Molecular Pharmacology Laboratory, Division of Molecular Cardiology and Biophysics, Victor Chang Cardiac Research Institute, Darlinghurst, NSW, Australia.
St Vincent's Clinical School, University of New South Wales, NSW, Australia.
Br J Pharmacol. 2018 Nov;175(21):4047-4059. doi: 10.1111/bph.14160. Epub 2018 Mar 25.
Cardiovascular disease (CVD) remains the largest cause of mortality worldwide, and there is a clear gender gap in disease occurrence, with men being predisposed to earlier onset of CVD, including atherosclerosis and hypertension, relative to women. Oestrogen may be a driving factor for female-specific cardioprotection, though androgens and sex chromosomes are also likely to contribute to sexual dimorphism in the cardiovascular system (CVS). Many GPCR-mediated processes are involved in cardiovascular homeostasis, and some exhibit clear sex divergence. Here, we focus on the G protein-coupled oestrogen receptor, endothelin receptors ET and ET and the eicosanoid G protein-coupled receptors (GPCRs), discussing the evidence and potential mechanisms leading to gender dimorphic responses in the vasculature. The use of animal models and pharmacological tools has been essential to understanding the role of these receptors in the CVS and will be key to further delineating their sex-specific effects. Ultimately, this may illuminate wider sex differences in cardiovascular pathology and physiology.
This article is part of a themed section on Molecular Pharmacology of GPCRs. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.21/issuetoc.
心血管疾病（CVD）仍然是全球最大的死亡原因，并且在疾病发生方面存在明显的性别差距，与女性相比，男性更容易出现心血管疾病的早期发病，包括动脉粥样硬化和高血压。雌激素可能是女性特有的心脏保护的驱动因素，但雄激素和性染色体也可能导致心血管系统（CVS）的性别二态性。许多 G 蛋白偶联受体介导的过程参与心血管稳态，其中一些表现出明显的性别差异。在这里，我们专注于 G 蛋白偶联雌激素受体、内皮素受体 ET 和 ET 以及类二十烷酸 G 蛋白偶联受体（GPCR），讨论导致血管中性别二态反应的证据和潜在机制。使用动物模型和药理学工具对于理解这些受体在 CVS 中的作用至关重要，并且将是进一步描述它们的性别特异性作用的关键。最终，这可能阐明心血管病理学和生理学中更广泛的性别差异。
本文是 GPCR 分子药理学主题部分的一部分。要查看本节中的其他文章，请访问 http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.21/issuetoc.
