Antidiuretic hormone release

Wilke RA. Posterior pituitary sigma receptors and drug-induced syndrome of inappropriate antidiuretic hormone release. Ann Intern Med 1999 131(10) 799. 

Hyponatraemia may result if sodium loss occurs in patients who drink a large quantity of water when taking a diuretic. Other mechanisms are probably involved, including enhancement of antidiuretic hormone release. Such patients have reduced total body sodium and extracellular fluid and are oedema-free. Discontinuing the diuretic and restricting water intake are effective. The condition should be distinguished from hyponatraemia with oedema which develops in some pahents with congestive... 

The author thought that SIADH had resulted from severe pleurisy secondary to intrapleural administration of picibanil rather than to direct stimulation of antidiuretic hormone release. 

Proper attention to plasma expansion must be continued into the intraoperative and postoperative periods. A number of neurohormonal changes take place that affect urine output, and patients may have substantial third-spacing of fluid depending on the operation and the preexisting condition of the patient. Furthermore, postoperative patients are prone to hyponatremia from renal generation of electrolyte-free water and from antidiuretic hormone release. As in acute resuscitation, the administration of hypotonic solutions in the perioperative period does not prevent the decrease in extracellular volume that often occurs. Therefore, although excess fluid administration is to be avoided in the perioperative setting, isotonic crystalloid solutions should be used when fluids are indicated to prevent intravascular depletion and circulatory insufficiency. 

Renal hypoperfusion without systemic hypotension most commonly results from bilateral renal artery occlusion, or unilateral occlusion in a patient with a single functioning kidney. In these conditions, the sodium-retentive hormones are activated by the decline in renal parenchymal perfusion. However, systemic arterial blood pressure is usually elevated, leading to an inhibition of antidiuretic hormone release. Consequently, the urinary indices will reflect enhanced sodium reabsorption (i.e., a low fractional excretion of sodium), but the urinary solutes may not be maximally concentrated. 

These agents decrease the transport of amino acids into cells and mediate inhibition of purine synthesis inhibition of RNA. DNA. and protein synthesis disruption of lipid metabolism inhibition of glycolysis changes in antidiuretic hormone release and disruption of cell membrane integrity and membrane function. 

Syndrome of inappropriate antidiuretic hormone is defined by water retention, dilutional hyponatraemia and decreased volume of highly concentrated urine. There are several causes which can result in SIADH, neoplasms ectopic secreting AVP, ectopic release of AVP by various diseases or drugs, exogenous administration of AVP, desmopressin, lysipressin or large doses of OT (iatrogenic SLADH). 

The posterior pituitary is innervated by direct nervous stimulation from the hypothalamus, resulting in the release of specific hormones. The hypothalamus synthesizes two hormones, oxytocin and vasopressin. These hormones are stored in and released from the posterior pituitary lobe. Oxytocin exerts two actions (1) it promotes uterine contractions during labor, and (2) it contracts the smooth muscles in the breast to stimulate the release of milk from the mammary gland during lactation. Vasopressin is an antidiuretic hormone (ADH) essential for proper fluid and electrolyte balance in the body. Specifically, vasopressin increases the permeability of the distal convoluted tubules and collecting ducts of the nephrons to water. This causes the kidney to excrete less water in the urine. Consequently, the urine becomes more concentrated as water is conserved. 

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... 

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. 

Vasopressin (antidiuretic hormone) is a peptide synthesized in the hypothalamus and secreted from the neurohypophysis of the pituitary gland. This substance plays an important role in the long-term regulation of blood pressure through its action on the kidney to increase reabsorption of water. The major stimulus for release of vasopressin is an increase in plasma osmolarity. The resulting reabsorption of water dilutes the plasma toward its normal value of 290 mOsM. This activity is discussed in more detail in Chapter 10 (the endocrine system) and Chapter 19 (the renal system). 

In order to make adjustments in the water load, the reabsorption of the remaining 20% of the filtered water from the distal tubule and the collecting duct is physiologically controlled by antidiuretic hormone (ADH), also referred to as vasopressin. Antidiuretic hormone, synthesized in the hypothalamus and released from the neurohypophysis of the pituitary gland, promotes the... 

Carbamazepine Tegretol, Epitol Tablet 200 mg 200-1,800 m day in 2-4 divided doses. Use alone or in combination with other medications Blocks voltage-sensitive Na+ channels Stimulates the release of antidiuretic hormone and decreases Na+... 

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. 

Neurohypophysis. Release of vasopressin (antidiuretic hormone) results in lowered urinary output (p. 164). Levels of vasopressin necessary for vasoconstriction will rarely be produced by nicotine. 

The actions of nicotine on the central nervous system are the result of a composite of stimulatory and depressant effects. These can include tremors, convulsions, respiratory stimulation or depression, and release of antidiuretic hormone from the pituitary. Nausea and emesis are frequently observed after the initial use of nicotine in the form of tobacco smoke. However, tolerance to these effects rapidly develops. This is in contrast to the effects of nicotine on the cardiovascular system, where tolerance develops much more slowly. 

The permeability properties of the distal convoluted tubule are regulated by antidiuretic hormone (ADH, or vasopressin). In hypotonic conditions, ADH secretion by the posterior pituitary is suppressed and the distal convoluted tubule is impermeant to water. Conversely, in hypertonic or volume-contracted states, ADH is released by the posterior pituitary and increases the permeability and water reabsorption by the distal convoluted tubule. 

Historically vasopressin and oxytocin, two nonapep-tides, were the first peptide neurohormones to be considered they are stored in the neurohypophysis and released into the bloodstream upon an appropriate stimulus. In the periphery, oxytocin stimulates the contraction of epididymal and uterine smooth muscle (see Chapter 62) and vasopressin (antidiuretic hormone) facilitates the reabsorption of water from the kidney tubules. In addition to these well-accepted roles as neurohormones, there is convincing evidence that these compounds function as neurotransmitters they both possess potent inhibitory actions on neurohypophyseal neurons. The significance of their neurotransmitter function is not yet clear. 

The opioids have pronounced effects on the release of hormones from both the pituitary and the hypothalamus. Stimulation of some of the opioid receptors in hypothalamic nuclei decrease the release of dopamine, thus increasing release of prolactin. Opioids bind in the supraoptic nuclei of the hypothalamus and increase the release of antidiuretic hormone (vasopressin). 

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