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Cardiac concentric remodelling induced by non-aromatizable (dihydro-)testosterone is antagonized by oestradiol in ovariectomized rats

Artikel i vetenskaplig tidskrift
Författare Åsa Tivesten
Entela Bollano
Henrik Nyström
Camilla Alexanderson
Göran Bergström
Agneta Holmäng
Publicerad i J Endocrinol
Volym 189
Nummer/häfte 3
Sidor 485-91
Publiceringsår 2006
Publicerad vid Wallenberglaboratoriet
Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Sidor 485-91
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Androgens/*pharmacology, Animals, Dihydrotestosterone/*pharmacology, Echocardiography, Estradiol/*pharmacology, Female, Heart/*drug effects, Heart Ventricles/drug effects/physiology/ultrasonography, Insulin-Like Growth Factor I/genetics, Ovariectomy, RNA, Messenger/analysis, Rats, Rats, Sprague-Dawley, Receptors, Androgen/genetics/metabolism, Reverse Transcriptase Polymerase Chain Reaction
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Previous studies on the cardiovascular effects of androgens in females, most of them using testosterone treatment, have yielded conflicting results. Testosterone is metabolized into oestradiol (E2) and dihydrotestosterone (DHT) within cardiovascular tissues. The aim of the present study was to explore the cardiovascular effects exerted by E2 and the non-aromatizable androgen DHT and to study possible interactions between these in female rats. Ovariectomized rats were treated with DHT, E2, or DHT+E2 for 6 weeks. DHT increased left-ventricular posterior wall thickness, assessed by echocardiography, whereas left-ventricular dimension, as well as total heart weight and calculated left-ventricular mass, were unchanged. DHT also increased the levels of insulin-like growth factor-I mRNA in the left ventricle. E2 abolished the effect of DHT on left-ventricular remodelling and insulin-like growth factor-I mRNA when the two treatments were given in combination. E2 also reduced androgen receptor mRNA levels in the heart. Neither E2 nor DHT changed blood pressure measured by telemetry. In conclusion, treatment with the endogenous non-aromatizable androgen DHT causes cardiac concentric remodelling in ovariectomized rats, possibly mediated by increased local levels of insulin-like growth factor-I. The effect of DHT on cardiac wall thickness was antagonized by E2, possibly through downregulation of cardiac androgen receptors. These mechanisms may be of importance for the concentric left-ventricular geometric pattern developing in women after menopause.

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