Urine antidiuretic hormone effects

Antidiuretic hormone (ADH), also referred to as vasopressin, has two major effects, both of which are reflected by its names (1) antidiuresis (decrease in urine formation by the kidney) and (2) vasoconstriction of arterioles. 

Antidiuretic hormone promotes the reabsorption of water from the tubules of the kidney, or antidiuresis. Specifically, it acts on the collecting ducts and increases the number of water channels, which increases the diffusion coefficient for water. This results in the body s conservation of water and the production of a low volume of concentrated urine. The reabsorbed water affects plasma osmolarity and blood volume. This effect of ADH on the kidney occurs at relatively low concentrations. At higher concentrations, ADH causes constriction of arterioles, which serves to increase blood pressure. Antidiuretic hormone secretion is regulated by several factors ... 

Li+ also inhibits several hormone-stimulated adenylate cyclases which, in some cases, appear to be related to side effects of Li+ therapy. For instance, Li+ inhibits the hydro-osmotic action of vasopressin, the antidiuretic hormone which increases water resorption in the kidney [136]. This effect is associated with polyuria, a relatively harmless side effect sometimes experienced with Li+ treatment, which arises from the inability of the kidney to concentrate urine. Li+ has been shown to inhibit vasopressin-stimulated adenylate cyclase activity in renal epithelial cells. Additionally, Li+ is reported to enhance the vasopressin-induced synthesis of prostaglandin E2 (PGE2) in vitro in kidney. PGE2 inhibits adenylate cyclase activity by stimulation of Gj, and, therefore, this effect may contribute to the Li+-induced polyuria. 

FIGURE 78-1. Diagnostic algorithm for the evaluation of hyponatremia. (CHF, congestive heart failure EABV, effective arterial blood volume SIADH, syndrome of inappropriate antidiuretic hormone UNa, urine sodium concentration Uosm, urine osmolality.)... 

Ethanol is a diuretic. This effect may be caused by its ability to inhibit secretion of antidiuretic hormone from the posterior pituitary, which leads to a reduction in renal tubular water reabsorption. The large amount of fluid normally consumed with ethanol also contributes to increased urine production. 

Fig. 19 (A) Cross-sectional view of the Alzet osmotic pump, an osmotic pressure-activated drug-delivery system. (B) The effect of 7 days of subcutaneous delivery of antidiuretic hormone (vasopressin) on the daily volume of urinary excretion and urine osmolality in the Brattleboro rats with diabetes insipidus.

The endocrine effects are interesting but not of much clinical importance. Menses may be suppressed breasts may lactate in the female or become swollen in the male. Gonadotropin, estrone, estradiol, pregnandiol, and 17-ketosteroids may be reduced in the urine. The depression of gonadotropin may lead to false negative pregnancy tests. There appears to be some central suppression of the antidiuretic hormone (6). 

Alcohol inhibits the release of vasopressin (antidiuretic hormone see Chapter 29) from the posterior pituitary gland, resulting in enhanced diuresis. The volume loading that accompanies imbibing complements the diuresis that occurs as a result of reduced vasopressin secretion. Alcoholics have less urine output than do control subjects in response to a challenge dose with ethanol, suggesting that tolerance develops to the diuretic effects of ethanol. Alcoholics withdrawing from alcohol exhibit increased vasopressin release and a consequent retention of water, as well as dilutional hyponatremia. 

DDAVP is a synthetic form of the antidiuretic hormone vasopressin. Without vasopressin, the body does not conserve water and a large amount of very dilute urine is excreted. The body will attempt to have the client replace the fluid by producing the symptom of extreme thirst. Lack of thirst indicates the medication is effective. 

There are two components to the regulation of ECE sodium the total amount of sodium retained and its concentration. The former is regulated by mechanisms that directly affect sodium, whereas the latter is essentially regulated via water balance. Thus, whatever sodium is retained in ECF is clothed with the appropriate amount of water to maintain the normal plasma sodium concentration within narrow limits deviations of less than 1% (hard to measure in the laboratory) trigger corrective responses. Thus, a raised plasma sodium concentration (e.g., after water loss) stimulates both thirst and renal water conservation antidiuretic hormone (ADH) from the posterior pituitary reduces urine output through its effect on the renal collecting ducts. Even one of these mechanisms can defend body water thus diabetes insipidus (inadequate production or effect of ADH) does not cause severe dehydration but polydipsia (increased fluid intake thirst is a sensation). 

Desmopressin is a posterior pituitary hormone that has antidiuretic effects that decrease urinary volume and inaease urine osmolality. It is indicated in control of primary nocturnal enuresis control of central aanial diabetes insipidus and maintenance of hemostasis in patients with hemophilia A and type 1 von Willebrand disease during surgery and postoperatively. 

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