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harlanmorrison

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The LAD was isolated and placed in either prostaglandin or potassium chloride (KCl), another contracting agent, and testosterone. This study tested the effect of endothelial denudation as well as washing the vessels with either Krebs–Henseleit bicarbonate (KHB), or N‐nitro‐l‐arginine methyl ester (l‐NAME). Deenadayalu et al18 performed a similar study using the left anterior descending (LAD) coronary arteries of swine hearts. Statistical significance was observed at both 1 and 10 μmol/L of testosterone, and there was no difference between the groups with and without endothelium.16 This suggests that testosterone has a direct smooth muscle–relaxing effect and does not require endothelium to induce vasodilation. After 7 minutes in prostaglandin, arteries were washed and exposed to testosterone or control solution. Effects of a therapy on blood vessels that have been subjected to endothelial denudation would suggest that the drug is working through an endothelium‐independent and NO‐mediated‐independent mechanism, such as directly on the tunica media (smooth muscle layer) of an artery. There is little information regarding the mechanism by which testosterone exerts its cardioprotective effect regarding ischemic injury; thus, more research is required.
Nonetheless, the results of the TOM trial provide important cautionary information regarding the potential for TRT to be harmful in at least some populations of older men and points to the need for larger studies. Further, subjects in the TOM trial had higher baseline BMI, higher triglycerides, and lower HDL than individuals included in the second study. However, it is important to remember that all of these studies, regardless of findings, have methodological weaknesses that limit their interpretive value. Furthermore, another meta-analysis found that TRT appeared to confer mortality benefit specifically in hypogonadal men with Type 2 diabetes . Given the absence of a clear, causal relationship, clinical use of TRT is predicated on the presence of hypogonadal symptoms rather than cardiometabolic disease. Overall, these types of longitudinal analyses also fail to provide evidence of a direct, causal relationship between androgen exposure and CVD.
Studies show both a decrease in the Akt prosurvival pathway in testosterone‐treated male animals and upregulation of the Akt prosurvival pathway in male animals without endogenous testosterone or with a blocked androgen receptor, suggesting that testosterone gives way to an increase in death signaling and therefore attenuates cardiomyocyte survival. To further investigate the effects of testosterone on apoptosis, Wang et al56 isolated hearts from adult male rats, orchiectomized male rats, and testes‐intact male rats given flutamide. What this study showed was that an increase in either testosterone or DHT inhibited IL‐6 production dependent on the androgen receptor, which then led to a decrease in inflammation.50 Hofbauer et al51 also showed testosterone and DHT at a 10−7 mol/L concentration inhibit IL‐6 mRNA expression. To better understand the increased incidence of autoimmune diseases in females compared with males, Bebo et al48 examined the inflammatory factors in autoimmune encephalomyelitis in mice. These data suggest that testosterone alone increases neutrophil infiltration and therefore may increase inflammation when compared with mice without testosterone.43 Increased inflammation following acute myocardial infarction may lead to increased rupture in the myocardium.
Since day-to-day variation of T concentrations in a given individual can be large , these single low measurements may not be as meaningful as multiple measurements over time. The inconsistency among the longitudinal data may in part be due to the design of such studies and the reliance on single, or even duplicate measures of serum T. Moreover, appropriately powered randomized controlled trials of TRT, the gold standard for determining the risks and benefits of a clinical intervention, have not been performed. Articles from American Journal of Physiology - Heart and Circulatory Physiology are provided here courtesy of American Physiological Society Therefore, it is reasonable to propose that 1) an insufficiency of androgens during pregnancy, particularly 5β-DHT, could contribute, at least in part, to the development of preeclampsia/eclampsia and 2) exogenously administered 5β-DHT may be therapeutically relevant for the treatment of gestational HT.
This metabolite is a powerful androgen at the genomic level, with higher potency than even Tes, but its nongenomic vasorelaxing efficacy and potency are notably less than those of Tes (8, 10, 48). Since 5β-DHT has little or no affinity for the intracellular AR and is totally devoid of androgenic properties (14), then the acute vasorelaxing effect of 5β-DHT is most likely mediated by an AR-independent, nongenomic mechanism. Thus 5α-DHT is a potent androgen with a strong affinity for the intracellular androgen receptor (AR), whereas its 5β-isomer (5β-DHT), which does not bind to the AR, is totally devoid of androgenic properties but is highly efficacious in producing vasorelaxation. To avoid confusion, it must be recognized that Tes and its metabolites are clearly distinguishable by their fundamentally different configurations (Fig. 2).
The studies describing the relationship between testosterone and atherosclerosis have brought about controversy. In contrast to the studies described above, some studies show that exogenous testosterone exacerbates atherosclerosis. Hatakeyama et al37 described the effect of testosterone on tumor necrosis factor alpha (TNFα)–induced expression of vascular cell adhesion molecule 1 (VCAM‐1) in human aortic endothelial cells (HAECs). Nathan et al36 suggested that aromatase, an enzyme that converts testosterone to estrogens, may play an important role in limiting atherosclerosis in males. These segments were then cultured for 21 days in a standard medium containing differing concentrations of testosterone.
Furthermore, it should be noted that numerous studies have shown that high pharmacological concentrations of Tes (10–100 μM) induce vasodilation in endothelium-denuded vessels, suggesting an endothelium-independent mechanism (8, 10, 12, 24, 47, 48, 60, 63, 73). Interestingly, in studies employing small vessel wire myography, it has been reported that micromolar concentrations of Tes induce vasodilation of rat pulmonary arteries (23), human subcutaneous resistance arterioles (32), and porcine small prostatic arteries (43). This acute effect of Tes and other androgens has been observed at micromolar concentrations in a variety of large arteries (aorta, coronary and umbilical arteries) as well as small resistance arteries (mesenteric, prostatic, pulmonary, and subcutaneous) from several animal species (rat, mouse, rabbit, pig, and dog) and humans (2, 8, 10, 32, 48, 60, 71). While this effect frequently has been observed in large arteries at micromolar concentrations, more recent studies have reported vasorelaxation of smaller resistance arteries at nanomolar (physiological) concentrations. Additionally, breaking a blood vessel can result in the formation of blood clots, resulting in a life-threatening situation if the blood clot travels to the lungs or heart. Testosterone plays an essential role in the maintenance of cardiovascular health. Optimal oxygen supply to the blood vessels improves their function and health and helps combat vascular stiffness.
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