Objective: To determine whether atrial natriuretic peptide (ANP) attenuates the vasocon-strictor effects of angiotensin II (AII), a thromboxane mimetic (U46619), and endothelin-1 in the human fetal-placental vasculature and to determine whether nitric oxide (NO) has a role in the vasodilator activity of ANP. Methods: Isolated placental cotyledons were dually perfused, with fetal perfusion pressure used as an index of vascular response. The effects of AII (10-10-10-6 mol/L bolus injection), endothelin-1 (10-7 mol/L bolus), and U46619 (10-9-10-6 mol/L bolus or 10-8 mol/L infusion) were established in the absence or presence of ANP (10-8 mol/L). The role of NO as a mediator of ANP action was investigated by perfusion with n-nitro-L-arginine (NNLA, 10-3 mol/L), an inhibitor of NO synthase. Statistical significance was determined by analysis of variance. Results: Atrial nutriuretic peptide caused significant attenuation of vasoconstrictor responses to AII, but weak attenuation of endothelin-1 and no attenuation of U46619. Use of NNLA did not affect the attenuation of AII-induced vasoconstriction by ANP. Conclusion: Atrial natriuretic peptide is a vasodilator of the fetal-placental vasculature constricted with AII and endothelin-1, but not with U46619. Nitric oxide does not mediate the action of ANP.
|Number of pages||5|
|Journal||Journal of the Society for Gynecologic Investigation|
|State||Published - 1 Jan 1995|
- Atrial natriuretic peptide
- nitric oxide
- thromboxane mimetic