To determine if alterations in arterial pressure influenced fetal heart rate variability (HRV), experiments were carried out in chronically catheterized fetal sheep aged 128–138 d. Arterial pressure was raised or lowered by intravenous infusion of phenylephrine or sodium nitroprusside, and the effects on heart rate (HR) and HRV were measured (HRV, as the coefficient of variation (CV) in mean pulse interval or by power spectral analysis). Experiments were carried out before and during &bgr;-adrenoceptor blockade with propranolol or before and during cardiac vagal blockade with atropine. There were positive relationships between mean arterial pressure and HRV (slope = 0.074 ± 0.001,r= 0.81 ± 0.06,p< 0.001, measured as the CV of pulse interval) and between mean arterial pressure and power spectral density (slope = 4 ± 0.5,r= 0.89 ± 0.02,p< 0.001) in the frequency range 0.04–0.08 Hz. &bgr;-adrenoceptor blockade had no effect on these relationships, but they were abolished by cardiac vagal blockade. The sigmoid relationship between fetal HR and mean arterial pressure,i.e.the cardiac baroreflex, was affected, however, by blockade of cardiac sympathetics and abolished by blockade of cardiac vagal activity. Thus, fetal HRV was affected by alterations in arterial pressure, and these effects depended on the integrity of the cardiac vagus, not on alterations in cardiac sympathetic activity. Therefore, although baroreflex control of fetal HR depends on the integrity of both sympathetic and parasympathetic efferent pathways, baroreceptor-induced changes in HRV depend only on the cardiac vagus.