Right ventricular adaptation to pulmonary hypertension (PH) is an important prognostic factor. Pulmonary artery (PA) smooth muscle activation attenuates arterial dysfunction during acute PH. We investigated the role of the pulmonary artery vascular smooth muscle activation on the right ventricular-vascular coupling during acute PH. PA flow, pressure, and diameter, right ventricular and aortic pressures were recorded in six anesthetized sheep. Acute PH was induced by phenylephrine (APH) and PA mechanical constriction (PPH). We calculated the PA buffering function, the incremental elastic modulus and pulmonary vascular compliance. Pulmonary vascular impedance and right ventricular hydraulic power were calculated through Fourier approach. We also quantified the magnitude and timing of the reflected wave. Right ventricular-vascular coupling was assessed by the energy transmission ratio. Pulmonary buffering function and vascular compliance increased (P<0.05) and arterial wall stiffness decreased (P<0.05) during APH with respect to PPH. Although total input resistance increased and reflected wave came back earlier during PH states (P<0.05), only PPH produced a rightward shift of the pulmonary impedance and a more prominent reflected wave. Accordingly, APH determined a minor increase of total hydraulic power with a smaller pulsatile to total power ratio and energy transmission ratio (P<0.05). In conclusion, isobaric PA vasoconstriction prevents the pulsatile hydraulic load to increase by preserving the PA buffering function and the reflected wave magnitude. Thus, vascular smooth muscle activation of the main PA improves the energy transfer from the right ventricle to the hypertensive pulmonary circulation, and this may play relevant role in the right ventricular adaptation to acute PH.