Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple system atrophy (MSA) is a heterogeneous group of central neurological degenerations often associated with diffuse deterioration of the hypothalamic cholinergic neurons. In the hypothesis of an altered cholinergic regulation of vasopressin release, we evaluated vasopressin response to metoclopramide (20 mg i.v.), a cholinomimetic agonist, in 12 MSA patients. In the same patients the hemodynamic and osmolal control of vasopressin was also evaluated. We found that MSA patients had significantly lower basal plasma vasopressin values and higher plasma osmolality than control subjects. However, they displayed a normal vasopressin response to osmotic stimulation. During head-up tilting, orthostatic hypotension occurred in all patients, and the vasopressin response to hypotension was severely blunted in 5 of 12 patients, thus demonstrating the presence of a lesion of the afferent noradrenergic pathways. Metoclopramide increased vasopressin in control subjects, whereas MSA patients did not display any increase in vasopressin. These results clearly indicate that cholinergic neurons that regulate vasopressin release are damaged in MSA. Such an alteration may be dissociated from the lesion of the afferent noradrenergic pathways. As a consequence of the altered vasopressin release, MSA patients show lower plasma vasopressin levels with consequent propensity to dehydration and hypovolemia, which may further aggravate their hypotension.
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PMID:Altered vasopressin response to metoclopramide in multiple system atrophy: evidence of a cholinergic defect in the hypothalamus. 131 10

Metoclopramide was orally administered (10 or 20 mg) to 22 subjects, 75 min before parabolic flight. Serum levels of ACTH, EPI, NE, and vasopressin (AVP) were unaltered by metoclopramide. AVP and ACTH (1.2 and 36 pg.ml-1) were elevated 77 and 3.8-fold (92.3 and 135 pg.ml-1) following emesis, after 40 parabolas (68.7 and 140 pg.ml-1) and landing (8.7 and 79 pg.ml-1). Seven subjects displaying no nausea and no emesis demonstrated smaller elevations (8.2 and 2.2-fold). Of 15 vomiting subjects, 7 reported no nausea and had lower elevations of AVP with faster recoveries. These findings are consistent with Rowe's suggestion (1979) that nausea may correlate with AVP release. Inhibition of AVP release by fluid shifts during microgravity might account for our findings and astronaut-reported episodes of vomiting without nausea. Elevations in EPI followed emesis or exposure to 40 parabolas whether emesis occurred or not. Only emesis elevated NE (578 to 840 pg.ml-1).
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PMID:Hormonal responses of metoclopramide-treated subjects experiencing nausea or emesis during parabolic flight. 282 88

There is reason to believe that the dopaminergic system plays a role in the control of salt and water metabolism in the neonate. Therefore, we performed a series of studies designed to test this assumption and reveal the relationship between dopamine (DA) and other factors known to affect salt and water balance. The postnatal course of urinary dopamine excretion was assessed in a group of premature infants kept on low or high salt diet. A clear association between sodium depletion and increased DA excretion, and between reduction in DA excretion and restoration of salt balance was demonstrated. In premature infants with cardiopulmonary distress, DA therapy resulted in an increase in sodium and water diuresis, enhanced plasma renin activity (PRA) and decreased plasma prolactin level; the plasma aldosterone (pAldo) level remained stable. Metoclopramide (MTC), a specific DA antagonist given to premature infants to treat functional gastrointestinal disturbances, induced an increase in Na+ and water excretion which was associated with significant falls in plasma and urinary aldosterone, but left PRA unaltered. Arginine vasopressin excretion also fell after MTC, but this change was not associated with increased free water clearance. These results suggest that endogenous DA has no apparent influence on PRA and, contrary to findings in adults, it stimulates the secretion of aldosterone and vasopressin and thus tubular sodium and water reabsorption.
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PMID:Dopaminergic control of neonatal salt and water metabolism. 315 91

A decreased concentration of vasopressin (AVP) in the plasma of patients with Alzheimer's disease has been shown recently and suggests damage to hypothalamic neurosecretory cells. To verify this, osmolar and hypotension (sodium nitroprusside) stimulations on AVP release were applied. The effect of metoclopramide, a powerful stimulator of AVP, was also assessed. Patients with Alzheimer's disease released AVP normally after hypotension. However, AVP response to osmotic stimulation was altered in eight out of 10 patients, owing to low osmoreceptor sensitivity and/or high threshold. Metoclopramide increased AVP in controls but not in patients. Normal AVP response to hypotension in patients with Alzheimer's disease makes it unlikely that there is a significant anatomical loss or damage of hypothalamic neurosecretory cells. Alterations in osmoreceptor function and AVP unresponsiveness to metoclopramide point to damage in the control of AVP release in Alzheimer's disease.
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PMID:Alterations in vasopressin regulation in Alzheimer's disease. 320 98

The vasopressin response of rats to i.p. injection of hypertonic sodium chloride (1.5 mol/l) was compared with that following i.v. infusion of 1.05 mol sodium chloride/l. The two regimes produced a similar vasopressin response in terms of the osmotic threshold, although the slopes of the plot of plasma vasopressin levels against plasma osmolality were not identical. Pretreatment with naloxone and levallorphan increased the resting vasopressin levels and effectively potentiated vasopressin release in response to hypertonic saline by reducing the osmotic threshold for hormone release. Thus, opioid peptides appear to exert an inhibitory effect on vasopressin release under resting and stimulated conditions. The adrenoreceptor antagonists propranolol, phenyoxybenzamine and phentolamine produced a fall in resting vasopressin concentrations while propranolol and phenoxybenzamine potentiated the osmotic release of vasopressin in association with a fall in the osmotic threshold. This would suggest that noradrenergic pathways are excitatory at rest while having an inhibitory effect on the osmotic response. Metoclopramide also produced a fall in resting plasma vasopressin concentrations while increasing the osmotic response. In contrast haloperidol did not affect the vasopressin response.
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PMID:A comparison of the vasopressin response of rats to intraperitoneal and intravenous administration of hypertonic saline, and the effect of opioid and aminergic antagonists. 335 18

This study was performed in order to investigate the dopaminergic mechanism involved in the control of arginine-vasopressin (AVP) secretion in normal men. Plasma AVP concentrations were measured before and after the administration of an i.v. bolus of 10 mg metoclopramide or domperidone to twelve healthy males. Metoclopramide, a cerebral and peripheral antagonist of dopaminergic receptors, significantly stimulated AVP secretion, whereas domperidone, a dopamine antagonist which does not cross the blood-brain barrier, was without effect. These data suggest that metoclopramide stimulates the release of AVP by blocking dopaminergic receptors in structures located inside the blood-brain barrier. Alternatively, it is possible that the stimulation of AVP release induced by metoclopramide does not occur through inhibition of dopamine receptors but rather through interaction with other neuroendocrine pathways.
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PMID:Different effects of metoclopramide and domperidone on arginine-vasopressin secretion in man. 376 59

alpha MSH is present in high concentrations in the intermediate lobe of the fetal pituitary and has been implicated as a regulator of fetal adrenal steroidogenesis and fetal growth. However, there are few data regarding alpha MSH levels in fetal plasma or the control of fetal alpha MSH secretion. We measured alpha MSH immunoactivity in the plasma of chronically catheterized fetal lambs (gestational age, 116-138 days), newborn lambs, and adult sheep both in the baseline state and after dopamine receptor blockade with metoclopramide. The effect of metoclopramide on the release of another proopiomelanocortin-derived peptide, N-acetyl-beta-endorphin (N-acetyl-beta EP), which is synthesized together with alpha MSH in the intermediate lobe, was also studied. Baseline fetal plasma alpha MSH was significantly greater than maternal alpha MSH [35.6 +/- 2.2 (+/- SEM) vs. 10.0 +/- 1.0 pg/ml]. In eight studies in five fetal lambs, alpha MSH rose to a peak level of 121 +/- 23 pg/ml 15 min after metoclopramide administration to the fetus. Simultaneous maternal alpha MSH levels did not change, suggesting that the alpha MSH in fetal plasma was of fetal pituitary origin. Gel filtration of pooled fetal plasma extracts revealed that the alpha MSH immunoactivity eluted in the same position as the alpha MSH standard. Metoclopramide caused the secretion of nearly equimolar amounts of alpha MSH and N-acetyl-beta EP into fetal plasma. In four fetal lambs, basal N-acetyl-beta EP levels of 156 +/- 34 pg/ml rose to 305 +/- 65 pg/ml 15 min after metoclopramide treatment. Metoclopramide also stimulated plasma alpha MSH in newborn and adult sheep. In six newborn lambs, alpha MSH rose from 45.2 +/- 13 to 211 +/- 38 pg/ml 15 min after metoclopramide treatment, whereas in four adult sheep, a basal alpha MSH level of 11.1 +/- 2.2 pg/ml rose to 20.1 +/- 2.7 pg/ml 15 min after metoclopramide. In addition, metoclopramide stimulated fetal and neonatal PRL secretion, but had no effect on plasma vasopressin concentrations or acid-base and blood gas values. These studies indicate that immunoreactive alpha MSH and N-acetyl-beta EP are secreted into ovine fetal plasma and that the secretion of these peptides in the fetus appears to be under tonic dopamine inhibition, as is the case in the adult sheep and newborn lamb.
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PMID:Dopaminergic regulation of alpha-melanocyte-stimulating hormone and N-acetyl-beta-endorphin secretion in the fetal lamb. 380 22

Bromocriptine (5-100 microgram; 6.7 X 10(-9) - 1.3 X 10(-7) mol.), SK&F 38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine, 0.5-5 mg; 1.7 X 10(-6)-1.7 X 10(-5) mol.) and apomorphine (20-200 microgram; 6.4 X 19(-8)-6.4 X 10(-7) mol.) administered into rat kidneys perfused with physiological solution containing vasopressin and pretreated with an alpha-adrenoreceptor antagonist produced vasodilator responses similar to dopamine (50-100 microgram; 2.6 X 10(-8)-5.3 X 10(-7) mol.). THe responses to bromocriptine, SK&F 38393 and apomorphine were found to be significantly reduced by the dopamine receptor antagonist ergometrine (50 microgram; 1.1 X 10(-7) mol.). Metoclopramide (250 microgram; 7.4 X 10(-7) mol.) was found to be an effective antagonist of dopamine, bromocriptine, SK&F 38393 and apomorphine. Apomorphine (20, 50 microgram; 6.4 X 10(-8), 1.6 X 10(-7) mo.) was found to act as a partial agonist on dopamine receptors in this preparation.
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PMID:A comparison of the responses to some dopamine-receptor agonists and antagonists in the isolated perfused rat kidney. 697 30

1. The anti-emetic drug metoclopramide has been shown to stimulate secretion of the antidiuretic hormone arginine vasopressin. Since metoclopramide is used to treat nausea, which is another potent stimulus to vasopressin secretion, the aim of this study was to determine whether metoclopramide might limit free water excretion and so cause hyponatraemia. 2. Metoclopramide 20 mg (0.2-0.3 mg/kg), prochlorperazine 12.5 mg (0.1-0.2 mg/kg) and placebo were administered intravenously in a double blind randomized crossover way at 2 week intervals and the effects on urine flow rate, plasma osmolality, thirst ratings and plasma sodium and atrial natriuretic peptide concentrations determined in water-loaded (10 mL/kg) healthy young men. 3. There were no differential effects on any variable of either drug versus placebo. 4. These results indicate that metoclopramide is unlikely to cause any significant water retention in a clinical setting or precipitate hyponatraemia.
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PMID:Effects of anti-emetics on water excretion in humans. 815 53

Pharmacologic therapy used during acute variceal bleeding may control the bleeding episode, minimized transfusion requirements, and prevent early rebleeding. Several options for pharmacologic therapy exist in this setting and include: vasopressin in combination with nitroglycerin, terlipressin, somatostatin, and octreotide. Metoclopramide and domperidone may also be useful but require additional study. At present, octreotide, administered intravenously as soon as variceal bleeding is suspected, is favored.
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PMID:Pharmacological prevention of rebleeding. 1033 44


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