Mills I H, Obika L F, Newport P A
Contrib Nephrol. 1978;12:132-44. doi: 10.1159/000401661.
Large doses of angiotensin when infused intravenously or into the renal artery cause natriuresis. The initial effect is release of prostaglandin (probably PGE) and this leads to release of kallikrein. This latter step can be inhibited by noradrenaline. Activation of the kallikrein/kinin system is followed by release of a large molecular weight natriuretic hormone which is absent in glomerulonephritis. A small molecular weight hormone follows the large one and probably effects natriuresis by inhibition of renal Na/K ATPase. This inhibition is reversed by noradrenalint or renal nerve stimulation. Natriuresis is the result of a chain reaction and not a single specific natriuretic hormone.
静脉内或肾动脉内注入大剂量血管紧张素会引起利钠作用。最初的效应是前列腺素（可能是PGE）的释放，这会导致激肽释放酶的释放。后一步骤可被去甲肾上腺素抑制。激肽释放酶/激肽系统激活后会释放一种大分子利钠激素，而肾小球肾炎患者体内不存在这种激素。大分子激素之后会出现一种小分子激素，它可能通过抑制肾钠/钾ATP酶来发挥利钠作用。去甲肾上腺素或肾神经刺激可逆转这种抑制作用。利钠作用是连锁反应的结果，而非单一特定利钠激素所致。
