Regulation of Extracellular Fluid Osmolarity and Sodium Concentration PDF

Regulation of extracellular fluid osmolarity and sodium concentration Prof. Dr. Senol Dane Nile University of Nigeria  Regulation of extracellular fluid osmolarity and Na concentration are closely linked because Na is the most abundant ion in the ECF. Plasma N...

Regulation of extracellular fluid osmolarity and sodium concentration Prof. Dr. Senol Dane Nile University of Nigeria  Regulation of extracellular fluid osmolarity and Na concentration are closely linked because Na is the most abundant ion in the ECF. Plasma Na concentration is regulated within close limits of 140-145 mEq/L (about 142 mEq/L). Osmolarity is about 300 mOsm/L. They are precisely controlled because they determine the distribution of fluid between the IC and EC compartments. ESTIMATING PLASMA OSMOLARITY FROM PLASMA SODIUM CONCENTRATION Plasma osmolarity (Posm) is estimated from the plasma Na concentration Posm = PNa+ × 2.1 (mmol/L) If plasma Na concentration of 142 mEq/L, the plasma osmolarity is 298 mOsm/L. To be more exact, in conditions associated with renal disease, the contribution of the plasma concentrations of two other solutes, glucose and urea, should be included.  Na ions and associated anions (bicarbonate and Cl) represent 94% of the EC osmoles, with glucose and urea contributing 3-5% of the total osmoles. Urea permeates cell membranes easily, its effect is little. The sodium ions in the ECF and associated anions are the principal determinants of fluid movement across the cell membrane.  Two primary systems are involved in regulating the Na concentration and osmolarity of ECF: (1) the osmoreceptor-ADH system (2) the thirst mechanism  OSMORECEPTOR-ADH FEEDBACK SYSTEM If osmolarity (plasma Na concentration) increases above normal because of water deficit, this feedback system operates as follows: 1. An increase in extracellular fluid osmolarity (an increase in plasma Na concentration) causes the nerve cells called osmoreceptors, located in the anterior hypothalamus near the supraoptic nuclei, to shrink. 2. Shrinkage of the osmoreceptors causes them to send nerve signals to nerve cells in the supraoptic nuclei, which then relay these signals down the stalk of the pituitary gland to the posterior pituitary. 3. These action potentials stimulate the release of ADH, which is stored in secretory granules (or vesicles) in the nerve endings. 4. ADH enters the blood stream and is transported to the kidneys, where it increases the water permeability of the late distal tubules, cortical collecting tubules, and medullary collecting ducts. Osmorecept or- antidiuretic hormone (ADH) feedback mechanism for regulating extracellular fluid osmolarity in response to  Water is conserved in the body while sodium and other solutes are excreted in the urine. This causes dilution of the solutes in the extracellular fluid, correcting the initial concentrated extracellular fluid. The opposite sequence of events occurs when the extracellular fluid becomes too dilute (hypo-osmotic). With excess water ingestion and a decrease in extracellular fluid osmolarity, less ADH is formed, the renal tubules decrease their permeability for water, less water is reabsorbed, and a large volume of dilute urine is formed. This concentrates the body fluids and returns plasma osmolarity toward normal. ADH RELEASE FROM THE POSTERIOR PITUITARY The hypothalamus contains neurons that synthesize ADH in its supraoptic and paraventricular nuclei. These nuclei have axonal extensions to the posterior pituitary. ADH is transported down the axons of the neurons to their tips, terminating in the posterior pituitary gland. When the supraoptic and paraventricular nuclei are stimulated by increased osmolarity, ADH is released into the systemic circulation.  Also, the anteroventral region of the third ventricle (AV3V region) is important in controlling osmolarity and ADH secretion. Lesions of the AV3V region cause multiple deficits in the control of ADH secretion, thirst, sodium appetite, and blood pressure. Electrical stimulation of this region or stimulation by angiotensin II can increase ADH secretion, thirst, and sodium appetite.  The AV3V region and the supraoptic nuclei have osmoreceptors that are excited by small increases in extracellular fluid osmolarity. These cells send nerve signals to the supraoptic nuclei to increase secretion of ADH. They also induce thirst in response to increased extracellular fluid osmolarity STIMULATION OF ADH RELEASE BY DECREASED ARTERIAL PRESSURE AND/OR BLOOD VOLUME ADH release is also controlled by cardiovascular reflexes that respond to decreases in blood pressure and/or blood volume, including (1) the arterial baroreceptor reflexes and (2) the cardiopulmonary reflexes. These reflexes originate in high-pressure regions of the circulation (the aortic arch and carotid sinus) and in the low- pressure regions (the cardiac atria). Afferent stimuli are carried by the vagus and glossopharyngeal nerves to the nuclei of the tractus solitarius. Signals from these nuclei goes to the hypothalamic nuclei.  Increased osmolarity, decreased arterial pressure and decreased blood volume increase ADH secretion. If blood pressure and blood volume are reduced, such as occurs during hemorrhage, increased ADH secretion causes increased water reabsorption by the kidneys, helping to restore blood pressure and blood volume toward normal. Control of ADH Secretion THIRST The kidneys minimize fluid loss during water deficits through the osmoreceptor-ADH feedback system. Adequate fluid intake is necessary to counterbalance whatever fluid loss does occur through sweating and breathing and through the gastrointestinal tract. Fluid intake is regulated by the thirst mechanism together with the osmoreceptor-ADH mechanism, maintains precise control of extracellular fluid osmolarity and sodium concentration. Many of the same factors that stimulate ADH secretion also increase thirst. THIRST CENTERS AV3V region promotes ADH release and stimulates thirst. Located anterolaterally in the preoptic nucleus is another center for thrist. The neurons of the thirst center respond to injections of hypertonic salt solutions by stimulating drinking behavior. These cells function as osmoreceptors to activate the thirst mechanism. Increased osmolarity of the cerebrospinal fluid in the third ventricle has the same effect to promote drinking. Control of thrist Role of Angiotensin II and Aldosterone in Controlling Extracellular Fluid Osmolarity and Sodium Concentration Angiotensin II and aldosterone play an important role in regulating Na reabsorption by the renal tubules. When Na intake is low, increased levels of these hormones stimulate Na reabsorption by the kidneys and prevent large sodium losses. Conversely, with high sodium intake, decreased formation of these hormones permits the kidneys to excrete large amounts of Na.