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)

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.
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PMID:Plasma vasopressin in uncontrolled diabetes mellitus. 10 67

The hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.
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PMID:Vasopressin: deficiency, excess and the syndrome of inappropriate antiduretic hormone secretion. 10 6

Pretreatment with the neuropeptide DG-AVP (desglycrinamide9-arginine8-vasopressin) at two dose levels (25 and 125 mcg/kg) did not reduce intravenous morphine self-administration (0.25 mg/kg/inj) by morpine dependent monkeys, in comparison to pretreatment with saline or DG-AVP vehicle placebo. Food self-administration was also unaffected by DG-AVP pretreatment in comparison to control conditions. These data do not confirm previous reports of a dose-dependent suppression of heroin self-administration in rat following DG-AVP pretreatment [14].
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PMID:Effects of the neuropeptide DG-AVP on morphine and food self-administration by dependent rhesus monkey. 10 66

The ability of somatostatin to modify the water premeability of the toad bladder was examined. Somatostatin had a small effect on basal water flow and antagonized the hydrosmotic effect of vasopressin. Water flow induced by cyclic AMP was enhanced. These results may explain the diuretic and hyposthenuric effects of somatostatin in vivo.
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PMID:Antagonism of vasopressin-induced water flow by somatostatin. 10 4

The neurohypophyseal hormones vasopressin and oxytocin modulate memory processes. Vasopressin facilitates, while oxytocin attenuates memory consolidation and retrieval. These influences are located in different regions of the molecules. Thus, the neurohypophyseal hormones act as precursor molecules for neuropeptides involved in memory processes. The covalent ring structures of both vasopressin and oxytocin mainly affect consolidation; the linear parts, retrieval processes; while nearly the whole oxytocin or vasotocin molecule is needed for attenuation of consolidation and retrieval. Regional studies, utilizing microdissection techniques in combination with a sensitive radioenzymatic catecholamine assay, revealed a distinct pattern of effects on cerebral alpha-methyl-p-tyrosine methylester-induced catecholamine disappearance following intraventricular vasopressin administration in limbic midbrain structures. In situations in which the amount of bioavailable vasopressin in the brain is absent, as is the case in the Brattleboro rat with hereditary diabetes insipidus, or neutralized in normal Wistar rats following the intraventricular administration of antivasopressin serum, regional catecholamine disappearance in most cases is altered in a direction opposite to that observed after intracerebroventricular vasopressin administration. These results indicate that vasopressin modulates memory processes by modulation of neurotransmission in distinct catecholamine systems. Recent experiments suggest that the influence of vasopressin on memory consolidation is mediated by the dorsal noradrenergic bundle via terminal regions of this bundle.
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PMID:Neurohypophyseal principles and memory. 11 Jun 23

A new method for the simultaneous visualization of brain peptides and monoamine neurotransmitters was employed to analyze the integrated morphology of hypothalamic catecholamines and neurophysins in young and old monkeys. Immunocytochemical analysis using bovine neurophysin revealed a dual papulation of light and dark stained cells in the paraventricular nucleus in young and old macaques. In general, both populations of neurons stained with less density in old macaques indicating the possibility of a reduced content of neurophysin. Further analysis using specific neurophysin antisera for vasopressin or oxytocin revealed an appreciable decrease in the number of vassopressin-containing perikarya in the 20 year monkey whereas oxytocin-synthesizing neurons did not show a similar change in numbers with age. Qualitatively, terminal innervation patterns of hypothalamic catecholamines remained strikingly constant in spite of marked reductions in dark-stained neurophysin perikarya of the paraventricular nucleus.
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PMID:Integrated morphology of neuronal catecholamines and neurophysin in the aged macaque. 11 79

Five patients with refractory gastrointestinal bleeding from Mallory-Weiss tears of the esophagus were successfully treated with intraarterial infusions of vasopressin. Although transcatheter embolization has been shown to control the hemorrhage from these lesions, increased experience with and ease of vasopressin infusion suggest that infusion therapy should be the primary treatment method when more conservative measures are inadequate. Embolization techniques may be reserved for cases in which vasopressin therapy is contraindicated or unsuccessful.
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PMID:Intraarterial vasopressin infusion for treatment of Mallory-Weiss tears of the esophagogastric junction. 11 3

The effects of intracerebral injection of angiotensin II (AII) on both water intake and arginine-vasopressin (AVP) release were tested on unanesthetized rhesus monkeys (Macaca mulatta). Injection of 10(-10) mol of peptide was administered with a cannula microinjection system stereotaxically implanted into different diencephalic structures. The preoptic area, anterior part of third ventricle, caudate nucleus, and septum appeared to be the injection sites most effective in eliciting both drinking behavior and AVP release when the animal did not have access to water. On the contrary, when water was presented, AVP release was blocked after AII microinjections in the preoptic area and the third ventricle. No drinking was observed after microinjection in the supraopticus nucleus although AVP release was stimulated. These data suggest that AII might be effective in the regulation of water balance by centrally controlling both the input (drinking) and the output (ADH secretion) of water.
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PMID:Vasopressin release and drinking induced by intracranial injection of angiotensin II in monkey. 11 63

Serum gastrin increased in patients with pernicious anaemia after a beef-meal, but decreased after an oral load of glucose, xylose or sodium chloride. 50 g of glucose and 25 or 75 g of xylose suppressed serum gastrin to approximately 40% of basal values at 60 min and were slightly more effective than 10 g of sodium chloride. There was no rise in beef-meal stimulated serum gastrin concentration in vagotomized patients and only a slight rise in two patients with duodenal ulcer when an oral dose of 10 g of sodium chloride was given together with the beef-meal. 25 g of xylose suppressed basal serum gastrin concentration significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in all subjects examined. Further studies indicated, however, that vasopressin was only effective when pharmacological plasma concenten orally and intraduodenally were compared in six patients with pernicious anaemia. Serum gastrin concentration decreased approximately to the same extent in both experiments. It is concluded that the inhibitory effect of glucose on gastrin secretion most likely is mediated hormonally via osmo-receptors located in the small intestine.
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PMID:Inhibition of gastrin secretion by hypertonic solutions in patients with pernicious anaemia and duodenal ulcer. 11 45

A patient with a syndrome of inappropriate antidiuretic hormone secretion secondary to an undifferentiated bronchogenic carcinoma with distant metastases was treated with demethylchlortetracycline. Up until recently, treatment of this syndrome was based on water restriction and when the plasma sodium concentration became extremely low, hypertonic saline solution administration. Recently it has been demonstrated that the antibiotic demethylchlortetracycline inhibits the action of the antidiuretic hormone on the renal tubules. The drug has been used successfully in five patients with the syndrome of inappropriate antidiuretic hormone secretion. The administration of 900 mg of demethylchlortetracycline per day for 7 days in our patient produced an increase of free water clearance, diuresis, plasma sodium concentration, and plasma osmolarity. Urinary excretion of sodium and urinary osmolarity declined. Furthermore, the neurological symptoms attributed to hyponatremia improved markedly. The patient lost 6 kg during treatment, probably because of negative water balance induced by demethylchlortetracycline. Even though the administration of demethylchlortetracycline did not produce significant decreases in the glomerular filtration rate or renal blood flow in our patient, it is advisable to control the renal function in individuals treated with this drug since it may on occasion determine renal insufficiency.
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PMID:[Treatment of the syndrome of inappropriate antidiuretic hormone secretion with demethylchlortetracycline (author's transl)]. 11 37


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