Volume nonosmotic

Causes of nonosmotic release of arginine vasopressin, commonly known as antidiuretic hormone, include hypovolemia decreased effective circulating volume as seen in patients with congestive heart failure nephrosis cirrhosis and syndrome of inappropriate antidiuretic hormone (SIADH) release. 

To appreciate the refinements that this thermodynamic treatment introduces into the customary expression describing the osmotic responses of cells and organelles, we compare Equation 2.18 with Equation 2.15, the conventional Boyle-Van t Hoff relation. The volume of water inside the chloroplast is VM,n because n v is the number of moles of internal water and Vw is the volume per mole of water. This factor in Equation 2.18 can be identified with V — b in Equation 2.15. Instead of being designated the nonosmotic volume, b is more appropriately called the nonwater volume, as it includes the volume of the internal solutes, colloids, and membranes. In other words, the total volume (V) minus the nonwater volume (b) equals the volume of internal water (Ew ). We also note that the possible hydrostatic and matric contributions included in Equation 2.18 are neglected in the usual Boyle-Van t Hoff relation. In summary, although certain approximations and assumptions are incorporated into Equation 2.18 (e.g., that solutes do not cross the limiting membranes and that the... 

Nonosmotic release of ADH occurs when the effective arterial blood volume (EABV) decreases by approximately 5% to 10%. The EABV is the vascular component of the ECF that is responsible for organ perfusion. A change in the EABV promotes an afferent response from baroreceptors in the chest and neck and activation of the renin-angiotensin system, leading to synthesis of angiotensin 11. Angiotensin 11 then stimulates both nonosmotic release of ADH and thirst. The volume stimulus overrides osmotic inhibition of ADH release, and conservation of water fosters restoration of blood pressure and EABV at the expense of hypo-osmolality. 

Hyponatremia (serum sodium <135 mEq/L) is the most common electrolyte abnormality in hospitalized patients, with a reported incidence of about 2.5%. ° Brain injury results from either the acute effects of hypo-osmolality or from too rapid correction of hypo-osmolality in patients with symptomatic hyponatremia, and is associated with a 20% incidence of significant morbidity and a mortality rate as high as 25%. Hyponatremia is predominantly the result of an excess of extracellular water relative to sodium because of impaired water excretion. The kidney normally has the capacity to excrete large volumes of dilute urine after ingestion of a water load. Nonosmotic... 

Diuretic-induced hyponatremia occurs more frequently in patients treated with thiazide diuretics than in patients who are receiving loop diuretics. In addition to causing extracellular volume depletion and nonosmotic stimulation of ADH, thiazides interfere with urinary dilution and water excretion by blocking tubular sodium and potassium reabsorption in the distal tubule. Water is then retained in excess of sodium by virtue of nonosmotic release of ADH and excretion of urine with a concentration of sodium and potassium that exceeds that of the plasma. 

Hyponatremia associated with an increase in ECF volume occurs in conditions in which renal sodium and water excretion are impaired. Patients with cirrhosis, congestive heart failure, and nephrotic syndrome have an expanded ECF volume and edema, but a decreased EABV. The decreased EABV results in renal sodium retention, and eventually ECF volume expansion and edema. At the same time, there is nonosmotic release of ADH and retention of water in excess of sodium, thus perpetuating the hyponatremia. 

ECF volume deficit (ECFVd) is dependent on the patient s weight, age, and the degree of volume depletion, and is difficult to precisely estimate. An ECFVd loss that is equal to a 10% to 15% decrease in body weight is associated with the development of postural hypotension. An ECFVd loss as low as 5%, however, can result in hyponatremia caused by nonosmotic ADH release as a result of stimulation of baroreceptors located in the chest and neck. The ECFVd of patients can be estimated as illustrated in this case a 42-year-old male weighs 70 kg on initial examination and presents with postural hypotension and has a serum sodium of 125 mEq/L ... 

EFFECTS ON URINARY EXCRETION Loop diuretics profoundly increase the urinary excretion of Na+ and Cl" (i.e., up to 25% of the filtered load of Na+) and markedly increase the excretion of Ca + and Mg +. Furosemide but not bumetanide also has weak carbonic anhydrase-inhibiting activity that increases the urinary excretion of HCO " and phosphate. AU inhibitors of the Na+-K+-2CL symporter increase the urinary excretion of K+ and titratable acid, due in part to increased delivery of Na+ to the distal tubule. The mechanism by which increased distal delivery of Na+ enhances excretion of K+ and H+ is discussed in the section on inhibitors of Na+ channels. Other mechanisms contributing to enhanced K+ and H+ excretion include flow-dependent enhancement of ion secretion by the collecting duct, nonosmotic vasopressin release, and activation of the renin-angiotensin-aldosterone axis. Loop diuretics acutely increase the excretion of uric acid, whereas their chronic administration reduces uric acid excretion, possibly due to enhanced transport in the proximal tubule secondary to volume depletion or to competition between the diuretic and uric acid for the organic acid secretory mechanism in the proximal tubule. 

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