β-Human atrial natriuretic polypeptide (β-hANP) is an antiparallel dimer of α-human ANP (a-hANP) that was isolated from human atria. Using synthetic β-hANP and a radioimmunoassay for α-hANP that also detects β-hANP, we have previously demonstrated that β-hANP is converted into α-hANP in human plasma in vitro. In the present study, we compared the effects of intravenous administration of β-hANP (100 μg) to five normal human volunteers with those of an equimolar administration of α-hANP (50 μg) to the same subjects, and we also investigated the possible mechanisms of actions of β-hANP. Although the administration of α-hANP caused a significant decrease in blood pressure with a reactional increase of heart rate, β-hANP elicited minimal change of blood pressure. In contrast, β-hANP exerted more potent and longer lasting diuretic and natriuretic activities than did α-hANP. Net changes in urine volume and sodium excretion induced by β-hANP (579 ± 65 ml, 56.0 ± 9.9 mEq) were significantly greater than those elicited by α-hANP (396 ± 50 ml, 34.7 ± 4.9 mEq; p < 0.05, respectively). The administration ofβ-hANP revealed a longer retention of the ANP-like immunoreactivity level in plasma, compared with that of α-hANP. High performance gel permeation chromatography coupled with the radioimmunoassay revealed that β-hANP (Afr=6000) was also converted into α-hANP (Mr=3000) in human plasma in vivo. The demonstrated conversion of β-hANP into α-hANP could be relevant to the observed effects of β-hANP in humans.
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