Burns Kevin D, Li Ningjun
Division of Nephrology, The Ottawa Hospital and University of Ottawa, 1967 Riverside Drive, Room 535A, Ontario K1H 7W9, Canada.
Curr Hypertens Rep. 2003 Apr;5(2):165-71. doi: 10.1007/s11906-003-0074-1.
The kidney contains a renin-angiotensin system that appears to regulate systemic blood pressure. Angiotensin II (Ang II) has stimulatory effects on sodium transport in multiple nephron segments via binding to plasma membrane AT(1) receptors. In the proximal tubule, Ang II production is substantial. The stimulatory effect of Ang II on proximal sodium transport is enhanced by renal nerves, and is associated with internalization of apical and basolateral receptors. In the cortical collecting duct, AT(1) receptors stimulate transport through apical sodium channels, and in the inner medulla, urea transport is enhanced by Ang II, contributing to increased sodium and water reabsorption. AT(1) receptors may also be linked to increased expression of certain tubular sodium transporters. In contrast to the stimulatory effects of AT(1) receptors on sodium transport, AT(2) receptors expressed in the adult kidney are linked to increased urinary sodium excretion and decreased blood pressure. This suggests that renal tubular AT(1) receptor activation serves as a protective mechanism to increase sodium reabsorption and blood pressure when extracellular fluid volume is threatened, whereas AT(2) receptors dampen this response. The interplay between these two receptor pathways in the kidney could have significant effects on long-term blood pressure control.
肾脏含有一个肾素 - 血管紧张素系统，该系统似乎可调节全身血压。血管紧张素II（Ang II）通过与质膜AT(1)受体结合，对多个肾单位节段的钠转运具有刺激作用。在近端小管中，Ang II的产生量很大。肾神经可增强Ang II对近端钠转运的刺激作用，且这与顶端和基底外侧受体的内化有关。在皮质集合管中，AT(1)受体通过顶端钠通道刺激转运，而在内髓质中，Ang II可增强尿素转运，有助于增加钠和水的重吸收。AT(1)受体也可能与某些肾小管钠转运体的表达增加有关。与AT(1)受体对钠转运的刺激作用相反，成年肾脏中表达的AT(2)受体与尿钠排泄增加和血压降低有关。这表明，当细胞外液量受到威胁时，肾小管AT(1)受体的激活作为一种保护机制，可增加钠重吸收和血压，而AT(2)受体则可减弱这种反应。肾脏中这两种受体途径之间的相互作用可能对长期血压控制产生重大影响。
