RELEASE OF KALIURETIC PEPTIDE DURING IMMERSION-INDUCED CENTRAL HYPERVOLEMIA IN HEALTHY HUMANS

Kaliuretic peptide, a new peptide hormone consisting of amino acids 79 -98 of the 126 amino acid atrial natriuretic factor (ANF) prohormone, is synthesized in the heart and is a potent stimulator of potassium ex cretion. The mechanism(s) controlling the release of kaliuretic peptid e heretofore has not been defined. Because water immersion to the neck provides an acute central volume expansion identical to that produced by 2 liters of saline but without the plasma compositional change, im mersion to the neck (NI) was utilized to assess kaliuretic peptide res ponses to acute central blood volume expansion in seven seated sodium- replete normal subjects. Since atrial natriuretic factor (ANF; amino a cids 99-126 of the prohormone) originates from the amino acids adjacen t to kaliuretic peptide in the ANF prohormone but is proteolytically c leaved from the rest of the prohormone before release, measurement of ANF was incorporated into this study to determine if there are differe nces with respect to release of these two portions of the ANF prohormo ne. Both kaliuretic peptide and ANF increased promptly with NI, with A NF peaking at 1 hr of immersion, whereas kaliuretic peptide peaked at the 3rd hr of immersion. With cessation of Immersion, ANF decreased to preimmersion levels within 0.5 hr while kaliuretic peptide was still significantly (P < 0.05) elevated at 1 hr postimmersion. These finding s indicate that kaliuretic peptide and ANF are released simultaneously but that kaliuretic peptide peak circulating concentration and its re turn to preimmersion values are prolonged compared with ANF, These las t findings suggest a slower clearance from the circulation for kaliure tic peptide. The diuretic peak response to NI corresponded in a tempor al manner to the peak circulating concentration of kalluretic peptide, suggesting a possible physiologic role for kaliuretic peptide in modu lating volume homeostasis in humans.