ProANFs 1-30, 31-67, and 79-98, as well as ANF have significant blood pressure-lowering and diuretic properties. ProANFs 1-30 and 31-67 also have natriuretic properties in humans that are significantly (P < .001) prolonged compared with ANF. ProANF 79-98, although not possessing any natriuretic property, is the strongest stimulator of potassium excretion of the four atrial natriuretic peptides.
The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 [i.e. pro-ANF-(1-30)], 31-67 [i.e. pro-ANF(31-67)], 79-98 [i.e. pro-ANF-(79-98)], and 99-126 [i.e. atrial natriuretic factor (ANF)] of 126-amino acid ANF prohormone have a negative feedback on their own and each others' release. Thirty healthy human subjects were studied with infusion of 100 ng/kg BW.min for 60 min of each of the respective peptides. Pro-ANF-(1-30) decreased the circulating concentrations of pro-ANF-(31-67) and ANF 51% and 89%, respectively. Pro-ANF-(31-67) decreased the circulating concentration of ANF by 55% and the peptides immunologically recognized by the pro-ANF-(1-30) RIA by 58% [this assay recognizes pro-ANF-(1-30) (50%) and pro-ANF-(1-98) (50%)]. Pro-ANF-(79-98) decreased the circulating concentration of ANF by 40%, pro-ANF-(31-67) by 31%, and the peptides recognized by the pro-ANF-(1-30) RIA by 46%. ANF decreased the circulating concentration of pro-ANF-(31-67) by 40% and the peptides recognized by pro-ANF-(1-30) RIA by 38%. Infusion of pro-ANF-(1-30), -(31-67), -(79-98), and -(99-126) also decreased the excretion of the other atrial natriuretic peptides measured in the urine by 32-84%. Infusion of vehicle only did not result in any decrease in these atrial natriuretic peptides in either plasma or urine. These data taken together indicate that each of the respective atrial natriuretic peptides inhibits the release, rather than breakdown, of each other, as increased breakdown would have resulted in their urinary concentrations being increased. This study further indicates that because pro-ANF-(1-98) was decreased in the circulation secondary to pro-ANF-(31-67) and pro-ANF-(79-98) infusions, they inhibit their own release, as they are both derived from pro-ANF-(1-98).
The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 (long acting natriuretic peptide), 31-67 (vessel dilator) and 79-98 (kaliuretic peptide) as well as 99-126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P < 0.001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P < 0.01) decreased plasma aldosterone levels which remained significantly (P < 0.001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P < 0.01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P < 0.001) than following ANF infusion.
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