Selective Passage of Prostaglandins across the Lung

Abstract

STIMULATION of the splenic nerves releases prostaglandins from the spleen to give concentrations of as much as 0.2 µg/ml. in splenic venous blood¹. The release of prostaglandins might influence organs remote from the site of release, for prostaglandins can exert potent actions on smooth muscle². The lung has recently been shown to determine the fate of many vasoactive substances; some are activated—conversion of angiotensin I to angiotensin II (ref. 3)—and some inactivated. The degree of inactivation seems to be specific for a given substance, ranging from almost complete (bradykinin⁴, 5-hydroxytryptamine⁵, prostaglandins E₁ E₂ and F_2α (ref. 1)), to minor (noradrenaline⁶), to allowance of their free passage (adrenaline⁶ and angiotensin II (ref. 7)). The removal of prostaglandins by the lung restricts their activities to the organs from which they are released and between their organ of origin and the site in the pulmonary circulation where they are inactivated¹. A prostaglandin which passed through the lungs after its release from an organ could be considered a circulating hormone, as long as it is not rapidly degraded in the blood. Ferreira and Vane¹ reported that prostaglandins E₁ E₂ and F_2α were stable in blood, though rapidly inactivated by the lung. Removal of prostaglandins A₁ and A₂ by the lung was not determined because the assay organs are insensitive to them. Vascular smooth muscle, however, unlike other smooth muscle, is reactive to low concentrations of prostaglandins A₁ and A₂ (refs. 8–10) and the renal vasculature is probably most sensitive to prostaglandins A₁ and A₂ (refs. 10 and 11). Because the renal vasculature is also sensitive to prostaglandins E₁ and E₂ (ref. 12), it has been used as an index of the fate of prostaglandins infused into the venous and arterial circulations.