Aim: Hypoxic pulmonary vasoconstriction (HPV) can be modulated through either elevation of [Ca2+]i by Ca2+-dependent mechanism or inhibition of MLCP by Ca2+-independent mechanism.TRPC channels constitute the major Ca2+ pathways for the elevated [Ca2+](i,) which is considered a classic trigger for HPV.However, it is generally believed that RhoA/ROCK pathway can modulate Ca2+ sensitivity to influence HPV by regulating MLC phosphorylation and dephosphorylation.