The mechanism of adenosine A1 receptor–induced intrarenal vasoconstriction is unclear; it depends on sodium intake and may be mediated by changing the intrarenal activity of the nitric oxide (NO) and/or cyclooxygenase (COX) pathway of arachidonic acid metabolism. The effects of 2-chloro-N6-cyclopentyl-adenosine (CCPA), a selective A1 receptor agonist, on renal hemodynamics were examined in anesthetized rats maintained on high sodium (HS) or low sodium (LS) diet. Total renal (i.e., cortical) blood flow (RBF) as well as superficial cortical (CBF), outer medullary (OMBF), and inner medullary (IMBF) flows were determined by laser-Doppler. In HS rats, suprarenal aortic infusions of 8–40 nmol/kg/hr CCPA decreased IMBF (15%) and other perfusion indices (22%–27%); in LS rats, IMBF increased 3% (insignificant) and other indices decreased 13%–24%. In LS rats, pretreatment with N-nitro-L-arginine methyl ester prevented the A1 receptor–mediated decrease in RBF and CBF but not OMBF; the response in IMBF was not altered. Pretreatment with indomethacin prevented the decreases in RBF, CBF, and OMBF and did not change the response of IMBF. Thus, within the cortex the vasoconstriction that follows A1 receptor activation results both from inhibition of NO synthesis and from stimulation of vasoconstrictor products of the COX pathway. In the outer medulla, the latter products seem exclusively responsible for CCPA-induced vasoconstriction. The observation that in LS rats IMBF was not affected by stimulation of adenosine A1 receptors suggests that limiting salt intake may help protect medullary perfusion against vasoconstrictor stimuli which have the potential to disturb long-term control of arterial pressure.

中文翻译：

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简短的交流

腺苷A1受体诱导肾内血管收缩的机制尚不清楚；它取决于钠的摄入量，并且可能通过改变花生四烯酸代谢的一氧化氮（NO）和/或环氧合酶（COX）途径的肾内活性来介导。2-氯-N的影响6β-环戊基腺苷 (CCPA) 是一种选择性 A1 受体激动剂，在维持高钠 (HS) 或低钠 (LS) 饮食的麻醉大鼠中检查了肾血流动力学的影响。通过激光多普勒确定总肾（即皮质）血流量（RBF）以及浅皮质（CBF）、外髓（OMBF）和内髓（IMBF）流量。在 HS 大鼠中，肾上主动脉输注 8–40 nmol/kg/hr CCPA 降低 IMBF (15%) 和其他灌注指数 (22%–27%)；LS大鼠的IMBF增加3%（不显着），其他指标下降13%~24%。在 LS 大鼠中，用 N-硝基-L-精氨酸甲酯进行预处理可防止 A1 受体介导的 RBF 和 CBF 减少，但不能防止 OMBF 减少；IMBF 中的响应没有改变。吲哚美辛预处理可防止 RBF、CBF 和 OMBF 的降低，并且不会改变 IMBF 的反应。因此，在皮层内，A1受体激活后的血管收缩是由于抑制NO合成和刺激COX途径的血管收缩产物所致。在外髓质中，后者的产物似乎专门负责 CCPA 诱导的血管收缩。在 LS 大鼠中，观察到 IMBF 不受腺苷 A1 受体刺激的影响，这表明限制盐摄入量可能有助于保护髓质灌注免受血管收缩刺激的影响，血管收缩刺激可能会干扰动脉压的长期控制。