Why the study?
Does atrial natriuretic peptide infusion increase urine flow and sodium excretion in animal models of chronic sodium-retaining disorders (heart failure and nephrotic syndrome)?
Does atrial natriuretic peptide infusion increase urine flow and sodium excretion in animal models of chronic sodium-retaining disorders (heart failure and nephrotic syndrome)?
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The diuretic and natriuretic responses to atrial natriuretic peptide are blunted in animal models of chronic sodium-retaining disorders like congestive heart failure and nephrotic syndrome.
Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.
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Koepke et al. (1987) studied this question.
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