THE ACTION OF 2 NATRIURETIC PEPTIDES (ATRIAL-NATRIURETIC-PEPTIDE AND BRAIN NATRIURETIC PEPTIDE) IN THE HUMAN PLACENTAL VASCULATURE

OBJECTIVE: Our purpose was to compare the actions of atrial natriureti c peptide and brain natriuretic peptide in the human placental vascula ture. STUDY DESIGN: Isolated placental cotyledons were dually perfused with fetal perfusion pressure used as an index of vascular response. The effect of angiotensin II (10(-10) to 10(-6) mol/L bolus injection) was established in the absence or presence of atrial natriuretic pept ide (10(-8) mol/L) or brain natriuretic peptide (10(-8) mol/L final co ncentration). The role of nitric oxide as a mediator of natriuretic pe ptide action was investigated by perfusion of n-nitro-L-arginine (10(- 3) mol/L), an inhibitor of nitric oxide synthase. Attenuation of the a ction of atrial natriuretic peptide by placental peptidases was studie d by perfusion with the peptidase inhibitor benzamidine (2 x 10(-2) mo l/L). Statistical significance was determined by analysis of variance and paired t test. RESULTS: Significant attenuation of vasoconstrictor responses to angiotensin II occurred within both atrial natriuretic p eptide and brain natriuretic peptide; however, brain natriuretic pepti de was more effective. n-Nitro-L-arginine did not affect the attenuati on of angiotensin II-induced vasoconstriction by atrial or brain natri uretic peptides. In the presence of benzamidine atrial natriuretic pep tide exerted a significantly greater vasodilator effect. CONCLUSION: B rain natriuretic peptide is a more potent vasodilator of the placental vasculature than is atrial natriuretic peptide. The low efficacy of a trial natriuretic peptide may be related to placental peptidases. Nitr ic oxide does not mediate the action of atrial natriuretic peptide or brain natriuretic peptide.