Vessel dilator, long acting natriuretic peptide, and kaliuretic peptide increase circulating prostaglandin E-2

Prostaglandin E-2 (PGE(2)) increases in the circulation of persons with con gestive heart failure (CHF), but the cause of this increase is unknown. Pro staglandins are not stored, therefore, they cannot be released in response to congestive heart failure itself but rather need to have their synthesis stimulated by a hormone or some other substance. Prostaglandin E-2's biolog ic properties are nearly identical to four peptide hormones originating fro m amino acids 1-30 [long acting natriuretic peptide], 31-67 [vessel dilator ], 79-98 [kaliuretic peptide] and 99-126 [atrial natriuretic peptide, ANP] of the 126 amino acid AMP prohormone. ANP previously has been found to have no effect on circulating PGE(2) concentrations in persons with CHF. The pr esent investigation was designed to determine if one or more of the other t hree atrial natriuretic peptides might increase PGE(2) when infused at thei r respective 100 ng/kg body weight/minute concentrations for 60 minutes in persons with congestive heart failure. Vessel dilator increased PGE(2) 8-fo ld (P<0.001) in the first 20 minutes of its infusion with PGE(2) remaining 2-3 fold increased (P<0.05) for 60 minutes after stopping its infusion. Lon g acting natriuretic peptide did not increase PGE(2) until 40 minutes of it s infusion but it caused the maximal increase (27-fold; P<0.001) of PGE(2) of the three peptide hormones tested. Kaliuretic peptide's stimulated incre ase of PGE(2) also began in a delayed fashion but its effects lasted the lo ngest, with PGE(2) being increased (P<0.05) for two hours after the cessati on of kaliuretic peptide's infusion. This investigation demonstrates that 1 ) three endogenous peptide hormones increase PGE(2) in the circulation and 2) suggests that the known increase in PGE(2) in CHF may be in part seconda ry to these peptides.