Wynne F L, Khalil R A
Research and Development, Department of Veterans Affairs Medical center, Harvard Medical School West Roxbury, Massachusetts 02132, USA.
J Endocrinol Invest. 2003 Feb;26(2):181-6. doi: 10.1007/BF03345150.
The greater incidence of coronary artery disease in men compared to women has often suggested possible harmful effects of male sex steroids that could promote coronary atherogenesis and vasoconstriction. However, antiatherogenic and coronary vasodilator effects of testosterone have also been suggested. The interaction of testosterone (T) with its specific receptors may trigger not only long-term genomic effects, but also acute non-genomic vasodilator responses. Testosterone may activate the endothelium and stimulate the nitric oxide-cGMP and/or the hyperpolarization-mediated vascular relaxation pathway. T may also inhibit the signaling mechanisms of smooth muscle contraction such as [Ca2+]i and protein kinases. The T-induced stimulation of endothelium-dependent mechanisms of vascular relaxation and inhibition of the mechanisms of coronary smooth muscle contraction represent potential beneficial effects of T against coronary artery disease.
与女性相比,男性冠状动脉疾病的发病率更高,这常常表明男性甾体激素可能具有促进冠状动脉粥样硬化和血管收缩的有害作用。然而,也有人提出睾酮具有抗动脉粥样硬化和冠状动脉扩张作用。睾酮(T)与其特异性受体的相互作用不仅可能触发长期的基因组效应,还可能引发急性非基因组血管舒张反应。睾酮可能激活内皮细胞,刺激一氧化氮 - 环磷酸鸟苷(cGMP)和/或超极化介导的血管舒张途径。T还可能抑制平滑肌收缩的信号传导机制,如细胞内钙离子浓度([Ca2+]i)和蛋白激酶。T诱导的血管舒张内皮依赖性机制的刺激以及冠状动脉平滑肌收缩机制的抑制代表了T对冠状动脉疾病的潜在有益作用。