Institute of Endocrinology, Chaim Sheba Medical Center, Tel Hashomer, Ramat Gan, 52521, Israel.
Curr Hypertens Rep. 2013 Jun;15(3):190-5. doi: 10.1007/s11906-013-0338-3.
Although obesity is a well-known risk factor for hypertension, the mechanisms by which hypertension develops in obese patients are not entirely clear. Animal models of obesity and their different susceptibilities to develop hypertension have revealed some of the mechanisms linking obesity and hypertension. Adipose tissue is an endocrine organ secreting hormones that impact blood pressure, such as elements of the renin-angiotensin system whose role in hypertension have been established. In addition, the appetite-suppressing adipokine leptin activates the sympathetic nervous system via the melanocortin system, and this activation, especially in the kidney, increases blood pressure. Leptin secretion from adipocytes is increased in most models of obesity due to leptin resistance, although the resistance is often selective to the anorexigenic effect, while the susceptibility to the hypertensive effect remains intact. Understanding the pathways by which obesity contributes to increased blood pressure will hopefully pave the way to and better define the appropriate treatment for obesity-induced hypertension.
虽然肥胖是高血压的一个众所周知的危险因素，但肥胖患者中高血压发展的机制尚不完全清楚。肥胖动物模型及其对高血压的不同易感性揭示了一些将肥胖与高血压联系起来的机制。脂肪组织是一种内分泌器官，分泌影响血压的激素，如肾素-血管紧张素系统的成分，其在高血压中的作用已得到确立。此外，抑制食欲的脂肪因子瘦素通过黑皮质素系统激活交感神经系统，这种激活，特别是在肾脏中，会增加血压。由于瘦素抵抗，大多数肥胖模型中脂肪细胞的瘦素分泌增加，尽管这种抵抗通常对厌食作用具有选择性，而对高血压作用的敏感性仍然完整。了解肥胖导致血压升高的途径有望为肥胖引起的高血压的治疗铺平道路，并更好地定义其治疗方法。
