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Rgs5 Targeting Leads to Chronic Low Blood Pressure and a Lean Body Habitus

机译：Rgs5靶向导致慢性低血压和瘦身习惯

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RGS5 is a potent GTPase-activating protein for Giα and Gqα that is expressed strongly in pericytes and is present in vascular smooth muscle cells. To study the role of RGS5 in blood vessel physiology, we generated Rgs5-deficient mice. The Rgs5?/? mice developed normally, without obvious defects in cardiovascular development or function. Surprisingly, Rgs5?/? mice had persistently low blood pressure, lower in female mice than in male mice, without concomitant cardiac dysfunction, and a lean body habitus. The examination of the major blood vessels revealed that the aortas of Rgs5?/? mice were dilated compared to those of control mice, without altered wall thickness. Isolated aortic smooth muscle cells from the Rgs5?/? mice exhibited exaggerated levels of phosphorylation of vasodilator-stimulated phosphoprotein and extracellular signal-regulated kinase in response to stimulation with either sodium nitroprusside or sphingosine 1-phosphate. The results of this study, along with those of previous studies demonstrating that RGS5 stability is under the control of nitric oxide via the N-end rule pathway, suggest that RGS5 may balance vascular tone by attenuating vasodilatory signaling in vivo in opposition to RGS2, another RGS (regulator of G protein signaling) family member known to inhibit G protein-coupled receptor-mediated vasoconstrictor signaling. Blocking the function or the expression of RGS5 may provide an alternative approach to treat hypertension.
机译：RGS5是G iα和G qα的有效GTPase激活蛋白，在周细胞中强烈表达，并存在于血管平滑肌细胞中。为了研究RGS5在血管生理中的作用，我们制备了 Rgs5 缺陷小鼠。 Rgs5 ？/？小鼠正常发育，心血管发育或功能无明显缺陷。出乎意料的是， Rgs5 ？/？小鼠的血压持续低下，雌性小鼠比雄性小鼠低，没有伴随的心脏功能障碍和瘦身习惯。对主要血管的检查显示，与对照小鼠相比， Rgs5 α/β小鼠的主动脉扩张，而壁厚没有改变。从 Rgs5 ？/？小鼠中分离出的主动脉平滑肌细胞对硝普钠刺激下的血管扩张剂刺激的磷蛋白和细胞外信号调节激酶的磷酸化水平过高或鞘氨醇1-磷酸。这项研究的结果以及先前的研究表明，RGS5的稳定性受N端规则途径的一氧化氮控制，这表明RGS5可能通过减弱体内血管舒张信号而与RGS2相对，从而平衡了血管紧张度。已知RGS（G蛋白信号调节剂）家族成员可抑制G蛋白偶联受体介导的血管收缩剂信号传导。阻断RGS5的功能或表达可能提供治疗高血压的另一种方法。

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