Kuz'min O B, Kriukova R A
Fiziol Zh SSSR Im I M Sechenova. 1984 Mar;70(3):355-9.
Blockade of kidneys' beta-1 adrenoreceptors with talinolol entailed in anesthetized rats a sodium- uretic response accompanied by inhibition of sodium reabsorption and an increase of the blood flow in cortical and external layers with no PO2 changes, at that. Haloperidol prevented the increase of blood flow in the external layer but did not affect the cortical hemodynamic shift or the depressing influence of talinolol on the channel transport of sodium. The inhibiting agent for the kallikrein-kinin system contrical and the inhibiting agent for prostaglandin synthesis indomethacin did not alter the kidney response to the drug under study. The hemodynamic shift as well as the inhibition of sodium reabsorption seem to be unrelated either to excitation of receptors sensitive to dopamine, or to activation of the kallikrein-kinin system or stimulation of prostaglandin synthesis.
在麻醉大鼠中，用他林洛尔阻断肾脏的β-1肾上腺素能受体会引发钠利尿反应，同时抑制钠重吸收，并增加皮质和外层的血流量，此时PO2无变化。氟哌啶醇可阻止外层血流量增加，但不影响皮质血流动力学变化或他林洛尔对钠通道转运的抑制作用。激肽释放酶-激肽系统抑制剂康催纽和前列腺素合成抑制剂吲哚美辛均未改变肾脏对所研究药物的反应。血流动力学变化以及钠重吸收的抑制似乎与对多巴胺敏感的受体兴奋、激肽释放酶-激肽系统激活或前列腺素合成刺激均无关。
