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Antidiuresis

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. [Pg.124]

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 ... [Pg.124]

Other factors regulating ADH secretion include blood volume and blood pressure. A decrease in blood volume of 10% or more causes an increase in ADH secretion sufficient to cause vasoconstriction as well as antidiuresis. A decrease in mean arterial blood pressure of 5% or more also causes an increase in ADH secretion. The resulting water conservation and vasoconstriction help increase... [Pg.125]

ADH, a nonapeptide, released from the posterior pituitary gland promotes re-absorption of water in the kidney. This response is mediated by vasopressin receptors of the V2 subtype. ADH enhances the permeability of collecting duct epithelium for water (but not for electrolytes). As a result, water is drawn from urine into the hyperosmolar inter-stitium of the medulla. Nicotine augments (p. 110) and ethanol decreases ADH release. At concentrations above those required for antidiuresis, ADH stimulates smooth musculature, including that of blood vessels ( vasopressin ). The latter response is mediated by receptors of the Vi subtype. Blood pressure rises coronary vasoconstriction can precipitate angina pectoris. Lypres-sin (8-L-lysine vasopressin) acts like ADH. Other derivatives may display only one of the two actions. [Pg.164]

Garcia-Miranda, P., Feral, M. J., and llundain, A. A. (2010). Effect of antidiuresis on renal creatine metabolism. /. Physiol. Pharmacol. 61(1), 83-88. [Pg.241]

Robinson D, Cardozo L, Akeson M, Hvistendahl G, Riis A, Norgaard JP. Antidiuresis a new concept in managing female daytime urinary incontinence. BJU Int 2004 93 996-1000. [Pg.484]

Endocrine responses Stimulatory effects p antidiuresis Hypothalamus, possible pituitary... [Pg.450]

Tolerance develops to the narcotic and analgesic actions of morphine, so that increasingly larger doses are needed to render patients pain free. Tolerance develops to many effects of morphine such as analgesia, euphoria, narcosis, respiratory depression, hypotension, and antidiuresis. Morphine-induced bradycardia may be experienced. However, no tolerance develops to morphine-induced miosis or constipation. If the administration of morphine is discontinued, the tolerance is lost and the preaddiction analgesic doses of morphine become effective once more. [Pg.464]

Vasopressin interacts with two types of receptors. Vi receptors are found on vascular smooth muscle cells and mediate vasoconstriction (see Chapter 17 Vasoactive Peptides). V2 receptors are found on renal tubule cells and mediate antidiuresis through increased water permeability and water resorption in the collecting tubules. Extrarenal V2-like receptors mediate release of coagulation... [Pg.876]

ALDO-R agonist [antidiuresis, anti-natriuresis i.e. H20 retention, Na+ retention K+ loss from kidneys]... [Pg.459]

Morphine causes antidiuresis by releasing antidiuretic hormone, and this can be clinically important. [Pg.334]

Apprehension and fear caused an increase in blood levels, but the induction of anesthesia was not a strong stimulus. ADH levels are often raised in the preoperative patient owing to fiuid deprivation, and intravenous fluids will frequently cause a reduction in plasma ADH activity. Skin incision in a patient under general anesthesia constitutes a stimulus which can be abolished by the additional use of a local anesthetic in the skin (M6). Traction on the root of the mesentery of the small intestine was shown to be a distinct stimulus. Osmoreceptors are involved in the control of ADH release, which is inhibited when tonicity is low and is increased as tonicity rises (H12). However, after injury when the plasma is often hypotonic for many reasons and the urine concentrated, the promotion of further antidiuresis is paradoxical and unrelated to normal mechanisms of osmolality control. Plasma volume changes and associated deprivation of intake in the immediate post injury period take precedence over tonicity control mechanisms. Thus many stimuli which in themselves are not associated with blood volume changes can evoke an ADH response. [Pg.266]

Water and electrolyte disturbances, including inappropriate antidiuresis, can occur in patients who have taken high doses of colchicine (2,3), including hypernatremia and polyuria (4). [Pg.883]

Andrivet P, Adnot S, Brun-Bulsson C, Chabrier PE, Darmon JY, Braquet P, et al. Involvement of ANF in the acute antidiuresis during PEEP ventilation. JAppI Physiol 1988 65(5) 1967-74. [Pg.543]

Yohimbine has US FDA approval to reverse the effects of xylazine in dogs. Toxic effects are similar to those observed in humans. Hypertension, tachycardia, central nervous system stimulation, and antidiuresis may occur. [Pg.2868]

Gain of Function of the Vasopressin 112 Receptor Nephrogenic Syndrome of Inappropriate Antidiuresis... [Pg.177]

Soule S, Florkowski C, Potter H et al (2008) Intermittent severe, symptomatic hyponatrae-mia due to the nephrogenic syndrome of inappropriate antidiuresis. Ann Clin Biochem 45 520-523... [Pg.187]

Marcialis MA, Faa V, Fanos V et al (2008) Neonatal onset of nephrogenic syndrome of inappropriate antidiuresis. Pediatr Nephrol 23 2267-2271... [Pg.187]

Kocan M, See HB, Sampaio NG et al (2009) Agonist-independent interactions between beta-arrestins and mutant vasopressin type II receptors associated with nephrogenic syndrome of inappropriate antidiuresis. Mol Endocrinol 23 559-571... [Pg.187]

Hormonal Factors. A number of publications have centered on the mode of action and the Inhibition of the antidiuretic hormone (ADH, vasopressin). It was shown that ADH in the rat may regularly cause diuresis as well as the generally observed antidiuresis. This biphasic action is dose-dependent, i.e., small doses of the hormone injected or infused... [Pg.65]

McKinley MJ. Denton DA, Weisinger RS. Sensors for antidiuresis and thirst—osmoreceptors or CSF sodium detectors Brain Res 1978 141 89-103. [Pg.398]

For example, at low and high rates of urine flow, the minimal and maximal values of the may vary from 30% to 60% of the glomerular filtration rate. This occurs because various tubular segments are permeable to urea and allow passive reabsorption to occur under conditions of antidiuresis. The fractional excretion of urea (FE ,pa) is calculated as [(urine urea/ plasma urea)/(urine creatinine/plasma creatinine) x... [Pg.629]


See other pages where Antidiuresis is mentioned: [Pg.162]    [Pg.313]    [Pg.389]    [Pg.153]    [Pg.371]    [Pg.691]    [Pg.1720]    [Pg.51]    [Pg.700]    [Pg.150]    [Pg.188]    [Pg.192]    [Pg.168]    [Pg.66]    [Pg.3341]    [Pg.47]    [Pg.97]    [Pg.730]    [Pg.153]    [Pg.1991]    [Pg.187]    [Pg.187]    [Pg.66]    [Pg.25]    [Pg.566]   
See also in sourсe #XX -- [ Pg.124 ]

See also in sourсe #XX -- [ Pg.371 ]




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Syndrome of inappropriate antidiuresis

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