac contraction.
{"title":"Neuropeptide Y (NPY) inhibits spontaneous contraction of the mouse atrium by possible activation of the NPY1 receptor.","authors":"Y Oki, H Teraoka, T Kitazawa","doi":"10.1111/aap.12055","DOIUrl":"https://doi.org/10.1111/aap.12055","url":null,"abstract":"<p><p>Neuropeptide Y (NPY) causes various central and peripheral actions through activation of G-protein-coupled NPY receptors. Although a species-dependent difference in cardiac actions of NPY has been reported, the responses to NPY have not been examined in mice, widely used experimental animals. This study aimed to clarify the responses to NPY and the receptor subtype involved in the responses in mouse atrium. Neuropeptide Y caused negative inotropic and negative chronotropic actions in spontaneous beating right atria. Negative inotropic actions were more marked than negative chronotropic actions. Therefore, negative inotropic actions were studied in detail for evaluation of the NPY-induced cardiac actions in mouse atrium. Neuropeptide Y-induced negative inotropic actions were not affected by atropine but were abolished in the atria from pertussis toxin-treated mice. In isolated atrial preparations from reserpine-treated mice, NPY-induced negative inotropic actions were significantly attenuated. [Leu31, Pro34]-NPY, but not peptide YY, was effective in decreasing spontaneous contraction in atrial preparations. Although Y<sub>1</sub> , Y<sub>2</sub> , Y<sub>4</sub> and Y<sub>5</sub> receptor mRNAs were expressed almost equally in the brain, NPY<sub>1</sub> receptor mRNA was dominantly expressed in the atrium. In conclusion, NPY caused negative inotropic and chronotropic actions through activation of the Y<sub>1</sub> receptor in the mouse atrium. A high expression level of Y<sub>1</sub> mRNA in the atrium suggests a functional role of NPY in the regulation of mouse cardiac contraction.</p>","PeriodicalId":8872,"journal":{"name":"Autonomic & autacoid pharmacology","volume":"37 2","pages":"23-28"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35027465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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