Hemodynamic, Renal, andHormonal Responses toBrainNatriuretic Peptide Infusion inPatients With Congestive HeartFailure

Background. Thisstudy was designed toexamine thehemodynamic, renal, andhormonal effects ofbrainnatriuretic peptide (BNP)infusion inpatients withcongestive heartfailure (CHF)andincontrol subjects. Methods andResults. We infused synthetic humanBNP ata rateof0.1ug/kg/min. BNP infusion decreased pulmonary capillary wedgepressure(control, from5±1to2±1mm Hg, pCHF,from21±3to14±4mm Hg,p<0.05) andsystemic vascular resistance (control, from1,264+75 to934±52dyne*sec*cm-5;CHF,from2,485±379 to1,771±195 dyne*sec . cm-5;p<0.01, respectively) andincreased stroke volumeindex(control, from49.9±2.7 to 51.5±2.3 ml/m2, p=NS;CHF,from25.6±3.8 to32.0±3.9 ml/m2,p<0.01). BNP infusion significantly increased urinevolume(control, from2.3±0.7 to7.5±+1.9 ml/min; CHF,from 0.8±0.2 to5.3±1.0ml/min;p<0.01, respectively), excretion ofsodium(control, from79.2+21.6 to332.8±70.9 1LEq/min; CHF,from77.4±20.8 to753.5± 108.0,uEq/min; p<0.01, respectively), andexcretion ofchloride (control, from72.5±18.4to256.0±43.3 ,Eq/min; CHF,from 74.0+19.6to708.8± 103.3,uEq/min; p<0.01, respectively). Urinary excretion ofsodiumandof chloride inresponsetoBNP infusion was higher inpatients withCHF thanincontrol subjects (pnatriuretic peptide (control, from65±11to84±14pg/ml;CHF,from262±65to301±62pg/ml; p<0.05, respectively) anddecreased plasmaaldosterone concentrations inbothgroups(control, from 43.3±+12.1 to27.3±7.1 pg/ml; CHF,from91.1±34.3 to66.3+±27.2 pg/ml;p<0.05, respectively). Conclusions. We conclude thatBNP infusion improves left ventricular function inpatients withCHF byvasodilation andprominent natriuretic action. (Circulation 1991;84:1581-1588) A rial natriuretic peptide (ANP) isacirculating hormone withawiderangeofpotent biological effects, including natriuresis, diuresis, vasodilatation, andinhibition oftherenin-angiotensin-aldosterone