Acute effects of physiological increments of alpha-atrial natriuretic peptide in man

Seven dehydrated volunteers received three hour infusions of 0.8 pmol kg-1 min-1 of human alpha-atrial natriuretic peptide (h-alpha ANP) or vehicle alone (Ve) in a single-blind, randomized cross-over design. H-alpha ANP infusion increased plasma h-alpha ANP from 4.2 +/- 0.4 to 20.3 +/- 6.4 pm. H-alpha ANP suppressed plasma renin activity from 3.30 +/- 0.48 to 1.37 +/- 0.35 ng ml-1 hr-1 (P less than 0.001 vs. Ve). Plasma aldosterone was unaltered by h-alpha ANP. Fractional excretion of filtered sodium (FENa) changed from 0.92 +/- 0.09 to 1.13 +/- 0.16% with h-alpha ANP, and from 1.02 +/- 0.09 to 0.69 +/- 0.11% with Ve (P less than 0.01 h-alpha ANP vs. Ve). FEK was unchanged. FEpo4 increased from 7.2 +/- 1.2 to 9.2 +/- 1.2% and FELi from 22.1 +/- 1.4 to 24.9 +/- 3.0% with h-alpha ANP (both P less than 0.05 vs. Ve). H-alpha ANP decreased mean urinary osmolality by approximately 150 mOsmol kg-1 compared to Ve (P less than 0.01). GFR, RPF and filtration fraction were unchanged by h-alpha ANP, H-alpha ANP was associated with a significant tachycardia (P less than 0.01 vs. Ve) but with no significant change in arterial pressure. These results suggest that small increments of plasma h-alpha ANP, mimicking physiological changes, are natriuretic at least partly by reducing proximal tubular reabsorption of sodium, and also impair urinary concentration.