Possible role of prostaglandins in the pathogenesis of pulmonary hypertension

Abstract

Pulmonary hypertension is known to occur at high altitudes, due to hypoxia and is considered to be more common in women taking oral contraceptives, situations known to decrease the synthesis of prostaglandin E and possibly prostacyclin with simultaneous increase in thromboxane A2 synthesis. Decreased bradykinin synthesis or persistence of foetal type of pulmonary vasculature are considered to predispose to the development of primary pulmonary hypertension. Bradykinin is a potent stimulator of prostaglandin E synthesis, a known vasodilator. Thus it is possible that primary pulmonary hypertension could be due to a fall in the synthesis of vasodilators like prostaglandin E and/or prostacyclin and a relative or absolute increase in vasoconstrictors like thromboxane A2 and/or prostaglandin F2 alpha.