Dehkordi O, Yun J C, Ho S S, Gill J R, Keiser H
Department of Physiology and Biophysics, Howard University, College of Medicine, Washington, D.C.
Ren Physiol Biochem. 1989 Mar-Apr;12(2):104-17. doi: 10.1159/000173184.
Renal arterial infusion of acetylcholine (ACh) in the dog normally produces a sustained rise in sodium excretion (UNaV) and in renal plasma flow (RPF). When prostaglandin (PG) synthesis is inhibited, ACh induces only a transient increase in UNaV and RPF followed by a progressive decline in UNaV and RPF, and a rise in renin secretory rate (RSR). Renal arterial infusion of PGE2 but not a vasodilator such as bradykinin restored the response to ACh to normal in indomethacin (Indo)-treated dogs. During renal arterial infusion of dibutyryl cyclic AMP (6 mg/min), ACh also produced a sustained increase in UNaV and RPF despite an inhibition of PG synthesis by Indo. Renal arterial infusion of verapamil (60 micrograms/min) or diltiazem (60 micrograms/min) also prevented the subsequent fall in RPF when ACh was infused; RSR, however, did not show a rise. The results suggest that synthesis of PGE2 with stimulation of cAMP is required for sustained ACh action. When PGE synthesis is inhibited, ACh may produce renal vasoconstriction by increasing intracellular Ca2+ concentration. The partial effect of calcium channel blockers suggests that release of calcium from intracellular stores as well as calcium entry may mediate the response.
在犬体内，肾动脉注入乙酰胆碱（ACh）通常会使钠排泄量（UNaV）和肾血浆流量（RPF）持续升高。当前列腺素（PG）合成受到抑制时，ACh仅引起UNaV和RPF短暂增加，随后UNaV和RPF逐渐下降，肾素分泌率（RSR）升高。肾动脉注入PGE2可使吲哚美辛（Indo）处理的犬对ACh的反应恢复正常，而注入血管舒张剂如缓激肽则无此作用。在肾动脉注入二丁酰环磷酸腺苷（6毫克/分钟）期间，尽管Indo抑制了PG合成，但ACh仍使UNaV和RPF持续增加。肾动脉注入维拉帕米（60微克/分钟）或地尔硫䓬（60微克/分钟）也可防止注入ACh后RPF随后的下降；然而，RSR并未升高。结果表明，持续的ACh作用需要合成PGE2并刺激cAMP。当PG合成受到抑制时，ACh可能通过增加细胞内Ca2+浓度而导致肾血管收缩。钙通道阻滞剂的部分作用表明，细胞内钙库释放钙以及钙内流可能介导了该反应。
