Acute pulmonary hypertension (PH) may arise with or without an increase in vascular smooth muscle (VSM) tone. Our objective was to determine how VSM activation affects both the conduit (CF) and wall buffering (BF) functions of the pulmonary artery (PA) during acute PH states. PA instantaneous flow, pressure and diameter of six sheep were recorded during normal pressure (CTL) and different states of acute PH, 1) passively induced by PA mechanical occlusion (PPH); 2) actively induced by intravenous administration of phenylephrine (APH); and 3) a combination of both (APPH). To evaluate the direct effect of VSM activation, isobaric (PPH versus APH) and isometric (CTL versus APPH) analyses were performed. We calculated the local BF from the elastic (E_PD) and viscous (_PD) indexes as _PD/E_PD, and the characteristic impedance (Z_C) from pressure and flow, to evaluate CF as 1/Z_C. We also calculated the absolute and normalized cross-sectional pulsatility (P_CS and NP_CS, respectively), the dynamic compliance (C_DYN), the cross-sectional distensibility (D_CS), and the pressure-strain elastic modulus (E_P). The isobaric analysis showed increase of CF, BF and _PD (P<0.01) and decrease of E_PD (P<0.05) during APH respect to PPH (concomitant with isobaric VSM activation-induced vasoconstriction, P<0.01). The isometric analysis showed increase of E_PD and _PD (P<0.01), non significant difference in BF (even in the presence of a significant mean PA pressure rise, from 14±6 to 25±8 mmHg, P<0.01), and decrease in CF (P<0.01) during APPH respect to CTL. Mechanical occlusions (PPH and APPH) reduced BF (P<0.01), and increased E_PD (P<0.05) with regard to their previous steady states (CTL and APH). Non significant differences were found in E_PD between PPH and APPH. VSM activation (APH and APPH) increased _PD (P<0.01) respect to their previous passive states (CTL and PPH), but no significant differences were found within similar levels of VSM activation. In conclusion, VSM plays a relevant role in main pulmonary artery function during acute pulmonary hypertension, since isobaric vasoconstriction induced by VSM activation improves both BF and CF, mainly due to the increase in _PD concomitant with the arterial compliance. C_DYN and D_CS were the more pertinent clinical indexes of arterial elasticity. Additionally, the _PD-mediated preservation of the BF could be evaluated by the geometric related indexes (P_CS and NP_CS), which appear to be qualitative markers of arterial wall viscosity status.