Bolus injection of anti-ANP in rats with surgically induced MI significantly depressed absolute and fractional urinary excretion of sodium without affecting mean arterial pressure or GFR.
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.
Awazu et al. (Fri,) conducted a other in Congestive heart failure (rat model). Purified rabbit anti-rat 25-amino acid atrial natriuretic peptide (ANP) immunoglobulin G (IgG) vs. Nonimmune IgG / normal or acutely water-deprived rats was evaluated on Renal sodium excretion and glomerular filtration rate. Bolus injection of anti-ANP in rats with surgically induced MI significantly depressed absolute and fractional urinary excretion of sodium without affecting mean arterial pressure or GFR.
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