Changes in aortic endothelium ultrastructure in male rats following castration, replacement with testosterone and administration of 5α-reductase inhibitor

Lu, Yingli; Kuang, Lin; Zhu, Hui; Wu, Hui; Wang, Xuefang; Pang, Yu-Ping; Wang, Ningjian; Yu, Danlu

doi:10.1111/j.1745-7262.2007.00327.x

Cited by 39 publications

(31 citation statements)

References 10 publications

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“…Additionally, testosterone may promote a nongenomic effect potentially induced directly in the absence of a receptor, through a nontranscriptional effect, or by a distinct nonclassical receptor that is possibly associated with the plasma membrane [46]. It was reported that testosterone deprivation in rats, submitted to castration or to 5 α -reductase inhibitor treatment (inhibits the conversion of testosterone to dihydrotestosterone), produced injuries in aortic ECs detected by electron microscopy [47]. ECs ultrastructure in orchidectomized animals seemed severely crimpled, coarse, and protuberant; with ruined cell-cell connections, and adhesion of red blood cells to the surface.…”

Section: Testosterone Endothelial Health and Erectionmentioning

confidence: 99%

Testosterone, Endothelial Health, and Erectile Function

2011

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Experimental and clinical studies have reported that testosterone has a critical role in the maintenance of homeostatic and morphologic corpus cavernosum components, essential for normal erectile physiology. Although the exact mechanisms mediated by testosterone in erectile function are still under investigation, recent research has suggested an important role in the regulation of endothelial cell (EC) biological functions. Besides stimulating the production of EC mediators, testosterone is also thought to promote the vasculogenic reendothelialization process, mediated by bone marrow-derived endothelial progenitor cells. Additionally, testosterone seems to modulate other erectile tissue components, including trabecular smooth muscle cells, nerve fibers, and tunica albuginea structure, all essential for the erectile process. This paper summarizes current data regarding testosterone-induced cellular and molecular mechanisms that regulate penile tissue components, focusing particularly on the role of testosterone in endothelial health and erectile function.

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Section: Testosterone Endothelial Health and Erectionmentioning

confidence: 99%

Testosterone, Endothelial Health, and Erectile Function

2011

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“…It was also demonstrated that androgen deficiency contributes to endothelial damage in a castrated rat model (Lu et al 2007). Furthermore, investigations showed that testosterone and dihydrotestosterone upregulate nitric oxide synthase (NOS) expression and activity in male genital tissues, particularly in cavernous tissue (Lugg et al 1995;Marin et al 1999;Penson et al 1996;Zvara et al 1995).…”

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confidence: 99%

Androgen depletion in humans leads to cavernous tissue reorganization and upregulation of Sirt1–eNOS axis

Tomada

Almeida

et al. 2011

AGE

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Aging and physiological androgen decay leads to structural changes in corpus cavernosum (CC) that associate with erectile function impairment. There is evidence that such changes relate to nitric oxide (NO) bioavailability, an endothelial compound produced by the action of endothelial NO synthase (eNOS), and is regulated by sirtuin-1 (Sirt1), a NAD + -dependent protein deacetylase. Taking into account the reduced NO synthesis observed in aging and erectile dysfunction, we aimed to characterize human CC of androgen-deprived, young, and aged individuals postulating that androgen deprivation induces modifications similar to those observed in aging. Human penile fragments were collected from young individuals submitted to male-to-female sex reassignment procedure, who undergone an androgen deprivation chemical regimen, from young organ donors and from aged patients submitted to penile deviation surgery. They were processed for histomorphometric analysis of smooth muscle (SM) and connective tissues (CT), and dual-immunofluorescence of alpha-actin/vWf or Sirt1, and endothelin-1/eNOS. Estrogen receptors were analyzed by immunohistochemistry and semiquantification of Sirt1, eNOS, and phospho-Akt was assayed by Western blotting. Androgen withdrawal, similarly to aging, leads to a noteworthy reduction of SM-to-CT ratio in CC. However, in contrast to young and aged, a significant increase in penile Sirt1 expression accompanied by an increase in total eNOS expression was observed in androgen-depleted individuals. No changes were evidenced in phospho-Akt system and estrogen receptors were undetectable. These findings indicate that Sirt1 regulates the expression of eNOS in human CC employing mechanisms influenced by androgen depletion.

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“…The median serum concentration of total testosterone was 17.0 nmol l 21 , SHBG was 40.7 nmol l 21 , BT was 7.29 nmol l 21 and FT was 0.29 nmol l 21 . The geometric mean CCS was 36.665.0, which was calculated using the following equation: exp [mean (log CCS)].…”

Section: Resultsmentioning

confidence: 99%

“…17,18 Additionally, testosterone could stimulate endothelial progenitor cells, which plays a key role in endothelial repair. 19,20 Lu et al 21 have proposed that decreased testosterone is associated with ultrastructural damage of the aortic endothelium. In this regard, hypogonadism has been reported to contribute to the development of metabolic syndrome.…”

Section: Discussionmentioning

confidence: 99%

Inverse relationship between bioavailable testosterone and subclinical coronary artery calcification in non-obese Korean men

Park¹,

Shim²,

Lee³

et al. 2012

Asian J Androl

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Although low testosterone levels in men have been associated with high risk for cardiovascular disease, little is known about the association between male sex hormones and subclinical coronary disease in men with apparently low cardiometabolic risk. This study was performed to investigate the association between male sex hormones and subclinical coronary artery calcification measured as coronary calcium score in non-obese Korean men. We examined the relationship of total testosterone, sex hormone-binding globulin, bioavailable testosterone and free testosterone with coronary calcium score in 291 non-obese Korean men (mean age: 52.869.3 years) not having a history of cardiovascular disease. Using multiple linear regression, we evaluated associations between log (sex hormone) levels and log (coronary calcium score) after adjusting for confounding variables in 105 men with some degree of coronary calcification defined as coronary calcium scoreo1. In multiple linear regression analysis, bioavailable testosterone was inversely associated with coronary calcium score (P50.046) after adjusting for age, body mass index, smoking status, alcohol consumption, regular exercise, mean blood pressure, resting heart rate, C-reactive protein, fasting plasma glucose, total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, hypertension medication and hyperlipidemia medication, whereas total testosterone, sex hormone-binding globulin and free testosterone were not (P50.674, P50.121 and P50.102, respectively). Our findings indicate that bioavailable testosterone is inversely associated with the degree of subclinical coronary artery calcification in non-obese men.

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Changes in aortic endothelium ultrastructure in male rats following castration, replacement with testosterone and administration of 5α-reductase inhibitor

Abstract: These results suggest that low concentrations of T and DHT are associated with ultrastructural damage of the aortic endothelia in male rats.

Cited by 39 publications

References 10 publications

Testosterone, Endothelial Health, and Erectile Function

Testosterone, Endothelial Health, and Erectile Function

Androgen depletion in humans leads to cavernous tissue reorganization and upregulation of Sirt1–eNOS axis

Inverse relationship between bioavailable testosterone and subclinical coronary artery calcification in non-obese Korean men

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