The "push-pull" effect denotes the reduced tolerance to +G_z (hypergravity) when +G_z stress is preceded by exposure to hypogravity, i.e. fractional, zero, or negative G_z. The purpose of this study was to test the hypothesis that an exaggerated, myogenically mediated rise in leg vascular conductance contributes to the push-pull effect, using heart-level arterial blood pressure as a measure of G-tolerance. The approach was to impose control (30 s of 30 ° head-up tilt) and push-pull (30 s of 30 ° head-up tilt immediately preceded by 10 s of -15 ° head-down tilt) gravitational stress after administration of hexamethonium (5 mg/kg) to inhibit autonomic ganglionic neurotransmission in 7 dogs. Cardiac output or thigh level arterial pressure (myogenic stimulus) was maintained constant by computer controlled ventricular pacing. The animals were sedated with acepromazine and lightly restrained in lateral recumbency on a tilt table. Following the onset of head-up tilt, the magnitude of the fall in heart-level arterial pressure from baseline was -11.6 ±2.9 and -17.1 ±2.2 mmHg for the control and push-pull trials, respectively (p <0.05) when cardiac output was maintained constant. Over forty percent of the exaggerated fall in heart-level arterial pressure was attributable to an exaggerated rise in hindlimb vascular conductance (p <0.05). Maintaining thigh-level arterial pressure constant abolished the exaggerated rise in hind-limb blood flow. Thus, a push-pull effect largely attributable to a myogenically-induced rise in leg vascular conductance occurs when autonomic function is inhibited.