Awazu M, Imada T, Kon V, Inagami T, Ichikawa I
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
Am J Physiol. 1989 Sep;257(3 Pt 2):R641-6. doi: 10.1152/ajpregu.1989.257.3.R641.
Effects of purified rabbit anti-rat 25-amino acid atrial natriuretic peptide (ANP) immunoglobulin G (IgG) on renal sodium excretion and glomerular filtration rate were studied in a rat model of congestive heart failure (CHF) having high circulating ANP levels. Bolus injection of anti-ANP into anesthetized rats with surgically induced myocardial infarction (MI) significantly and markedly depressed both absolute and fractional urinary excretion of sodium without affecting mean arterial pressure or glomerular filtration rate. By contrast, anti-ANP failed to affect these renal functions in normal or acutely water-deprived rats. Nonimmune IgG did not affect renal function in MI rats. These results indicate that high circulating ANP plays an important role in sodium homeostasis of congestive heart failure: by promoting sodium excretion, ANP opposes the tendency of sodium retention characteristic of CHF.
在循环心房利钠肽(ANP)水平较高的充血性心力衰竭(CHF)大鼠模型中,研究了纯化的兔抗大鼠25氨基酸心房利钠肽免疫球蛋白G(IgG)对肾钠排泄和肾小球滤过率的影响。将抗ANP大剂量注射到通过手术诱导心肌梗死(MI)的麻醉大鼠体内,显著且明显降低了钠的绝对尿排泄量和分数尿排泄量,而不影响平均动脉压或肾小球滤过率。相比之下,抗ANP对正常或急性缺水大鼠的这些肾功能没有影响。非免疫IgG对MI大鼠的肾功能没有影响。这些结果表明,循环中高水平的ANP在充血性心力衰竭的钠稳态中起重要作用:通过促进钠排泄,ANP对抗CHF特有的钠潴留倾向。