肾被交感神经广泛支配，在调节血压稳态中起重要作用。交感神经活动最终由中枢神经系统（CNS）控制。去甲肾上腺素是主要的交感神经递质，在肾脏的结前神经效应连接处释放，并调节肾素释放，肾血管抵抗，钠和水处理以及免疫细胞反应。在生理条件下，肾交感神经活动（RSNA）受周围机制（如肾反射，传入交感神经，中枢机制和传入感觉神经之间的复杂相互作用）调节。RSNA在高血压中升高，因此对于高血压的永存和高血压肾脏疾病的发展至关重要。肾交感神经传递不仅受RSNA的调节，还受结前α2-肾上腺素受体的调节。结前α2-肾上腺素能受体是自身受体，当被去甲肾上腺素激活时，抑制随后由交感神经冲动诱导的去甲肾上腺素释放。最终，α2-肾上腺素受体的缺失会通过调节肾脏的升压反应和钠处理而加重高血压。α2-肾上腺素受体也在血管，肾小管和免疫细胞中表达，从而发挥与血管紧张，钠排泄和炎症有关的作用。在当前的审查中，我们强调α2-肾上腺素受体在肾交感神经传递中的作用及其对高血压的影响。此外，我们专注于非肾上腺素α2-肾上腺素受体介导的生理和病理生理功能。详细，

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The kidney is extensively innervated by sympathetic nerves playing an important role in the regulation of blood pressure homeostasis. Sympathetic nerve activity is ultimately controlled by the central nervous system (CNS). Norepinephrine, the main sympathetic neurotransmitter, is released at prejunctional neuroeffector junctions in the kidney and modulates renin release, renal vascular resistance, sodium and water handling, and immune cell response. Under physiological conditions, renal sympathetic nerve activity (RSNA) is modulated by peripheral mechanisms such as the renorenal reflex, a complex interaction between efferent sympathetic nerves, central mechanism, and afferent sensory nerves. RSNA is increased in hypertension and, therefore, critical for the perpetuation of hypertension and the development of hypertensive kidney disease. Renal sympathetic neurotransmission is not only regulated by RSNA but also by prejunctional α2-adrenoceptors. Prejunctional α2-adrenoceptors serve as autoreceptors which, when activated by norepinephrine, inhibit the subsequent release of norepinephrine induced by a sympathetic nerve impulse. Deletion of α2-adrenoceptors aggravates hypertension ultimately by modulating renal pressor response and sodium handling. α2-adrenoceptors are also expressed in the vasculature, renal tubules, and immune cells and exert thereby effects related to vascular tone, sodium excretion, and inflammation. In the present review, we highlight the role of α2-adrenoceptors on renal sympathetic neurotransmission and its impact on hypertension. Moreover, we focus on physiological and pathophysiological functions mediated by non-adrenergic α2-adrenoceptors. In detail, we discuss the effects of sympathetic norepinephrine release and α2-adrenoceptor activation on renal sodium transporters, on renal vascular tone, and on immune cells in the context of hypertension and kidney disease.