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Antidiuretic hormone, response

Vasopressin (antidiuretic hormone [ADH]) secretion increases in response to decreased blood volume and/or reductions in effective blood volume via a decrease in inhibitory tone from both low-pressure and high-pressure baroreceptors to the hypothalamus. The neuronal pathways that mediate hemodynamic regulation of... [Pg.273]

FIGURE 10-3. Expected neurohumoral response to hypovolemia. ACTH, adrenocorticotropic hormone ADH, antidiuretic hormone CNS, central nervous system Na, sodium. (Reprinted from Jimenez EJ. Shock. In Civetta JM, Taylor RW, Kirby RR, eds. Critical Care. New York Lippincott-Raven 1997 369, with permission.)... [Pg.198]

Primary therapy is based on disease severity and type of hemorrhage.7 Most patients with mild to moderate disease and a minor bleeding episode can be treated with l-desamino-8-D-arginine vasopressin [desmopressin acetate (DDAVP)], a synthetic analog of the antidiuretic hormone vasopressin. DDAVP causes release of von Willebrand factor (vWF) and factor VIII from endogenous storage sites. This formulation increases plasma factor VIII levels by three- to fivefold within 30 minutes. The recommended dose is 0.3 mcg/kg intravenously (in 50 mL normal saline infused over 15 to 30 minutes) or subcutaneously or 300 meg intranasally via concentrated nasal spray every 12 hours. Peak effect with intranasal administration occurs 60 to 90 minutes after administration, which is somewhat later than with intravenous administration. Desmopressin infusion may be administered daily for up to 2 to 3 days. Tachyphylaxis, an attenuated response with repeated administration, may occur after several doses.8... [Pg.989]

Diabetes insipidus Polyuria due to the failure of renal tubules to reabsorb water in response to antidiuretic hormone. [Pg.1564]

As its name implies, the neurohypophysis is derived embryonically from nervous tissue. It is essentially an outgrowth of the hypothalamus and is composed of bundles of axons, or neural tracts, of neurosecretory cells originating in two hypothalamic nuclei. These neurons are referred to as neurosecretory cells because they generate action potentials as well as synthesize hormones. The cell bodies of the neurosecretory cells in the supraoptic nuclei produce primarily antidiuretic hormone (ADH) and the cell bodies of the paraventricular nuclei produce primarily oxytocin. These hormones are then transported down the axons to the neurohypophysis and stored in membrane-bound vesicles in the neuron terminals. Much like neurotransmitters, the hormones are released in response to the arrival of action potentials at the neuron terminal. [Pg.120]

Tissue electrodes [2, 3, 4, 5, 45,57], In these biosensors, a thin layer of tissue is attached to the internal sensor. The enzymic reactions taking place in the tissue liberate products sensed by the internal sensor. In the glutamine electrode [5, 45], a thick layer (about 0.05 mm) of porcine liver is used and in the adenosine-5 -monophosphate electrode [4], a layer of rabbit muscle tissue. In both cases, the ammonia gas probe is the indicator electrode. Various types of enzyme, bacterial and tissue electrodes were compared [2]. In an adenosine electrode a mixture of cells obtained from the outer (mucosal) side of a mouse small intestine was used [3j. The stability of all these electrodes increases in the presence of sodium azide in the solution that prevents bacterial decomposition of the tissue. In an electrode specific for the antidiuretic hormone [57], toad bladder is placed over the membrane of a sodium-sensitive glass electrode. In the presence of the antidiuretic hormone, sodium ions are transported through the bladder and the sodium electrode response depends on the hormone concentration. [Pg.205]

The anterior lobe secretes various trophic hormones, the posterior lobe is responsible for the secretion of oxytocin and antidiuretic hormone (vasopressin) and middle lobe secretes melanocyte-stimulating hormone (MSH) which may affect the synthesis of melanin. [Pg.269]

Antidiuretic hormone antagonists inhibit the effects of ADH in the collecting tubule. Conivaptan is a pharmacologic antagonist at Via and V2 receptors. Both lithium and demeclocycline appear to reduce the formation of cyclic adenosine monophosphate (cAMP) in response to ADH. [Pg.337]

Antidiuretic hormone antagonists are used to manage SIADH when water restriction has failed to correct the abnormality. This generally occurs in the outpatient setting, where water restriction cannot be enforced, or in the hospital when large quantities of intravenous fluid are needed for other purposes. Lithium carbonate has been used to treat this syndrome, but the response is unpredictable. Demeclocycline, in dosages of 600-1200 mg/d, yields a more predictable result and is less toxic. Appropriate plasma levels (2 mcg/mL) should be maintained by monitoring. Unlike demeclocycline, conivaptan is administered by IV injection, so it is not suitable for chronic use in outpatients. Lixivaptan and tolvaptan should soon be available for oral use. [Pg.337]

Antidiuretic hormone is also elevated in response to diminished effective circulating blood volume, as often occurs in congestive heart failure. When treatment by volume replacement is not desirable, hyponatremia may result. As for SIADH, water restriction is often the treatment of choice. In patients with congestive heart failure, this approach is often unsuccessful in view of increased thirst and the large number of oral medications being used. In these patients, conivaptan may be particularly useful because it has been found that... [Pg.337]

Polydipsia and polyuria are common but reversible concomitants of lithium treatment, occurring at therapeutic serum concentrations. The principal physiologic lesion involved is loss of responsiveness to antidiuretic hormone (nephrogenic diabetes insipidus). Lithium-induced diabetes insipidus is resistant to vasopressin but responds to amiloride. [Pg.641]

Water excretion is further controlled by the antidiuretic hormone from the posterior pituitary gland which acts to increase water resorption in the kidney through making the collecting tubule permeable to water for additional resorption beyond what took place in the tubule. The posterior pituitary gland secretes the hormone as a rapid and sensitive response... [Pg.1363]

Diabetes insipidus A disease marked by increased urination (polyuria) and excessive thirst (polydipsia) due to inadequate production of antidiuretic hormone (ADH) and/or a decrease in the renal response to ADH. [Pg.627]

The principal and intercalated cells of the collecting tubule aie responsible for Na+- K+ exchange and for H+ secretion and K+ reabsorption, respectively. Stimulation of aldosterone receptors in the principal cells results in Na+ reabsorption and K+ secretion. Antidiuretic hormone (ADH, vasopressin) receptors promote the reabsorption of water from the collecting tubules and ducts (Figure 23.3). This action is mediated by cAMP. [Pg.236]

Q8 Many of the symptoms of hypercalcaemia are non-specific. In excitable cells the membrane potential is stabilized (hyperpolarization) and the cells become less excitable fatigue, weakness, lethargy, confusion, anorexia, nausea and constipation are common. There are changes in the electrocardiogram (ECG), leading to heart block and other cardiac rhythm disturbances. A condition similar to diabetes insipidus also occurs with symptoms of polydipsia and polyuria. These symptoms are due to a reduction in the responsiveness of the renal tubules to antidiuretic hormone (ADH). [Pg.150]

Antidiuretic hormone (ADH) a hormone which is responsible for the regulation of water retention in the body. It is also called arginine vasopressin (AVP) or argipressin. [Pg.320]

Halothane can cause an increase in circulating concentrations of bromide and fluoride (20), which can be associated with impaired urine-concentrating ability in response to antidiuretic hormone (22). [Pg.1582]

As many as 10% of patients show signs of salt and fluid retention and edema (7). Increased intravascular fluid volume is responsible for dilution anemia and increasing cardiac load (SED-8, 216). There is still no explanation for the water-retaining effect, but it might reflect increased production of antidiuretic hormone. [Pg.2806]


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