Nandrolone-pretreatment enhances cardiac β2-adrenoceptor expression and reverses heart contractile down-regulation in the post-stress period of acute-stressed rats

Penna, Cláudia; Abbadessa, Giuliana; Mancardi, Daniele; Spaccamiglio, Angela; Racca, Silvia; Pagliaro, Pasquale

doi:10.1016/j.jsbmb.2007.05.005

Cited by 16 publications

(20 citation statements)

References 35 publications

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“…More recently left ventricular hypertrophy and increased myocardial susceptibility to I/R injury have also been shown in isolated hearts prepared from rats treated chronically with ND [13]. However, we recently have shown that subchronic treatment with ND for 14 days does not induce an evident left ventricular hypertrophy and, paradoxically, improves PostC cardioprotection [36]. Since cardiac hypertrophy is accompanied with alteration of function and expression of several proliferative modulators, such as kinases and phosphatates [53], many of which are involved in cardioprotection [10,21,22,34], we wondered whether treatment with ND, which induces cardiac hypertrophy, would alter the expression/activity of these enzymes and then would suppress the protective response to a PostC protocol.…”

Section: Introductionmentioning

confidence: 84%

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Ischemia/reperfusion injury is increased and cardioprotection by a postconditioning protocol is lost as cardiac hypertrophy develops in nandrolone treated rats

et al. 2010

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We hypothesized that Nandrolone (ND)-abuse induces cardiac hypertrophy, increases myocardial susceptibility to ischemia/reperfusion (I/R) injury, and reduces responsiveness to postconditioning (PostC) cardioprotection. Wistar-rats were ND-treated for 2-weeks (short_ND) or 10-weeks (long_ND). Vehicle-treated rats served as controls. Hearts were retrogradely perfused and left ventricular pressure (LVP) was measured before and after 30-min global ischemia. In subgroups of hearts, to induce cardioprotection a PostC protocol (five cycles of 10-s reperfusion and 10-s ischemia) was performed. β-adrenoreceptors, kinases (Akt and GSk-3β) and phosphatases (PP2A sub A and PP2A sub B) were examined by Western blot before and after ischemia. After 120-min reperfusion infarct-size was measured. Short_ND slightly increased cardiac/body weight ratio, but did not affect cardiac baseline nor post-ischemic contractile function or infarct-size when compared to vehicle hearts. However, PostC limited cardiac dysfunction much more in short_ND hearts than other groups. Although cardiac/body weight ratio markedly increased after long_ND, baseline LVP was not affected. Yet, post-ischemic contracture and infarct-size were exacerbated and PostC was unable to reduce infarct-size and ventricular dysfunction. While short_ND increased phosphatases, non-phosphorylated and phosphorylated Akt, long_ND reduced phosphatase-expression and Akt-phosphorylation. Both short_ND and long_ND had no effect on the GSK-3β-phosphorylation but increased the expression of β 2 -adrenoreceptors. In reperfusion, PostC increased Akt-phosphorylation regardless of protective effects, but reduced phosphataseexpression in protected hearts only. In conclusion: short_ND improves post-ischemic myocardial performance in postconditioned hearts. However, long_ND increases myocardial susceptibility to I/R injury and abolishes cardioprotection by PostC. This increased susceptibility might be related to steroid-induced hypertrophy and/or to altered enzyme expression/phosphorylation.

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Section: Introductionmentioning

confidence: 84%

“…To confirm equal protein loading, membranes were incubated with an anti-α-actin antibody (Sigma). [36,37].…”

Section: Western Blotting Analysismentioning

confidence: 99%

Ischemia/reperfusion injury is increased and cardioprotection by a postconditioning protocol is lost as cardiac hypertrophy develops in nandrolone treated rats

et al. 2010

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“…In general, the effects of stress on heart β 1 -AR and β 2 -AR receptors differ (Santos and Spadari-Bratfisch 2006). Restraint stress (acute, 1 hour) did not changed β 1 -AR or β 2 -AR (Penna et al 2007) while acute immobilization for 120 minutes changed β 2 -AR (Myslivecek et al 2004. Cold stress induced decrease of β 1 -AR and β 2 -AR and increased the number of β 3 -AR (Benes et al 2012).…”

Section: Discussionmentioning

confidence: 89%

Heart ventricles specific stress-induced changes in β-adrenoceptors and muscarinic receptors

Tillinger

Nováková²,

Križanová³

et al. 2014

gpb

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Abstract. The left and right ventricles fulfill different role in heart function. Here we compare chamber specific changes in local catecholamine concentrations; gene expression and the receptor protein amount of all three β-adrenoceptors (β-AR) in rat right heart ventricles exposed to acute (1 session) and repeated (7 sessions) immobilization stress (IMMO) vs. previously observed changes in left ventricles. Density of muscarinic receptors as main cardio-inhibitive receptors was also measured. In the right ventricles, noradrenaline and adrenaline were increased. No β 1 -AR changes were observed, in spite of the increased sympathetic activity. On the other hand, we have found a decrease of β 2 -AR gene expression (reduction to 30%) after 7 IMMO and protein (to 59%) after 1 IMMO. β 3 -AR gene expression was increased after 7 IMMO. Muscarinic receptor density was not changed. When comparing correlation in left and right ventricles, there was strong correlation between adrenaline and β 2 -AR gene expression, protein and β 3 -AR gene expression in the left ventricles while only correlation between adrenaline and β 2 -AR mRNA and protein in the right ventricles was found. Our results show that maintenance of cardiac homeostasis under stress conditions are to a great extent achieved by a balance between different receptors and also by a balanced receptor changes in left vs. right ventricles. Taken together, decrease of cardio-stimulating β 2 -AR represents a new important mechanism by which β 2 -AR contributes to the heart physiology.

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“…This long acting effects of Sustanon justifies why it is more attractive to be abused by athletes [2,12] . Regardless of these unique pharmacological structure and properties of Sustanon, only few studied attempted to investigate the adverse effects induced by Sustanon abuse, whereas other anabolic androgenic drugs such as Deca-Durabolin have been excessively studied by a number of investigators [14,15] . However, regarding the existence of this negative phenomenon in our Arab countries, the recent field study of Tahtamouni [5] in Jordan is believed to be one of the best studies which provided a strong evidences about the existence and the spread of this phenomenon in our Arab countries.…”

Section: Introductionmentioning

confidence: 99%

“…Overall, in regard the adverse effects caused by abusing these anabolic androgenic drugs, number of previous studies reported some of these effects including: cardiovascular disorders (particularly enlargement of the left ventricle) which can lead to sudden cardiac death, acute hepatitis and Jaundice, testicular dysfunction, infertility, hypertension, behavioral disorders in the form of sexual overstimulation and abnormal increase in the aggressive behavior [3.9,16-20] . However, by reviewing the literature of Sustanon abuse in particular, it was noticed that only very few studies have investigated the hormonal and nephritic adverse effects induced by such abuse among athletes [15,21] . The study of Modlinski and Fields [22] provided an explanation of the absence of sufficient information about some of the adverse effects such as the nephritic effects, as it indicated that because anabolic drugs abuse is elicited and occurred secretly among the athletes, most of our knowledge about the adverse effects of these drugs is obtained mainly from cases reports which reached the hospitals in some countries, therefore, our knowledge about some of these adverse effects such as the hormonal and nephritic effects are still very limited.…”

Section: Introductionmentioning

confidence: 99%

he Physiological Effects on Hormones levels and Kidneys Functions Induced by The Anabolic Androgenic Drug (Sustanon) in Male Guinea Pigs

Bisher¹

2009

American J. of Applied Sciences

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Problem statement:In recent years, the intentional abuse of anabolic androgenic drugs by athletes has increased rapidly in many countries to become a serious negative phenomenon. Athletes, specially in power sports, abuse these drugs such as Sustanon in high doses to obtain a rapid and huge increasing in the muscles mass and to improve their performance during the sport competitions. This abuse causes severe adverse effects among the abusers. Approach: The present physiological study was performed to answer the following question: could Sustanon abuse induce marked abnormal alterations in some hormones levels and in the kidneys functions?. The current study was needed due to the lack of sufficient information about the hormonal and nephritic adverse effects caused by Sustanon abuse in particular. This study on male Guinea pigs aimed to investigate the potential abnormal alterations in the levels of some hormones and in the kidney functions induced by repeated administration of two Sustanon doses. The treated animals were injected intramuscularly (i.m.) once a week with Sustanon doses as follow (15 mg to control group according to (t-test). The results have been described and discussed in full details within the text. Conclusion/Recommendations: The current hormonal results proved the occurrence of severe abnormal alterations in the serum levels of the thyroid gland hormones, Cortisol and Insulin under the influence of Sustanon treatment. This indicated that abusing Sustanon for long periods by athletes can cause serious pathological hormonal disorders in the abusers. In addition, the present nephritic results can be considered as strong proof that abusing Sustanon for long periods by athletes can induce severe defects and disorders in the kidney functions. This may lead to cause serious pathological damages in the kidneys structure in the late stages. Due to these serious adverse effects, it is recommended that much more official and medical restrictions should be applied to prevent abusers from obtaining these drugs in order to decrease the continuation of this negative health problem. In addition, the study recommends also that athletes and youths should be provided with much more medical information and enlightenment about the health risks and the complications of abusing these drugs through media.

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Nandrolone-pretreatment enhances cardiac β2-adrenoceptor expression and reverses heart contractile down-regulation in the post-stress period of acute-stressed rats

Cited by 16 publications

References 35 publications

Ischemia/reperfusion injury is increased and cardioprotection by a postconditioning protocol is lost as cardiac hypertrophy develops in nandrolone treated rats

Ischemia/reperfusion injury is increased and cardioprotection by a postconditioning protocol is lost as cardiac hypertrophy develops in nandrolone treated rats

Heart ventricles specific stress-induced changes in β-adrenoceptors and muscarinic receptors

he Physiological Effects on Hormones levels and Kidneys Functions Induced by The Anabolic Androgenic Drug (Sustanon) in Male Guinea Pigs

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