Littleton-Kearney Marguerite, Hurn Patricia D
Johns Hopkins Schools of Nursing and Medicine, 525 N. Wolfe Street, Room 460, Baltimore, MD 21205-2110, USA.
Biol Res Nurs. 2004 Apr;5(4):276-85. doi: 10.1177/1099800403262927.
Male sex is an acknowledged risk factor for many forms of cardiovascular disease, and vascular disease prevalence patterns appear to be different in men versus women. The vascular properties of the principal mammalian androgen, testosterone, are complex and linked to dose, duration of exposure, presence of underlying vascular disease, and, possibly, biological sex. Data from isolated vessels and animal models suggest that pharmacological doses of testosterone, or its potent intracellular metabolite dihydrotestosterone, produce vasodilation. Testosterone's major effect on vascular beds at physiologic concentrations remains unclear, with documentation of both vasodilatory and vasoconstrictive actions. Results of various studies suggest that testosterone can alter vascular tone through both endothelium-dependent and endothelium-independent mechanisms in a variety of vascular beds and vessel types. Testosterone's endothelium-dependent effects are likely mediated at least in part through nitric oxide (NO) elaboration, whereas mechanisms of endothelium-independent effects involve 1 or more types of smooth muscle ion conductance channels. Data from clinical studies indicate that, in men, androgen replacement may provide beneficial effects when coronary artery disease is present. Conversely, in women, testosterone may augment existing hypertension, increase risk for cardiovascular events, or promote atherogenesis. However, it should be emphasized that most of these observations are anecdotal or come from small-scale clinical studies, and limited information is available in women. New research is required to understand the potential efficacy of androgen therapy, or lack thereof. This review focuses on current understanding of testosterone's physiological effects on vascular behavior and of testosterone's putative role in vascular health and disease.
男性是多种心血管疾病公认的危险因素，而且男性与女性的血管疾病流行模式似乎有所不同。主要的哺乳动物雄激素睾酮的血管特性很复杂，与剂量、暴露持续时间、潜在血管疾病的存在以及可能的生物性别有关。来自离体血管和动物模型的数据表明，药理剂量的睾酮或其强效细胞内代谢物双氢睾酮可产生血管舒张作用。睾酮在生理浓度下对血管床的主要作用仍不清楚，有文献记载其既有血管舒张作用，也有血管收缩作用。各种研究结果表明，睾酮可通过多种血管床和血管类型中依赖内皮和不依赖内皮的机制改变血管张力。睾酮的内皮依赖性作用可能至少部分是通过一氧化氮（NO）的释放介导的，而不依赖内皮的作用机制涉及1种或多种类型的平滑肌离子传导通道。临床研究数据表明，在男性中，存在冠状动脉疾病时雄激素替代可能会带来有益效果。相反，在女性中，睾酮可能会加重现有的高血压，增加心血管事件风险或促进动脉粥样硬化形成。然而，应该强调的是，这些观察结果大多是轶事性的或来自小规模临床研究，女性方面的信息有限。需要开展新的研究来了解雄激素治疗的潜在疗效或其缺乏疗效的情况。本综述重点关注目前对睾酮对血管行为的生理作用以及睾酮在血管健康和疾病中假定作用的理解。
