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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Functional linkage as a direction for studies in oxidative stress: alpha-adrenergic receptors.
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Functional linkage as a direction for studies in oxidative stress: alpha-adrenergic receptors.

机译：功能连接作为研究氧化应激的方向：α-肾上腺素能受体。

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The alpha-adrenergic receptors (adrenoceptors) are activated by the endogenous agonists epinephrine and norepinephrine. They are G protein-coupled receptors that may be broadly classified into alpha1 (subclasses alpha1A, alpha1B, alpha1D) and alpha2 (subclasses alpha2A, alpha2B, alpha2C). The alpha1-adrenoceptors act by binding to G(alpha)q subunits of the G proteins, causing activation of phospholipase C (PLC). PLC converts phosphatidylinositol 4,5-bisphosphate into inositol trisphosphate (IP3) and diacylglycerol (DAG), which have downstream effects on cytosolic Ca2+ concentration. The alpha2-adrenoceptors bind to G(alpha)i thus inhibiting adenylyl cyclase and decreasing cAMP levels. DAG alters protein kinase C activity and cAMP activates protein kinase A. The downstream pathways of the two receptors may also interact. Activation of alpha1- and alpha2-adrenoceptors in vascular smooth muscle results in vasoconstriction. However, the densities of individual receptor subclasses vary between vessel beds or between vessels of various sizes within the same bed. In vasculature, the densities of adrenoceptor subclasses differ between conduit arteries and arterioles. These differences, along with differences in coupling mechanisms, allow for fine regulation of arterial blood flow. This diversity is enhanced by interactions resulting from homo- and heterodimer formation of the receptors, metabolic pathways, and kinases. Reactive oxygen species generated in pathologies may alter alpha1- and alpha2-adrenoceptor cascades, change vascular contractility, or cause remodeling of blood vessels. This review emphasizes the need for understanding the functional linkage between alpha-adrenoceptor subtypes, coupling, cross talk, and oxidative stress in cardiovascular pathologies.
机译：α-肾上腺素受体（肾上腺素受体）被内源性激动剂肾上腺素和去甲肾上腺素激活。它们是G蛋白偶联受体，可以大致分为alpha1（子类alpha1A，alpha1B，alpha1D）和alpha2（子类alpha2A，alpha2B，alpha2C）。 α1-肾上腺素受体通过与G蛋白的Gαq亚基结合而起作用，引起磷脂酶C（PLC）的活化。 PLC将磷脂酰肌醇4,5-二磷酸酯转化为肌醇三磷酸酯（IP3）和二酰基甘油（DAG），它们对胞质Ca2 +浓度具有下游影响。 α2-肾上腺素能受体与Gαi结合，从而抑制腺苷酸环化酶并降低cAMP水平。 DAG改变蛋白激酶C的活性，而cAMP激活蛋白激酶A。这两个受体的下游途径也可能相互作用。血管平滑肌中α1和α2肾上腺素受体的激活导致血管收缩。但是，各个受体亚类的密度在血管床之间或同一床内各种尺寸的血管之间变化。在脉管系统中，肾上腺素受体亚类的密度在导管动脉和小动脉之间有所不同。这些差异以及耦合机制的差异，使动脉血流的精细调节成为可能。由于受体的同型和异型二聚体形成，代谢途径和激酶之间的相互作用而增强了这种多样性。病理学中产生的活性氧可能会改变α1和α2肾上腺素能受体的级联，改变血管收缩力或引起血管重塑。这篇综述强调需要了解心血管疾病中α-肾上腺素受体亚型，偶联，串扰和氧化应激之间的功能联系。

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