Atrial natriuretic peptide (ANP) exerts hemodynamic effects by direct
venodilation in the chick embryo. We hypothesized that ANP-induced ven
odilation affects ventricular diastolic filling resulting in reduced v
entricular preload. Chick ANP (0.1 mu g in 10 mu L of normal saline) w
as suffused onto the vitelline vascular bed in stage 21 (3 1/2 d) chic
k embryos. Equivalent aliquots of normal saline were suffused as sham
controls, and normal embryos received no suffusion. We measured simult
aneously dorsal aortic blood velocity and atrioventricular blood veloc
ity with a 20-MHz pulsed-Doppler velocity meter. Analog wave forms wer
e digitally sampled at 500 Hz, and the dorsal aortic cross-sectional a
rea was used to calculate dorsal aortic blood flow. Passive ventricula
r filling volume equaled dorsal aortic stroke volume multiplied by the
fraction of passive area; active filling volume equaled dorsal aortic
stroke volume multiplied by the fraction of active area. Data were su
mmarized as mean +/- SEM (n greater than or equal to 7 per group) and
analyzed by analysis of variance. Cycle lengths were similar in ANP-su
ffused, sham control, and normal embryos. Dorsal aortic blood flow dec
reased from 0.49 +/- 0.04 mm(3)/s at baseline to 0.27 +/- 0.05 mm(3)/s
at 4 min post-ANP suffusion (p < 0.05) and was unchanged in sham cont
rol and normal embryos (p > 0.05). Passive ventricular filling was red
uced by ANP suffusion, whereas active filling was unaffected, resultin
g in a decreased passive/active filling ratio from 0.64 +/- 0.07 at ba
seline to 0.32 +/- 0.08 at 4 min in ANP-suffused embryos (p < 0.05). P
assive/active ratio was unchanged in sham control and normal embryos.
Thus, ANP-mediated vasodilation reduces cardiac output via decreased p
assive ventricular filling in the embryonic heart.