The present investigation was designed to determine whether atrial nat
riuretic peptides consisting of amino acids 1-30 [ie. pro-ANF-(1-30)],
31-67 [i.e. pro-ANF(31-67)], 79-98 [ie. pro-ANF-(79-98)], and 99-126
[i.e. atrial natriuretic factor (ANF)] of 126-amino acid ANF prohormon
e have a negative feedback on their own and each others' release. Thir
ty healthy human subjects were studied with infusion of 100 ng/kg BW m
in for 60 min of each of the respective peptides. Pro-ANF-(1-30) decre
ased the circulating concentrations of pro-ANF-(31-67) and ANF 51% and
89%, respectively. Pro-ANF-(31-67) decreased the circulating concentr
ation 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 circulat
ing concentration of pro-ANF-(31-67) by 40% and the peptides recognize
d by pro-ANF-(130) 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 veh
icle only did not result in any decrease in these atrial natriuretic p
eptides in either plasma or urine. These data taken together indicate
that each of the respective atrial natriuretic peptides inhibits the r
elease, rather than breakdown, of each other, as increased breakdown w
ould have resulted in their urinary concentrations being increased. Th
is study further indicates that because pro-ANF-(1-98) was decreased i
n the circulation secondary to pro-ANF-(31-67) and pro-ANF-(79-98) inf
usions, they inhibit their own release, as they are both derived from
pro-ANF-(1-98).