1. Immune system. Prostaglandins promote many aspects of the inflammatory process, including the development of pain and fever. Drugs that inhibit prostaglandin synthesis help to alleviate these symptoms.
2. Reproductive system. Prostaglandins may play a role in ovulation and corpus luteum function in the ovaries and in contraction of the uterus. Excessive production of PGE2 and PGI2 may be involved in premature labor, endometriosis, dysmenorrhea (painful menstrual cramps), and other gynecological disorders.
3. Digestive system. The stomach and intestines produce prostaglandins, which are believed to inhibit gastric secretions and influence intestinal motility and fluid absorption. Since prostaglandins inhibit gastric secretion, drugs that suppress prostaglandin production may make a patient more susceptible to peptic ulcers.
4. Respiratory system. Some prostaglandins cause constriction whereas others cause dilation of blood vessels in the lungs and of bronchiolar smooth muscle. The leukotrienes are potent bronchoconstrictors, and these compounds, together with PGF2a, may cause respiratory distress and contribute to bronchoconstriction in asthma.
5. Circulatory system. Some prostaglandins are vasoconstrictors and others are vasodilators. Thromboxane A2, a vasoconstrictor, and prostacyclin, a vasodilator, play a role in blood clotting, as previously described. In a fetus, PGE2 is believed to promote dilation of the ductus arteriosus—a short vessel that connects the pulmonary artery with the aorta. After birth, the ductus arteriosus normally closes as a result of a rise in blood oxygen when the baby breathes. If the ductus remains patent (open), however, it can be closed by the administration of drugs that inhibit prostaglandin synthesis.
6. Urinary system. Prostaglandins are produced in the renal medulla and cause vasodilation, resulting in increased renal blood flow and increased excretion of water and electrolytes in the urine.
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