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In order to examine the effect of alpha-ANP on fetal placental vascular tone, single placental lobules were bilaterally perfused and fetal inflow pressure recorded. The placental vasculature was sub-maximally pre-constricted by infusion of the nitric oxide synthase inhibitor N omega-nitro-L-arginine (NOLA) or the thromboxane A2-mimetic U46619. In the presence of continuous infusion of 59.3 mumol/l NOLA, producing a mean pressure increase of 43.7 +/- 1.7 mmHg (n = 8, mean +/- SEM), alpha-ANP (10.7 to 325 nmol/l) produced significant pressure decreases (P &lt; 0.05). In separate experiments (U46619 was either infused at concentrations (4.8 to 21.4 nmol/l) to produce a mean pressure increase (50.1 +/- 2.6 mmHg, n = 10) similar to that produced by NOLA infusion or was infused at a concentration (28.5 nmol/l) that produced a significantly higher pressure increase (104 +/- 15 mmHg), infusion of 1 mumol/l alpha-ANP significantly reduced perfusion pressure. However, 100 nmol/l alpha-ANP or less had no significant effect (n = 4-7). These results indicate that alpha-ANP attenuates NOLA-induced and U46619-induced vasoconstriction in the human placenta, but at concentrations higher than those in fetal or maternal plasma.

α-Atrial natriuretic peptide-induced attenuation of vasoconstriction in the fetal circulation of the human isolated perfused placenta