Antidiuretic Hormone (ADH)
Antidiuretic Hormone (ADH) is a hormone produced by the hypothalamus and released by the pituitary gland. It plays a key role in regulating the body's water balance by controlling the amount of water reabsorbed by the kidneys. ADH helps to reduce the amount of urine produced by the body, thereby conserving water and preventing dehydration.
8 Key excerpts on "Antidiuretic Hormone (ADH)"
eBook - ePub- Anthony W. Norman, Gerald Litwack(Authors)
- 2014(Publication Date)
- Academic Press(Publisher)
...Chapter 4 Posterior Pituitary Hormones Publisher Summary This chapter discusses posterior pituitary hormone. Two important hormones are secreted from the posterior pituitary in both males and females. These are vasopressin (VP), the antidiuretic hormone, and oxytocin (OT), which in females acts as the milk ejection factor. Both are non-apeptides, closely related in structure and apparently derived from the same ancestral gene. The primary recognized function of VP is to stimulate reabsorption of water from the distal tubular kidney. The release of VP is generated by the need to maintain the blood osmolarity of plasma within strict limits (homeostasis), especially with reference to increased Na + concentrations in blood produced by ingestion of NaCl. VP secretion is also increased when blood volume or blood pressure is decreased. VP synthesis in the hypothalamus appear to be close to the osmoreceptor sites that sense changes in electrolyte (solute) concentrations in the circulation and signal release of the hormone from the neuronal terminals in the posterior pituitary. The osmoreceptor is close to the thirst center in the hypothalamus and also interacts with the rennin–angiotensin system...
eBook - ePub- Phillip A. Low(Author)
- 2011(Publication Date)
- Academic Press(Publisher)
...Chapter 25. Vasopressin and Disorders of Water Homeostasis Joseph G. Verbalis The primary physiologic action of arginine vasopressin (AVP) is its function as a water-retaining hormone. The central sensing system (osmostat) for control of release of AVP is located in the hypothalamus anterior to the third ventricle that also includes the circumventricular organ, the organum vasculosum of the lamina terminalis (OVLT). The osmostat controls release of AVP to cause water retention, and also stimulates thirst to cause water repletion. Osmotic regulation of AVP release and thirst are usually tightly coupled, but experimental lesions and some pathologic situations in humans demonstrate that each can be regulated independently. The primary extracellular osmolyte to which the osmoreceptor responds is sodium. Under normal physiologic conditions, glucose and urea readily traverse neuron cell membranes and do not stimulate release of AVP. Basal osmolality in normal subjects lies between 280 and 295 mOsm/kg H 2 O, but for each individual osmolality is maintained within narrow ranges. Increases in plasma osmolality as little as 1% will stimulate the osmoreceptors to release AVP. Basal plasma levels of AVP are 0.5 to 2 pg/mL, which are sufficient to maintain urine osmolality above plasma osmolality and urine volume in the range of 2–3 L/day. When AVP levels are suppressed below 0.5 pg/ml, maximum urine osmolality decreases to less than 100 mOsm/kg H 2 O and a free water diuresis ensues to levels approaching 800–1000 ml/h (18–24 L/d). Increases in plasma osmolality cause a linear increase in plasma AVP and a corresponding linear increase in urine osmolality. At a plasma osmolality of approximately 295 mOsm/kg H 2 O, urine osmolality is maximally concentrated to 1000–1200 mOsm/kg H 2 O...
eBook - ePubThe Endocrine System
Systems of the Body Series
- Joy P. Hinson, Peter Raven, Shern L. Chew(Authors)
- 2013(Publication Date)
- Churchill Livingstone(Publisher)
...What would it be if he did not have diabetes insipidus and his serum osmolality was 331 mOsm/L? (Answer: It should be >2 × 331 = 662 mOsm/kg). In SIADH, the urine is usually more concentrated, i.e. has a higher osmolality, than plasma. The symptoms of SIADH are essentially those of hyponatraemia, with headache, nausea, vomiting, confusion and ultimately coma. SIADH has many causes including neoplasms such as lung cancer (which can secrete vasopressin), neurological disorders such as meningitis, lung disease such as pneumonia and tuberculosis, and prescribed drugs such as carbamazepine. Tubercular lung tissue has been shown to contain measureable amounts of arginine vasopressin, as have some forms of lung cancer. In pneumonia it is not clear whether the infection causes local secretion of arginine vasopressin in the lung or whether it affects hypothalamic production. Thirst If you look at Figure 3.1, the connection between dehydration acting on the hypothalamus and, as a result, the pituitary acting to regulate water balance, is thirst. Thirst is such a common experience that we assume it is a simple process, but the regulation of thirst is very complex, involving angiotensin II, arginine vasopressin and central and peripheral receptors. For a summary of the hormonal control of blood pressure, osmolality and thirst, see Chapter 13. Water intoxication occurs when an individual drinks more fluids than they can handle in a physiologically appropriate manner. It can have many causes, including the psychogenic polydipsia associated with schizophrenia, and the excessive drinking seen following ingestion of Ecstasy (MDMA), which usually occurs in a misguided attempt to avoid dehydration and hyperthermia. Other hypothalamic hormones In addition to oxytocin and vasopressin, the hypothalamus produces two neuropeptide hormones called the orexins, also known as hypocretins. These hormones, orexin A and orexin B, have about 50% homology...
eBook - ePub- Mehul T. Dattani, Charles G. D. Brook, Mehul T. Dattani, Charles G. D. Brook(Authors)
- 2019(Publication Date)
- Wiley-Blackwell(Publisher)
...Dilutional hyponatraemia is a potential hazard if desmopressin is administered in excess over a prolonged time period. Volume contraction and thiazide diuretics, amiloride and indomethacin are indirect forms of treatment for NDI. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt‐wasting syndrome (CSWS) are causes of hyponatraemia. Clinical evaluation, assessment of extracellular fluid space volume status, measurement of urinary electrolytes and responses to infusion of saline solutions can distinguish these conditions; therapy (water restriction/oral urea/vaptans or saline infusion) must be carefully chosen after determining the cause of hyponatraemia. The maintenance of the tonicity of extracellular fluids within 1–2% of normal (287 ± 7 mosm/kg) is crucial for cell function, and so homeostasis by the regulation of water intake and excretion is critical to all mammals. This requires the normal function of the hypothalamus and its surrounding brain tissue, the posterior pituitary secreting arginine vasopressin peptide (AVP) and the kidney. AVP is a nonapeptide produced by the magnocellular neurons of the supraoptic and paraventricular nuclei (PVN) of the hypothalamus and released from the posterior pituitary with its associated protein (neurophysin, NPII) by calcium exocytosis. Vasopressin is the principal hormonal regulator of urine volume and concentration and the controller of water homeostasis under normal conditions. Disorders of vasopressin secretion and of its action in the kidney are associated with disrupted water metabolism leading to diabetes insipidus. Regulation of Water Balance Anatomy of the Hypothalamic–Posterior Pituitary Axis The posterior pituitary consists of magnocellular neurons producing vasopressin and/or oxytocin...
eBook - ePub- Charles G. D. Brook, Mehul T. Dattani(Authors)
- 2012(Publication Date)
- Wiley-Blackwell(Publisher)
...CHAPTER 10 Water Balance Key learning points 1. Maintenance of plasma osmolality is by thirst and urine output, which is controlled by arginine vasopressin/antidiuretic hormone (AVP/ADH). 2. Extracellular volume is regulated by the renin–angiotensin–aldosterone system. 3. Vasopressin deficiency causes diabetes insipidus (DI). 4. Symptoms of DI are polydipsia and polyuria and distinction must be made between DI and primary polydipsia. 5. Resistance to vasopressin action causes nephrogenic DI (NDI). 6. The syndrome of inappropriate ADH secretion must be distinguished from cerebral salt wasting when hyponatremia follows central nervous system injury. 7. Water intake and excretion vary widely in normal persons but plasma osmolality is maintained strictly within the range of 275–295 mOsm/kg. Plasma osmolality above or below the range results in alterations in intracellular solute concentrations, patterns of cellular depolarization, cell morphology and critical aspects of cell function that can become life threatening. 8. To limit excursions in osmolality, thirst controls water intake and AVP controls urine concentration. Intact function of either thirst or vasopressin secretion can maintain normal plasma osmolality independently with adequate access to water. 9. The regulation of extracellular fluid volume is primarily under the control of the renin–angiotensin–aldosterone system (see Chapter 8) and occurs by modulation of sodium intake and excretion, in contrast to the regulation of osmolality by water intake and excretion. 10. Both hyponatremia and hypernatremia should be carefully corrected over a period of 24–48 h. Water intake and excretion vary widely in normal persons but plasma osmolality is maintained strictly within the range of 275–295 mOsm/kg...
eBook - ePub- Anthony W. Norman, Gerald Litwack(Authors)
- 1997(Publication Date)
- Academic Press(Publisher)
...and Wray, S. (1992). Ann. N.Y. Acad. Sci. 652, 14−28. V BIOLOGICAL AND MOLECULAR ACTIONS A Role of VP (Antidiuretic Hormone) in the Regulation of Body Fluids The primary action of arginine vasopressin (AVP) is in the inhibition of water diuresis (loss of water in the urine), and this action operates through the actions of membrane receptors in the kidney. AVP also elevates blood pressure and constricts coronary arteries, and it stimulates intestinal and uterine contractions, as well as slightly stimulating milk ejection. However, the last two activities modestly cross over to the major functions of OT. In most cases, the secretion of OT will be signaled separately from the signaling to release AVP. Figure 4-13 shows an overview of some of the main features of water balance (additional discussion is presented in Chapter 15). The hypothalamic osmoreceptor detects elevations in serum tonicity. The mechanism is thought to involve the shrinking of the osmoreceptor neuron to the point where a signal (chemical or electrical) is generated and transmits this signal down its axon to its nerve ending. Alternatively, the changed ionic environment produces a conformational alteration in the osmoreceptor, which generates the signal. The signal is then received by the cell body of the vasopressinergic neuron and transmitted to its own nerve ending for the release of VP–NP. Signals to baroreceptors that control the release of AVP–NP are exemplified by emotional states that inhibit the release of AVP–NP and lead to transitory frequency of urination. Nicotine intake and pain may also operate through baroreceptors of the CNS repressive center, which may stimulate AVP–NP release through adrenergic stimulation. The AVP–NP complex is briefly stable in blood, having an experimental half-life of 10−20 min. AVP dissociates from NP and binds to a membrane receptor located in distal tubular cells of the kidney...
eBook - ePub- John Laycock, Karim Meeran(Authors)
- 2012(Publication Date)
- Wiley(Publisher)
...Vasopressin plays a particularly important role in the regulation of water reabsorption because it is the principal controlling influence over the synthesis and intracellular direction of a specific aquaporin (AQP2). This AQP2 is located in the principal cells of the final concentrating segment of the nephron, the collecting duct. The AQP2 molecules are water channels which are inserted into the apical membranes of the principal cells of the collecting duct. Another aquaporin (AQP3) which is located in the basolateral membranes and is involved in the movement of water out of the principal cells into the interstitial fluid and ultimately the plasma is also believed to be at least partially under the control of vasopressin. Yet another AQP (AQP4), also located in the basolateral membranes, is not influenced by VP. Since vasopressin also stimulates sodium reabsorption along this section together with aldosterone (certainly in the cortical collecting duct), it helps provide the osmotic gradient necessary for the vasopressin–AQP2 (and vasopressin–AQP3) regulated water reabsorption. Oxytocin This hormone may have a minor influence on water reabsorption along the collecting ducts, and this action could involve the V2 receptors for vasopressin as well as the oxytocin receptors, although its affinity for V2 receptors is minimal. Central Regulation The CNS clearly plays an important role in exerting an overall control over the behaviours and mechanisms involved in maintaining salt and water balance. Regarding behaviours, there are various centrally regulated activities which ensure that salt and water, so crucial to life, are actively sought when required. For this purpose, salt craving and thirst are stimuli (drivers) which will direct any animal including humans to seek sources of these necessities. Salt appetite is believed to involve inhibitory serotoninergic and oxytocinergic neurones, at least in rodents...
eBook - ePub- Anthony W. Norman, Helen L. Henry(Authors)
- 2014(Publication Date)
- Academic Press(Publisher)
...V1a is fairly widely distributed and has a variety of functions in the vasculature and elsewhere. The localizations of the other two vasopressin receptors are more restricted. V2 in the kidney is responsible for the primary physiological effect of vasopression, water resorption, giving the hormone its other name, antidiuretic hormone. The V1b receptor, located mainly in the anterior pituitary corticotrophs, is known primarily for its effect on ACTH secretion, but has been found outside the pituitary where its functions have not yet been delineated. Table 4-1 Distribution and Activity of AVP Receptors AVP receptor subtype Tissue Physiological activity 2 nd messenger system V1a Vascular smooth muscle Vasoconstriction PLC: Ca 2+, IP 3, DAG Liver ↑ Glycogen breakdown Platelets ↑ Adhesion Brain Stress adaptation, social recognition, memory, other V1b Ant. pituitary corticotrophs ↑ ACTH release Same as V1a V2 Kidney: distal nephron, basolateral membrane ↑ aquaporin → ↑ water resorption cAMP: PKA PLC, phospholipase C; IP 3, inositol 1,4,5- triphosphate; DAG, diacylglycerol; cAMP, cyclic AMP; PKA-cyclic AMP-dependent protein kinase. Figure 4-5 The secondary structure of the V2 receptor for arginine vasopressin. Residues shown in red are positions of mutations leading to diabetes insipidus, the primary clinical manifestation of lack of AVP. B AVP Regulation of Water Handling The primary action of arginine vasopressin (AVP), also known as antidiuretic hormone, is the inhibition of water diuresis (loss of water in the urine), mediated by AVP V2 receptors in the distal nephrons of the kidney. AVP also elevates blood pressure and constricts coronary arteries as described in the following section. Figure 4-6 shows an overview of the main features of water balance. The hypothalamic osmoreceptor detects elevations in serum tonicity reflecting low blood volume...
