Evaluation of an anti-diuretic activity of fluvoxamine in albino rats

Abstract

INTRODUCTIONPrecise regulation of body fluid osmolality is essential. It is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and the rate of solute-free water excretion by the kidney, i.e., water balance. Abnormalities in this homeostatic system can result from genetic diseases, acquired diseases, or drugs and may cause serious and potentially life-threatening deviations in plasma osmolality. Anti-diuretic hormone (ADH) released from posterior pituitary has a crucial role in the control of water content of the body through its actions on the cells of the distal part of nephron and collecting tubules in the kidney. One of the main stimulus to ADH release is an increase in plasma osmolality which produces a sensation of thirst. A decrease in circulating blood volume, i.e., hypovolemia is another stimulus and here the stimuli arise from baroreceptors in cardiovascular system or from angiotensin release. ADH binds to the V 2 receptors in basolateral membrane of cells of distal tubule and collecting ducts of the nephron. Its main effect in collecting duct is to increase the rate of insertion of water channels into luminal membrane thus increasing the permeability of membrane to water thereby leading to water reabsorption from the nephron. Several drugs affect the action of ADH.Diabetes insipidus (DI) is either due to deficient secretion of arginine vasopressin (AVP), also known as ADH by the pituitary gland (central DI) or due to renal tubular unresponsiveness to AVP (nephrogenic DI). This leads to polyuria, polydipsia with hyposthenuria, causing dehydration and hypernatremia if the patient is deprived of water. 2Vasopressin acts as an anti-diuretic by reabsorbing water via the principle cells of collecting ducts and the thick ascending loop of Henle, thereby increasing the plasma blood volume and decreasing the plasma osmolality. 3 ABSTRACTBackground: Diabetes insipidus is a disease characterized by high amounts of urine excretion. Antidiuretic drugs are used to treat this condition. Hence, our study intends to evaluate the anti-diuretic effect of fluvoxamine, a selective serotonin reuptake inhibitors in albino rats. Methods: Albino rats were divided into three groups of six animals each. The control group was fed with distilled water 10 ml/kg body weight, standard group received 4 units of vasopressin and test group received fluvoxamine 18 mg/kg body weight. On the day of experiment, diuresis was induced in all the groups by giving frusemide in a dose of 20 mg/kg body weight after loading with saline at 25 ml/kg body weight. The animals were confined in diuretic cage for a period of 5 hrs and urine output was noted. Urine was analyzed for electrolyte concentration (Na