Veterinary Physiology-III

EICOSANOIDS

• Von Euler in 1934 isolated and named a substance isolated from seminal fluid as prostaglandins. Unlike the other hormones, prostaglandins are not localized in any particular tissue. Most prostaglandins act locally at the site of their production on a cell interaction–paracrine effect and also act by autocrine mechanism.
  • Eicosanoids are a large group of molecules derived from 20 carbon polyunsaturated fattyacids. The principal groups of hormones of this class are prostaglandins (PG), prostacyclins, leukotrienes (LT), thromboxanes (TX) and lipoxins (LX).
  • Arachidonic acid is the most abundant precursor for these hormones. Stores of arachadonic acid are present in membrane lipids and released through the action of various lipases.
  • The specific eicosanoids synthesized by a particular cell are dictated by the group of processing enzymes expressed in that cell.
  • Phospholipase A₂ releases arachidonic acid from membrane phospholipids. The released arachidonic acid is converted to prostaglandin H₂ (PGH₂) by cyclic oxygenase 1 (Cox 1) and cyclic oxygenase 2 (Cox 2)enzymes.
  • PGH₂is converted to prostacyclins, thromboxanes and prostaglandins by isomerase enzymes present in tissues.
  • ThromboxaneA₂ is synthesized by platelets and promotes vasoconstriction and platelet aggregation.
  • Prostacyclinis produced in the lungs and vascular endothelium, inhibits platelet aggregation and produces vasodilatation.
  • Leukotrienes mediate allergic response and inflammation; released when allergens combine with IgE antibodies on the mast cells and they produce bronchoconstriction, vasoconstriction and increases vascular permeability, attract neutrophils and eosinophils to site of inflammation.
  • Functionsof liopxins are not elucidated.
  • Eicosanoid hormones are rapidly inactivated by being metabolized and are typically active for only a few seconds.

Prostaglandins(PG)

• Prostaglandins have varied functions particularly important in female reproduction, parturition, cardiovascular system.
• They play a prominent role in causing pain, inflammation and fever.
• Glucocorticoids inhibit phospholipase A2 and act as anti inflammatory.
• PGs may be considered to regulate several physiological functions such as contraction of smooth muscles in reproductive organs, and functions in erection, ejaculation, sperm transport, ovulation and also luteolysis.
• They also regulate blood pressure, lipolysis, gastric secretion and blood clotting.
• Thromboxane A2 and PGF₂α are vasoconstrictors.
• Prostaglandins enhance the motility and secretions of the small intestine.
• PGE regulates the renal blood flow from cortex to the juxtaglomerular nephrons during stress. Inhalation of PGE causes bronchodilation while PGF causes bronchospasm.
• PGE 2 exert a characteristic effect in the longitudinal musculature of the oviduct, an increase in tonus in the proximal part, while relaxation in the rest of the organ. PGE2 increases release of GH, glucagon, progesterone and aldosterone. PGE2 inhibits gastric acid secretion, but stimulates contractions of the uterus and dilatation of the blood vessels and has no luteolytic effect. It stimulates the production of plasminogen activator and increases plasmin activity, involved in cell migration, mixing of theca and granulosa cells during CL formation.
• PGE 3 and PGF cause relaxation of the whole oviduct.
• PGE , PGA and PGI are vasodilators and increases renal perfusion leading to increase in Cl, Na and K level in watery urine.
• PGF2 facilitates adrenaline release.
• PGD2 is vasoconstrictor.
• High levels of estrogen promote oxytocin receptors in the endometrium stimulatePGF synthesis and its secretion from the endometrium. PGF₂ alpha potentiates the contractions of the uterus by estrogen during parturition.
• In females PGF2α is involved in the follicular rupture and ovulation, also aids sperm transport in males. From endometrium PGF passes directly through the walls of utero-ovarian vein into artery by counter current mechanism and causes vasoconstriction of the blood vessels supplying the CL, the hypoxia in CL leading to luteolysis.