vasoactive agents on pulmonary and cerebral artery smooth muscle cells.

The following letters are in response to Point:Counterpoint: “Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction ” that appears in this issue. To the Editor: Obviously, I’m prejudiced, but evidence for the PASMC as the main effector for HPV seems compelling, not only because of our work (1) kindly cited by Rochefort and Michelakis (5), but also because of work not mentioned. Murray et al. (2) showed that fetal calf PASMCs grown on a flexible membrane could generate tension when exposed to hypoxia. Olson et al.’s (3), provocative study in the dorsal aorta of the most primitive vertebrate, the cyclostome, suggests that hypoxic vasoconstriction is phylogenetically ancient an