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Describe the Mechanism of Action ,Types,Doses,Side Effects, Indications and Contraindications of of the Drugs Affecting Renal System- II (ANTI-DIURETICS)

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Describe the Mechanism of Action ,Types,Doses,Side Effects, Indications and Contraindications of of the Drugs Affecting Renal System- II (ANTI-DIURETICS) Describe the mechanism of action ,types,doses,side effects, indications and contraindications of of the drugs affecting renal system- II (ANTI-DIURETICS) DR. LILY DUBEY ASSISTANT PROFESSOR, DEPARTMENT OF PHARMACOLOGY BUNDELKHAND MEDICAL COLLEGE, SAGAR (M.P) ANTI DIURETICS Antidiuretics (more precisely ‘anti-aquaretics’) Inhibit water excretion (without affecting salt excretion) are drugs that reduce urine volume, particularly in Diabetes insipidus (DI) CLASSIFICATION Antidiuretic hormone (ADH, Vasopressin), ◦ Desmopressin ◦ Lypressin ◦ Terlipressin Thiazide diuretics, Amiloride. Miscellaneous: ◦ Indomethacin, ◦ Chlorpropamide ◦ Carbamazepine Actions Kidney Acts on the Collecting duct (CD) principal cells to increase their water permeability— Water from the duct lumen diffuses to the interstitium by equilibrating with the hyperosmolar renal medulla. V2 subtype of ADH receptors are present on the basolateral membrane of principal cells in CDs Activation of V2 receptors→↑↑ cAMP →Promote Exocytosis of ‘Aquaporin-2’ Water Channel Containing Vesicles (WCVs) through the apical membrane → ↑↑Aqueous channels inserted into the apical membrane. ↓↓ rate of endocytosis & degradation of WCVs. Activation of V2 receptors increases urea permeability of terminal part of CDs in inner medulla by stimulating a vasopressin regulated urea transporter (VRUT or UT-1)— ↑↑Medullary hypertonicity. V2 receptor mediated actions of AVP on AscLH→ reinforce medullary hypertonicity by activating the Na+K+2Cl¯ cotransporter in the short-term & increasing its synthesis in the long-term. V1 receptors also participate in the renal response to AVP. Activation of V1 receptors constricts vasa recta to diminish blood flow to inner medulla & reduces washing off effect& helps in maintaining high osmolarity in this region. Thus, it contributes to antidiuresis. Blood vessels : AVP constricts blood vessels through V1 receptors and can raise BP (hence the name vasopressin), much higher concentration is needed than for maximal antidiuresis. Cutaneous, Mesenteric, Skeletal muscle, Fat depot, Thyroid, & coronary beds are constricted. Uses A. Based on V2 actions (Desmopressin is the drug of choice) 1. Diabetes Insipidus of pituitary origin (Neurogenic) most important indication for vasopressin. ineffective in renal (nephrogenic) DI, since kidney is unresponsive to ADH. Lifelong therapy is required, except in some cases of head injury or neurosurgery, where DI occurs transiently. 2. Bedwetting in children and nocturia in adults: Intranasal or oral desmopressin at bedtime controls primary nocturia by reducing urine volume. 3. Renal concentration test : 5–10 U i.m. of Aqueous vasopressin or 2 μg of desmopressin causes maximum urinary concentration. 4. Haemophilia, von Willebrand’s disease AVP may check bleeding by releasing coagulation factor VIII & von Willebrand’s factor. Desmopressin is the preferred preparation in a dose of 0.3 μg/kg diluted in 50 ml saline & infused i.v. over 30 min B. Based on V1 actions 1. Bleeding esophageal varices : Vasopressin/ Terlipressin Stops bleeding by constricting mesenteric blood vessels & reducing blood flow through the liver to the varices, allowing clot formation. Terlipressin stops bleeding in ~80%. Mortality benifit. replaced AVP because of fewer adverse effects & greater convenience in use. Octreotide (a somatostatin analogue) is an alternative. ADVERSE EFFECTS Bradycardia, Urticaria & other allergies . Nasal Irritation, Congestion, Rhinitis, ulceration & epistaxis can occur on local application. Systemic side effects : belching, nausea, abdominal cramps, pallor, urge to defecate ↑ cardiac afterload & precipitate angina by constricting coronary vessels. C/I : Ischaemic heart disease, Hypertension, Chronic nephritis & Psychogenic Polydipsia. THIAZIDES Induce a state of sustained electrolyte depletion so that glomerular filtrate is more completely reabsorbed iso-osmotically in PT. Further, because of reduced salt reabsorption in the cortical diluting segment, a smaller volume of less dilute urine is presented to the CDs & the same is passed out. That salt restriction has Thirdly, thiazides reduce g.f.r. & thus the fluid load on tubules. Hydrochlorothiazide 25–50 mg TDS VASOPRESSIN ANTAGONISTS Tolvaptan : orally active nonpeptide selective V2 receptor antagonist. Treatment of hyponatraemia due to CHF, cirrhosis of liver or syndrome of inappropriate ADH secretion (SIADH). Increases free water clearance by the kidney (aquaretic) & helps to correct the low plasma Na+ levels. Mozavaptan (V2 selective antagonist) & Conivaptan: (V1a+V2 antagonist) are the other vasopressin antagonists that are in clinical use THANK YOU.
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