Influence of testosterone on mean arterial pressure: A physiological study in male and female normotensive WKY and hypertensive SHR rats

Loh, Su Yi; Salleh, Naguib

doi:10.1556/2060.104.2017.1.3

Cited by 26 publications

(7 citation statements)

References 45 publications

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“…It is worth noting that there are inconsistent reports on the effect of ovariectomy on blood pressure. Loh SY et al found that the mean arterial pressure of 8-week-old female SHR decreased after gonadectomy (Loh et al 2017). Masubuchi et al also showed that gonadectomy may affect blood pressure in adult female rats (Masubuchi et al1982).…”

Section: Discussionmentioning

confidence: 98%

mTOR inhibitor improves testosterone-induced myocardial hypertrophy in hypertensive rats

Chen

Yuan

et al. 2022

Journal of Endocrinology

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Compelling evidence have described the incidence of hypertension and left ventricular hypertrophy (LVH) in postmenopausal women is significantly increased worldwide. Our team’s previous research identified that androgen was an underlying factor contributing to increased blood pressure and LVH in postmenopausal women. However, little is known about how androgens affect LVH in postmenopausal hypertensive women. The purpose of this study was to evaluate the role of mTOR signaling pathway in myocardial hypertrophy in androgen-induced postmenopausal hypertension and whether mTOR inhibitors can protect the myocardium from androgen-induced interference to prevent and treat cardiac hypertrophy. For that, ovariectomized (OVX) spontaneously hypertensive rats (SHR) aged 12 weeks were used to study the effects of testosterone (T 2.85 mg/kg/weekly im) on blood pressure and myocardial tissue. On the basis of antihypertensive therapy (chlorthalidone 8mg/kg/day ig), the improvement of blood pressure and myocardial hypertrophy in rats treated with different dose gradients of rapamycin (0.8mg/kg/day Vs 1.5mg/kg/day Vs 2mg/kg/day ip) in OVX+ estrogens(E 9.6 mg/Kg/day, ig)+T group was further evaluated. After T intervention, the OVX female rats exhibited significant increments in the heart weight / tibial length (TL), area of cardiomyocytes and the mRNA expressions of atrial natriuretic peptide, β- myosin heavy chain and matrix metalloproteinase 9 accompanied by a significant reduction in the uterine weight/TL and issue inhibitor of metalloproteinase 1. Mammalian rapamycin receptor (mTOR), ribosomal protein S6 kinase (S6K1),4E-bindiong protein 1(4EBP1) and eukaryotic translation initiation factor 4E in myocardial tissue of OVX+E+T group were expressed at higher levels than those of the other four groups. On the other hand, rapamycin abolished the effects of T-induced cardiac hypertrophy, decreased the systolic and diastolic blood pressure of SHR, and inhibited the activation of mTOR/ S6K1/4EBP1 signaling pathway in a concentration-dependent manner. Collectively, these data suggest that the mTOR/S6K1/4EBP1 pathway is an important therapeutic target for the prevention of LVH in postmenopausal hypertensive female rats with high T levels. Our findings also support the standpoint that the mTOR inhibitor, rapamycin, can eliminate T-induced cardiomyocyte hypertrophy

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Section: Discussionmentioning

confidence: 98%

mTOR inhibitor improves testosterone-induced myocardial hypertrophy in hypertensive rats

Chen

Yuan

et al. 2022

Journal of Endocrinology

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“…However, most current studies have focused on the relationship between serum total testosterone (TT) and blood pressure (BP) regulation in male patients. 10 , 11 Studies on the role of bioavailable testosterone (BioT) in postmenopausal hypertensive women with LVH have rarely been reported. By analyzing the relationship between androgen and LVH in postmenopausal hypertensive women, this study aims to provide a new predictor and theoretical basis for target organ damage in postmenopausal hypertensive patients.…”

Section: Introductionmentioning

confidence: 99%

Association of free androgen index and sex hormone–binding globulin and left ventricular hypertrophy in postmenopausal hypertensive women

Chen

Wang

Pei

et al. 2021

J of Clinical Hypertension

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The aim of the present study was to explore the relationship between androgen and LVH in postmenopausal hypertensive women. Enrolled in this study were 378 postmenopausal hypertensive women who were admitted to the department of cardiology between December 2018 and December 2020. According to left ventricular mass index (LVMI) evaluated by echocardiography, the patients were divided into LVH group (n = 172) and non‐LVH group (n = 206). Their clinical characteristics were collected. Based on the result of propensity score matching analysis, 160 cases in each group were matched successfully. After correcting for confounding factors by various models, the results showed that free androgen index (FAI) and sex hormone–binding globulin (SHBG) were the influencing factors of LVH in postmenopausal women with hypertension. Patients with elevated SHBG were 5% less likely to develop LVH than those without elevated SHBG (OR: 0.950, 95% CI 0.922‐1.578). Postmenopausal hypertensive patients with elevated FAI were 16% more likely to have LVH than those without elevated FAI (OR: 1.608, 95% CI 0.807‐3.202). Multiple linear regression showed that LVMI increased by 61.82g/m2 for every 1 unit increase in FAI. In addition, SHBG decreased by 1 nmol/l, and LVMI increased by 0.177g/m2. Subgroup analysis showed that patients in the controlled BP group had a lower risk of LVH for every additional unit of SHBG compared with the uncontrolled BP group. The risk of LVH for each additional unit of FAI in the uncontrolled BP group was higher than that in the controlled BP group. The results of this present study showed that the occurrence of LVH was positively correlated with FAI and negatively correlated with SHBG in postmenopausal women with hypertension. The increase in FAI level and the decrease in SHBG level may be related to the occurrence and development of LVH in postmenopausal hypertension.

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“…Again, since no significant improvement of cardiac function were observed after testosterone supplementation, we considered the increment of SBP after supplementation of testosterone may be also depended on its efficacy on volume and strength of peripheral skeletal muscle. This is not surprising since the contraction of peripheral skeletal muscle may serve as a secondary pump to maintain the BP, particularly in the elderly (36,37). Furthermore, results our meta-analysis did not support that testosterone supplementation in CHF patients was associated with significantly improved prognosis.…”

Section: Discussionmentioning

confidence: 58%

Testosterone Supplementation in Patients With Chronic Heart Failure: A Meta-Analysis of Randomized Controlled Trials

2020

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Background: The effect of testosterone supplementation in patients with chronic heart failure (CHF) remains uncertain.Methods: A meta-analysis of randomized controlled trials (RCTs) was performed. RCTs that evaluate the chronic effect of testosterone supplementation on exercise capacity and cardiac function in CHF were identified via searching of PubMed, Embase, and the Cochrane's Library databases. Heterogeneity was evaluated by the Cochrane's Q test and I 2 statistics. A fixed-effect model was used if the heterogeneity was not significant (I 2 < 50%); otherwise, a random-effect model was applied.Results: Eight studies including 170 patients in the testosterone supplementation group and 162 in the control group were included. Overall, testosterone supplementation was not associated with an improved exercise capacity (walking test: standardized mean difference [SMD] = 0.36, p = 0.07). Sensitivity analyses limited to male patients showed similar results (SMD = 0.21, p = 0.15), and subgroup analyses also showed similar results in male HF patients with baseline total testosterone (TT) ≥ or < 10 nmol/L. However, patients with TT at endpoint ≥ 25 nmol/L was associated with improved exercise capacity (SMD = 1.12, p = 0.02), but not for those with TT at endpoint < 25 nmol/L (SMD = 0.24, p = 0.12). In addition, VO 2max (weight mean difference [WMD] = 0.85, p = 0.43), the functional classification (the New York Heart Association classification: WMD = −0.08, p = 0.16) and quality of life (Minnesota Living with Heart Failure [MLHF] questionnaire: WMD = −6.03, p = 0.12) were not significantly affected. Moreover, testosterone supplementation did not significantly affect left ventricular ejection fraction (WMD: −1.52%, p = 0.37), serum B-type natriuretic peptide (SMD: −0.19, p = 0.23), or a composite outcome of death or HF hospitalization (risk ratio [RR]: 1.02, p = 0.96). Although testosterone supplementation increased systolic blood pressure (BP) in CHF patients (WMD: 5.68 mmHg, p < 0.001), diastolic BP or heart rate was not significantly changed as compared to control.Conclusions: Testosterone supplementation within a physiological range is not associated with significantly improved exercise capacity, cardiac function, quality of life, or clinical outcome in CHF patients.

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Influence of testosterone on mean arterial pressure: A physiological study in male and female normotensive WKY and hypertensive SHR rats

Cited by 26 publications

References 45 publications

mTOR inhibitor improves testosterone-induced myocardial hypertrophy in hypertensive rats

mTOR inhibitor improves testosterone-induced myocardial hypertrophy in hypertensive rats

Association of free androgen index and sex hormone–binding globulin and left ventricular hypertrophy in postmenopausal hypertensive women

Testosterone Supplementation in Patients With Chronic Heart Failure: A Meta-Analysis of Randomized Controlled Trials

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