Leukotrienes are synthesised by leucocytes, mast cells, lung, heart, spleen, and so on. Leukotriene causes contraction of smooth muscles, broncho constriction, vasoconstriction, adhesion of white blood cells, and release of lysosomal enzymes.

PGI2 inhibits platelet aggregation. Thromboxanes TX A2 and PG E2 promote platelet aggregation and blood clotting that might lead to thrombosis. Thus, PG I2 acts as vasodilator, while TX A2 is a vasoconstrictor.

PGE decreases lipolysis, increases glycogen formation, and promotes calcium mobilisation from the bone.

PGE increases glomerular filtration rate (GFR) and promotes urine output. Excretion of Na+ and K+ is also increased by PGE.

PGE is a bronchodilator, whereas PGF acts as a constrictor of bronchial smooth muscles. Thus, PGE and PGF oppose the actions of each other in the lungs. PGE1and PGE2 are used in the treatment of asthma.

Macrophages secrete PGE, which decreases the immunological functions of B and T-lympocytes.

PGE inhibits gastric secretion. PGS are used for the treatment of gastric ulcers. However, PGS stimulates pancreatic secretion and increases the motility of intestine which often causes diarrhoea.

PGE2 and PGF2 are used for medical termination of pregnancy and induction of labour. Pain and fever Pyrogens (fever-producing agents) promote prostaglandin biosynthesis, leading to formation of PGE2 in the hypothalamus, the site of regulation of body temperature. PGE2, along with histamine and bradykinin, causes pain.

PGE2 induces symptoms of inflammation (redness, swelling, edema, and so on)due to arteriolar vasodilation.

PGE, PGA, and PGI2 are vasodilators in function. This results in increased blood flow and decreased peripheral resistance to lower the blood pressure. PGS serve as agents in the treatment of hypertension.