Dobrowolski L, Walkowska A, Kompanowska-Jezierska E, Kuczeriszka M, Sadowski J
Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Acta Physiol (Oxf). 2007 Jan;189(1):77-85. doi: 10.1111/j.1748-1716.2006.01627.x.
Adenosine-5'-triphosphate (ATP) affects intrarenal vascular tone and tubular transport via P2 receptors; however, the actual role of the system in regulation of renal perfusion and excretion remains unclear and is the subject of this whole-kidney study.
Effects of suprarenal aortic ATP infusion, 0.6-1.2 mg kg(-1) h(-1), were examined in anaesthetised rats maintained on low- (LS) or high-sodium (HS) diet. Renal artery blood flow (RBF, transonic flow probe) and the perfusion (laser-Doppler flux) of the superficial cortex (CBF) and outer and inner medulla (OM-BF, IM-BF) were measured, together with sodium and water excretion and urine osmolality.
Adenosine-5'-triphosphate did not change arterial pressure, RBF or CBF while the effects on medullary perfusion depended on sodium intake. In LS rats ATP increased IM-BF 19 +/- 6%, the effect was prevented by inhibition of nitric oxide (NO) with N-nitro-l-arginine methyl ester. In HS rats ATP decreased OM-BF 16 +/- 3% and IM-BF (7 +/- 4%, not significant); previous inhibition of cytochrome P450 with 1-aminobenzotriazol blunted the OM-BF decrease and reversed the previous decrease of IM-BF to a 13 +/- 8% increase. Inhibition of P2 receptors with pyridoxal derivative (PPADS) abolished medullary vascular responses to ATP. In HS rats pre-treated with PPADS, ATP increased tubular reabsorption, probably via adenosine formation and stimulation of P1 receptors.
The data indicate a potential role of ATP in the selective control of renal medullary perfusion, different in sodium depleted and sodium replete rats. The action of ATP appears to be mediated by the NO system and the cytochrome P450 dependent vasoactive metabolites.
三磷酸腺苷（ATP）通过P2受体影响肾内血管张力和肾小管转运；然而，该系统在调节肾灌注和排泄中的实际作用仍不清楚，这也是本全肾研究的主题。
在以低钠（LS）或高钠（HS）饮食维持的麻醉大鼠中，检测了经肾上主动脉输注ATP（0.6 - 1.2 mg·kg⁻¹·h⁻¹）的效果。测量了肾动脉血流量（RBF，采用跨音速血流探头）以及浅表皮质（CBF）、外髓和内髓（OM - BF、IM - BF）的灌注（激光多普勒血流），同时测量了钠和水的排泄以及尿渗透压。
ATP不改变动脉血压、RBF或CBF，而对髓质灌注的影响取决于钠摄入量。在LS大鼠中，ATP使IM - BF增加19±6%，用N - 硝基 - l - 精氨酸甲酯抑制一氧化氮（NO）可阻止该效应。在HS大鼠中，ATP使OM - BF降低16±3%，使IM - BF降低（7±4%，无统计学意义）；用1 -氨基苯并三唑预先抑制细胞色素P450可减弱OM - BF的降低，并使之前降低的IM - BF逆转，增加13±8%。用吡哆醛衍生物（PPADS）抑制P2受体可消除髓质血管对ATP的反应。在经PPADS预处理的HS大鼠中，ATP可能通过腺苷形成和P1受体刺激增加肾小管重吸收。
数据表明ATP在选择性控制肾髓质灌注中具有潜在作用，在钠缺乏和钠充足的大鼠中有所不同。ATP的作用似乎由NO系统和细胞色素P450依赖性血管活性代谢产物介导。
