Vasopressin secretion

Cholecystokinin (CCK) is produced in the intestine and the brain. It appears to be an important mediator of anxiety. It also stimulates vasopressin secretion and slows gastric emptying. In addition, it is an important humoral satiety signal (appetite control). Various antagonists have been developed and are currently being investigated with regard to their therapeutic potential. 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Samson, W. K., Aguila, M. C., Martinovic, J., Antunes-Rodrigues, J., and Norris, M., Hypothalamic action of atrial natriuretic factor to inhibit vasopressin secretion. Peptides 8,449-454 (1987). 

As noted above, MDA is a potent stimulator of monoamine release (see Table 7.1), and recent reports indicate that a number of MDMA metabolites are bioactive. For example, Forsling et al.61 showed that the metabolite 4-hydroxy-3-methoxymethamphetamine (HMMA) is more potent than MDMA as a stimulator of vasopressin secretion from rat posterior pituitaries in vitro. The neuroendocrine effects produced by in vivo administration of MDMA metabolites have not been examined. Monks et al.62 demonstrated that catechol metabolites of MDMA and MDA, namely, 3,4-dihydroxymethamphetamine (HHMA) and 3,4-dihydroxyamphetamine (HHA), exhibit neurotoxic properties when oxidized and conjugated with glutathione. Further characterization of the biological effects of MDMA metabolites is an important area of research. 

Altemus M, Cizza G, Gold P (1992) Chronic fluoxetine treatment reduces hypothalamic vasopressin secretion in vitro. Brain Res 593 311-313 Appenrodt E, Schnabel R, Schwarzberg H (1998) Vasopressin administration modulates anxiety-related behavior in rats. Physiol Behav 64 543-547 Arborelius L, Owens MJ, PlotskyPM, Nemeroff CB (1999) The role of corticotropin-releasing factor in depression and anxiety disorders. J Endocrinol 160 1-12 Argiolas A, Gessa GL (1991) Central functions of oxytocin. Neurosci Biobehav Rev 15 217-231... 

Whereas it is conceivable that a CRH/vasopressin hyperdrive contributes to behavioral, emotional, and hormonal symptoms of mood disorders, the question remains which mechanisms mediate this hyperactivity of CRH and vasopressin-secreting neurons. The gene expression of both neuropeptides is suppressed by ligand-activated glucocorticoid receptors. The efficiency of this negative feedback action of circulating corticosteroids depends on the number of corticosteroid receptors, their affinity, and the degree of interaction with other factors (e.g., heat shock protein) involved in the transcription machinery. 

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a condition in which secretion of ADH continues despite serum hypo-osmolarity. This results in fluid retention and hyponatremia that can lead to brain oedema, mental confusion and coma. The causes are hypothalamic-pituitary tumours or an ectopic vasopressin-secreting tumour. 

Cortisol deficiency results in impaired renal function (particularly glomerular filtration), augmented vasopressin secretion, and diminished ability to excrete a water load. 

In rat dorsolateral septal, supraoptic, and paraventricular nuclei, dopamine receptors inhibiting GABA release were pharmacologically identified as D4 (Table 1). In the supraoptic and paraventricular nuclei the D4 receptors reduce the GABAer-gic inhibition of the oxytocin- and vasopressin-secreting neurons and thus enhance neurophypophysial hormone release. 

The regulation of vasopressin secretion by DA is multifaceted, likely involving participation of one or more separate populations of DA neurons under different physiological situations. Although the possibility exists that extrahypothalamic DA neurons may be involved in reflex activation of vasopressin release (Cornish et al., 1997),... 

There is also experimental evidence that central DA neurons may be involved in inhibiting activated vasopressin secretion. In normal hydrated rats icv administration of DA suppresses anesthesia-induced vasopressin secretion (Forsling and Williams, 1984). Conversely, icv injection of a DA antagonist enhances vasopressin secretion in response to hemorrhage (Yamaguchi et al., 1990). No information is availability, however, regarding the identity of diencephalic neurons mediating the suppressive effects of DA on stimulated vasopressin release. 

Amico JA, Layden LM, Pomerantz SM, Cameron JL (1993) Oxytocin and vasopressin secretion in monkeys administered apomorphine and a D2 receptor agonist. Life Sci 52 1301-1309. 

Manzanares J, Lookingland KJ, Moore KE (1990a) Atrial natriuretic peptide-induced suppression of basal and dehydration-induced vasopressin secretion is not mediated by hypothalamic tuberohypophysial or tuberoinfundibular dopaminergic neurons. Brain Res 527 103-108. 

Yamaguchi K, Karakida T, Koike M, Hama H (1988) Central effects of catecholamine antagonists on angiotensin-induced vasopressin secretion in conscious rats. Acta Endocrinologica 775 82-88. 

Yamaguchi K, Hama H, Adachi C (1990) Inhibitory role of periventricular dopaminergic mechanisms in hemorrhage-induced vasopressin secretion in conscious rats. Brain Res 573 335-338. 

There are two types of disturbances in vasopressin secretion. In central diabetes insipidus, vasopressin secretion is reduced it can be treated by giving vasopressin or desmopressin, which has a longer half-life, by mouth or intranasally. In nephrogenic diabetes insipidus, the plasma vasopressin concentration may be normal but the kidney fails to respond. The latter type of diabetes insipidus does not respond to vasopressin therapy but, paradoxically, can be managed by giving a thiazide diuretic, for example chlortalidone, at a maintenance dose of 50 mg daily. 

Q8 What conditions could result in disorders of vasopressin secretion ... 

Q8 Disturbances of vasopressin secretion can be caused by tumours in the hypothalamus or pituitary gland, or trauma. Excess vasopressin is secreted following some types of brain damage and by certain tumours of the hypothalamus, prostate, pancreas or bladder. Decreased release may be caused by lesions in the posterior pituitary following inflammation or trauma. 

The authors reviewed nine other reported patients with MDMA-related SIADH, all of whom were women. They concluded that MDMA-associated SIADH is multifactorial and that MDMA may stimulate vasopressin secretion in susceptible individuals. They further suggested that hyponatremia can also occur secondary to voluntary increases in fluid or water intake aimed at preventing the adverse effects of MDMA. With appropriate treatment, full recovery is possible in almost all cases of this life-threatening condition. 

Besides the osmoreceptor mechanism of vasopressin release, the physiological regulation of vasopressin secretion also involves a pressure-volume mechanism that is distinct from the osmotic sensor. AVP release is regulated by baro-receptors that respond to alterations in blood volume. For example, a reduction in plasma volume or arterial pressure,... 

Bayiis, P, Gaskill M, Robertson G, Vasopressin secretion in primary polydipsia and cranial diabetes insipidus. Quart J Med NS 1981 50 345-58. 

El Majdoubi M, Poulain DA, Theodosis DT (1996) The glutamatergic innervation of oxytocin- and vasopressin-secreting neurons in the rat supraoptic nucleus and its contribution to lactation-induced synaptic plasticity. Eur J... 

Baylis PH. Osmoregulation and control of vasopressin secretion in healthy adults. Am J Physiol 1987 253(5 pt 2) R671-R678. 

Vasopressin promotes increased resorption of water in the renal distal tubule by stimulating insertion of water channels or aquaporins into the apical membranes of kidney tubules. Water is resorbed across the renal epithelium into the blood leading to a decrease in plasma osmolarity and an increase in the osmolarity of urine. In DI, this process is impaired, leading to excessive urine production, hi the absence of vasopressin, the kidney cannot resorb water and it flows out as urine. This condition can arise from a deficiency in vasopressin secretion from the posterior pituitary as a result of hypothalamic tumors, injury (as in the case of this patient) or infection. Alternately,... 

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