Ishikawa S, Saito T, Okada K, Kuzuya T, Kangawa K, Matsuo H
Biochem Biophys Res Commun. 1985 Aug 15;130(3):1147-53. doi: 10.1016/0006-291x(85)91735-8.
The present study was undertaken to determine whether human atrial natriuretic factor (hANF) produces guanosine-3', 5'-monophosphate (cGMP) and alters arginine vasopressin (AVP)- and forskolin (F)- induced adenosine-3', 5'-monophosphate (cAMP) production in the cultured rat renal papillary collecting tubule cells. hANF increased cellular cGMP levels in a dose dependent manner. AVP and F, however, did not affect cGMP production. hANF significantly inhibited AVP- and F-stimulated cAMP levels, but hANF by itself did not affect cellular cAMP production. Since F activates adenylate cyclase at a step of catalytic unit and the cellular action of AVP to activate adenylate cyclase is mediated through receptor-catalytic units, the present results indicate that hANF may directly inhibit the AVP- and F-stimulated adenylate cyclase in renal papillary collecting tubules.
本研究旨在确定人心房利钠因子(hANF)是否产生鸟苷-3',5'-单磷酸(cGMP),并改变精氨酸加压素(AVP)和福斯可林(F)诱导的培养大鼠肾乳头集合管细胞中环磷酸腺苷(cAMP)的产生。hANF以剂量依赖的方式增加细胞内cGMP水平。然而,AVP和F并不影响cGMP的产生。hANF显著抑制AVP和F刺激的cAMP水平,但hANF本身并不影响细胞内cAMP的产生。由于F在催化单位水平激活腺苷酸环化酶,且AVP激活腺苷酸环化酶的细胞作用是通过受体-催化单位介导的,因此本研究结果表明,hANF可能直接抑制肾乳头集合管中AVP和F刺激的腺苷酸环化酶。