Zorad S, Fickova M, Zelezna B, Macho L, Kral J G
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia.
Gen Physiol Biophys. 1995 Oct;14(5):383-91.
Angiotensin II exerts its action via at least two distinct receptor subtypes designated AT1 and AT2. AT1 receptors seem to be responsible for most of the known angiotensin II effects while the role of AT2 receptors is not yet clear. Adipocytes of adult rats express exclusively the AT1 subtype. Angiotensin II stimulates prostacyclin release in adult rat adipocytes and in mouse preadipocytes. In the latter prostacyclin release is completely blocked by an AT2 receptor antagonist. Adipocyte angiotensin II receptors seem to be regulated by age and fat mass. Blockade of these receptors by an AT1 antagonist seems to prevent adipose tissue hypertrophy. Moreover, adipose tissue contains all the main components of the renin-angiotensin system such as angiotensinogen, angiotensin converting enzyme, angiotensin II and angiotensin II receptors. Angiotensinogen expression in adipocytes is stimulated by a high fat diet concurrent with enlargement of fat mass, associated with insulin resistance. Angiotensin converting enzyme inhibitors improve insulin sensitivity. Taken together, there is evidence of interaction between insulin and angiotensin II in regulation of adipose tissue metabolism and cellularity. Clarification of these interactions could lead to significant progress in pharmacological treatment of obesity and its comorbidity.
血管紧张素II通过至少两种不同的受体亚型（即AT1和AT2）发挥作用。AT1受体似乎介导了大多数已知的血管紧张素II效应，而AT2受体的作用尚不清楚。成年大鼠的脂肪细胞仅表达AT1亚型。血管紧张素II可刺激成年大鼠脂肪细胞和小鼠前脂肪细胞释放前列环素。在后者中，前列环素的释放被AT2受体拮抗剂完全阻断。脂肪细胞血管紧张素II受体似乎受年龄和脂肪量的调节。用AT1拮抗剂阻断这些受体似乎可预防脂肪组织肥大。此外，脂肪组织含有肾素-血管紧张素系统的所有主要成分，如血管紧张素原、血管紧张素转换酶、血管紧张素II和血管紧张素II受体。高脂肪饮食在增加脂肪量的同时会刺激脂肪细胞中血管紧张素原的表达，这与胰岛素抵抗有关。血管紧张素转换酶抑制剂可改善胰岛素敏感性。综上所述，有证据表明胰岛素与血管紧张素II在调节脂肪组织代谢和细胞构成方面存在相互作用。阐明这些相互作用可能会在肥胖及其合并症的药物治疗方面取得重大进展。
