Rakugi H, Ogihara T, Nakamaru M, Saito H, Shima J, Sakaguchi K, Kumahara Y
Department of Geriatric Medicine, Osaka University Medical School, Japan.
J Cardiovasc Pharmacol. 1989;13 Suppl 6:S55-8.
Atrial natriuretic peptide (ANP) has been shown to inhibit angiotensin II (Ang II)-induced steroidogenesis and vasoconstriction. To investigate the role of Ang II in the renal response to ANP, a synthetic ANP (0.1 micron/kg/min, 60 min) was infused for 1 h in eight subjects with or without pretreatment with an inhibitor of the converting enzyme, enalapril (20 mg, p.o.), or Ang II (10 ng/kg/min). ANP infusion alone caused increases in urinary volume, urinary sodium excretion, and glomerular filtration rate (GFR). However, enalapril treatment abolished these diuretic and natriuretic effects of ANP. In this group, GFR was decreased and no tubular effects, which was estimated by urinary excretion of sodium and phosphate, were observed. The anti-natriuretic effects of exogenous Ang II were reversed by concomitant ANP infusion, which inhibited both proximal and postproximal sodium reabsorption induced by Ang II without changing the GFR. These results indicate that endogenous Ang II plays an obligatory role in the natriuretic response to ANP and also suggested that ANP inhibits Ang II-stimulated tubular reabsorption of sodium.
心房利钠肽（ANP）已被证明可抑制血管紧张素II（Ang II）诱导的类固醇生成和血管收缩。为了研究Ang II在肾脏对ANP反应中的作用，对8名受试者输注合成ANP（0.1微克/千克/分钟，持续60分钟），共1小时，这些受试者分别接受或未接受转化酶抑制剂依那普利（20毫克，口服）或Ang II（10纳克/千克/分钟）的预处理。单独输注ANP会导致尿量、尿钠排泄和肾小球滤过率（GFR）增加。然而，依那普利治疗消除了ANP的这些利尿和利钠作用。在该组中，GFR降低，且未观察到通过尿钠和磷酸盐排泄评估的肾小管效应。外源性Ang II的抗利钠作用被同时输注的ANP逆转，ANP抑制了Ang II诱导的近端和近端后钠重吸收，而不改变GFR。这些结果表明内源性Ang II在对ANP的利钠反应中起必要作用，也提示ANP抑制Ang II刺激的肾小管钠重吸收。
