[Vasomotor control of the pulmonary circulation]

It was demonstrated that pulmonary vessels, in contrast to systemic vessels, 1) have a low basal vascular tone, 2) constrict in response to hypoxia and 3) do not display significantly prominent vasomotion during autonomic nerve stimulation. However, details about these characteristics have not been clarified sufficiently by conventional methods; namely, measuring pressure-flow relationships and vascular tension of isolated larger conduit pulmonary vessels. Recent technological advances in studying pulmonary circulation now permit us to reveal that vasomotor responses to respiratory gases and neurohumoral factors differ not only quantitatively but also qualitatively between the central conduit and peripheral resistance vessels (approximately 100- to 500-micron diam.). They also reveal that an increase in pulmonary sympathetic nerve activity can cause pulmonary vasodilation as well as vasoconstriction. The former has been partly explained by the most recent findings regarding the distribution differences of NO synthases and K+ channels between the resistance and conduit vessels. Concerning the latter, initial vascular tone appears to play an important role. The increased pulmonary sympathetic nerve activity has a beta-receptor-mediated pulmonary vasodilator effect under low pulmonary vascular tone conditions but an alpha-receptor-mediated constrictor effect under enhanced vascular tone conditions. This may serve to maintain homeostasis of the pulmonary circulation and a good balance between the right and left ventricle outputs. Here, I have reviewed new developments related to the mechanisms for controlling pulmonary vascular tone under different states: normal, acute and chronic hypoxia, and hemorrhagic hypotension. I have also described the effects of inhaled NO and PGI2 as selective pulmonary vasodilators used for pulmonary hypertension.