Cardiovascular and Metabolic Consequences of Testosterone Supplements in Young and Old Male Spontaneously Hypertensive Rats: Implications for Testosterone Supplements in Men

Dalmasso, Carolina; Patil, Chetan N; Cardozo, Licy L. Yanes; Romero, Damián G.; Marañón, Rodrigo O

doi:10.1161/jaha.117.007074

Cited by 23 publications

(16 citation statements)

References 32 publications

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“…These findings show that testosterone is important in the hypertensive effect induced by Ang II as withdrawal (castration) prevented Ang II effects and replacement (testosterone) reversed the castration effects on Ang II-induced changes in blood pressure. This suggests that the development of Ang II-induced hypertension is androgen dependent, which appears to be similar to that observed in other in utero programming of increases in blood pressure [20,[43][44][45].…”

Section: Discussionsupporting

confidence: 79%

Testosterone plays a permissive role in angiotensin II-induced hypertension and cardiac hypertrophy in male rats†

Mishra

Gopalakrishnan

et al. 2018

Biology of Reproduction

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Sex hormone-dependent vascular reactivity is an underlying factor contributing to sex differences in blood pressure. Inappropriate activation of the renin-angiotensin system (RAS) is involved in vascular dysfunction and hypertension. This study evaluated the role of androgens (testosterone) in angiotensin II (Ang II) -induced increase in blood pressure, vascular reactivity and cardiac hypertrophy. Eight weeks-old male Wistar rats underwent sham operation, castration, or castration with testosterone replacement. After 12 weeks of chronic changes in androgen status, Ang II (120 ng/kg per minute) or saline was infused for 28 days via subcutaneous miniosmotic pump, and changes in blood pressure was measured. Vascular reactivity and Ang II receptor levels were examined in mesenteric arteries. Heart weight, cardiac ANP mRNA levels and fibrosis were also assessed. Ang II infusion increased arterial pressure in intact males. The Ang II-induced increase in hypertensive response was prevented in castrated males. Testosterone replacement in castrated males restored Ang II-induced hypertensive responses. Castration reduced vascular AT1R/AT2R ratio, an effect that was reversed by testosterone replacement. Ang II-induced hypertension was associated with increased contractile response of mesenteric arteries to Ang II and phenylephrine in intact and testosterone-replaced castrated males; these increases were prevented in castrated males. Ang II infusion induced increased left ventricle-to-body weight ratio and ANP mRNA expression, indicators of left ventricular hypertrophy, and fibrosis in intact and testosterone-replaced castrated males, and castration prevented the increase in these parameters caused by Ang II. This study demonstrate that testosterone plays a permissive role in development and maintenance of Ang II-induced vascular dysfunction, hypertension and cardiac hypertrophy.

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Section: Discussionsupporting

confidence: 79%

Testosterone plays a permissive role in angiotensin II-induced hypertension and cardiac hypertrophy in male rats†

Mishra

Gopalakrishnan

et al. 2018

Biology of Reproduction

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“…3 The average change in ambulatory BP in those men on antihypertensive therapy was prominent in men with underlying hypertension than those without hypertension. Furthermore, Dalmasso C et al 11 have reported that there are differential effects of testosterone on BP in the spontaneously hypertensive rat (SHR) depending on the age of the SHR -an effect that may be mediated in part by the reninangiotensin system.…”

Section: Discussionmentioning

confidence: 99%

Effects of the oral testosterone undecanoate Kyzatrex™ on ambulatory blood pressure in hypogonadal men

White

Bernstein²,

Rittmaster³

et al. 2021

J of Clinical Hypertension

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Testosterone replacement therapies have been shown to increase blood pressure (BP) in hypogonadal men. We studied the effects of a new formulation of testosterone undecanoate (Kyzatrex™) on ambulatory blood pressure (ABP) and heart rate, in 155 men with hypogonadism (mean age, 50.5 years, 76.8% white, 36.1% on antihypertensive therapy). The ABP, heart rate and clinical assessments were obtained at baseline and following 120 and 180 days of therapy. Mean changes from baseline in 24‐h ambulatory systolic BP of 1.7 mmHg (95% CI, 0.3, 3.1) at day 120 and 1.8 mmHg (95% CI, 0.3, 3.2) at day 180 were observed post‐treatment. For those men on antihypertensive drug therapy, increases in mean 24‐h systolic BP were greater than those not taking antihypertensive drugs (3.4 vs 0.7 mmHg at day 120 and 3.1 vs 1.0 mmHg at day 180, respectively). Changes from baseline in 24‐h diastolic BP and heart rate at day 120 were smaller (<1 mmHg and <1 beat/min, respectively). There were no relationships observed between testosterone concentration or hemoglobin levels with ABP. Multivariable analyses showed that baseline ambulatory BP and antihypertensive therapy were significantly correlated with BP changes. These data demonstrate small increases in ambulatory BP following 120 days on this oral testosterone undecanoate with no further changes at 180 days. Changes in ambulatory BP were minimal in patients not taking antihypertensive therapy.

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“…Hormones such as testosterone are often used as adjuvants, although various adverse reactions have been reported [ 40 , 41 ]. Therefore, developing effective medicines is a core issue in treating age-related reproductive decline.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of ginseng stem-leaf saponins on D-galactose-induced reproductive injury in male mice

Zhang

Yang

Zhang

et al. 2021

Aging

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Panax ginseng is a perennial plant in the Araliaceae family. In this study, we investigated the protective effects of ginseng stem-leaf saponins (GSLS) isolated from P. ginseng against D-galactose-induced reproductive function decline, oxidative stress, and inflammatory response. Reproductive injuries were induced in mice via the subcutaneous injection of D-galactose (300 mg/kg) for six weeks. The mice were then treated with GSLS by intragastric administration. GSLS inhibited markers of oxidative stress and inflammatory cytokines induced by D-galactose in serum, liver and kidney, whereas GSLS increased the activities of antioxidant enzymes. Compared to the mice treated only with D-galactose, GSLS treatment significantly increased the average path velocity, straight line velocity, curvilinear velocity, and amplitude of the lateral head displacement of mouse sperm. Meanwhile, GSLS significantly increased the testosterone level and reduced the cortisol, FSH, and LH levels. Histopathological examination revealed alterations in the number and the arrangement of spermatogenic cells in the seminiferous tubules of the mice in the GSLS group. GSLS treatment suppressed MAPKs pathway activation in testes. These results suggest that GSLS can attenuate D-galactose-induced oxidative stress and inflammatory response in serum, liver and kidney, and ameliorate reproductive damage by inhibiting MAPKs signaling pathway.

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Cardiovascular and Metabolic Consequences of Testosterone Supplements in Young and Old Male Spontaneously Hypertensive Rats: Implications for Testosterone Supplements in Men

Cited by 23 publications

References 32 publications

Testosterone plays a permissive role in angiotensin II-induced hypertension and cardiac hypertrophy in male rats†

Testosterone plays a permissive role in angiotensin II-induced hypertension and cardiac hypertrophy in male rats†

Effects of the oral testosterone undecanoate Kyzatrex™ on ambulatory blood pressure in hypogonadal men

Protective effects of ginseng stem-leaf saponins on D-galactose-induced reproductive injury in male mice

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