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)

It has been shown that several mammalian species increase the excretion of sodium in urine as they become dehydrated. This dehydration-induced natriuresis occurs despite simultaneous hypovolemia, and it can be blocked by an experimentally-induced reduction in the sodium concentration of CSF, or by ablation of the periventricular tissue in the vicinity of the lamina terminalis. These two experimental procedures also disrupt thirst and vasopressin secretion. There may therefore be common features involved in the central control of osmoregulatory thirst, vasopressin secretion and sodium excretion. Experimental evidence in sheep suggests that whenever the tonicity of body fluids increases, a centrally mediated natriuretic mechanism is engaged. This cerebral natriuretic mechanism may contribute along with other influences such as the extracellular fluid volume, aldosterone and atrial natriuretic peptide, to determine the rate of sodium excretion by kidneys. The efferent pathway from brain to kidney mediating osmoregulatory natriuresis is not known. It is probably hormonal, because renal denervation does not disrupt such natriuresis.
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PMID:Common aspects of the cerebral regulation of thirst and renal sodium excretion. 163 66

The effect of elevated cerebrospinal fluid Na+ concentration (CSF [Na+]) on the tolerance of blood loss, and concomitant cardiovascular and humoral responses were studied in conscious sheep. A slow (0.7 ml kg-1 min-1) venous haemorrhage was continued until the mean systemic arterial pressure suddenly decreased to less than 50 mmHg, or in the absence of hypotension, until a total blood loss of 25 ml kg-1. Significantly more blood had to be removed to induce hypotension in animals receiving an intracerebroventricular (i.c.v.) infusion (0.02 ml min-1) of 0.5 M NaCl (starting 30 min before haemorrhage and continued throughout the experiment) compared to control haemorrhages without concomitant i.c.v. infusion (22.7 +/- 1.2 ml vs 16.9 +/- 0.9 ml kg-1). In one animal, subjected to 0.5 M NaCl infusion, the blood pressure was still maintained at 25 ml kg-1 of haemorrhage. In spite of a larger blood loss, animals receiving i.c.v. infusion of hypertonic NaCl had an improved recovery of the blood pressure after haemorrhage, due to a better maintained cardiac output rather than to a reinforced increase of the vascular resistance. The improved cardiovascular responses to haemorrhage during elevated CSF [Na+] are not readily explained by the effects on the plasma concentrations of vasopressin, angiotensin II or noradrenaline, although the latter was augmented. The plasma protein concentration decreased already during the 30 min of hypertonic NaCl infusion preceding haemorrhage, and the haemodilution caused by the subsequent blood removal was aggravated, which indicates that this treatment also causes transfer of fluid to the plasma compartment. We conclude that elevated CSF [Na+] increases tolerance to haemorrhage and improves cardiovascular function after blood loss in sheep. Since the haemodynamic responses in many respects were similar to those reported in response to the systemic administration of a small volume of hypertonic NaCl solution in haemorrhagic shock, part of the effect of that treatment may be mediated via cerebral effects of increased Na+ concentration.
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PMID:Increased resistance to haemorrhage induced by intracerebroventricular infusion of hypertonic NaCl in conscious sheep. 163 46

Thoracic shifts of blood stimulate diuresis and natriuresis during spaceflight. The available literature is not conclusive as to whether thoracic afferent neurons are essential for this response. Possibly, an acute elevation in cerebrospinal fluid pressure (CSF-p) activates central compensatory mechanisms. This is because central venous pressure is elevated by thoracic blood shifts and may reduce the pressure gradient for drainage of CSF into the venous sinuses. We tested whether rats with constriction of the venous return at the level of the heart (0.4 mm maximum diameter) had CSF-p different from sham-operated controls. CSF-p in the immediate postoperative period, as well as 1 and 10 days after surgery, were within normal limits and did not differ (p greater than 0.05). Blood collected at the end of the experiment showed no group differences (p greater than 0.05) in the hematocrit, or concentrations of sodium, potassium or vasopressin. Thus, changes in CSF-p, per se, appear to be insufficient to explain the cardiovascular or salt/water balance readjustments observed in spaceflight. It is likely that compensatory systems are highly redundant.
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PMID:Cerebrospinal fluid pressure of conscious rats after venous constriction at the right atrium. 177 18

The influence of naloxone on the release in limbic brain areas of both oxytocin (OXT) and vasopressin, measured by radioimmunoassay, was studied in conscious parturient rats. Three consecutive 30-min push-pull perfusions (20 microliters artificial CSF/min) were made, via previously implanted guide cannulae, within the medio-lateral septum and dorsal hippocampus of parturient animals given saline or naloxone hydrochloride (5 mg/kg body weight) after delivery of the second pup. OXT release in the hippocampus, but not in the septum, was increased during parturition, compared to day 1 post partum. During the first 30-min collection period following naloxone administration, release of OXT was significantly elevated within the septum (44% compared to saline controls, p less than 0.002), but not in the dorsal hippocampus; vasopressin release was not affected. In contrast, on day 1 post partum, naloxone, administered 5 min after starting two consecutive perfusions failed to alter OXT release in septum or hippocampus in conscious rats. Naloxone, known to increase the release of OXT also from the posterior pituitary during parturition, speeded the parturition process significantly between the birth of pups 4 and 8 during push-pull perfusion of septum or hippocampus. The data suggest that endogenous opioid inhibition is involved in the regulation of central OXT release, but not vasopressin release, during parturition. Together with previous studies on OXT release from the posterior pituitary, it seems that during parturition there is coordinated endogenous opioid action on the release of OXT both into blood and into the brain.
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PMID:Naloxone increases the release of oxytocin, but not vasopressin, within limbic brain areas of conscious parturient rats: a push-pull perfusion study. 178 42

A rare case of an abscess in the cavum septi pellucidi (CSP) is described and previously reported cases are reviewed. A 60-year-old male was admitted to the hospital because a diagnosis of cerebellar hemisphere infarction was made on CT scan. Seven years earlier, the patient had undergone a craniotomy for aneurysm clipping, and a ventriculo-peritoneal shunt was installed for normal pressure hydrocephalus 14 days after the aneurysmal rupture. On his second hospitalization CT scan also demonstrated CSP but this was not associated with ventriculomegaly. He was placed on a rehabilitation regimen and his hospital course was uneventful. Two months later, however, he developed hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. After analysis of CSF obtained from the shunting device, a diagnosis of meningitis was made and CSF culture revealed E. coli infection. A part of the peritoneal tubing was torn and missing when the tube was removed from the peritoneal cavity and converted to outer drainage. Being treated with intrathecal and intravenous antibiotics administration, the meningitis subsided. However, CT scan taken twelve days after the onset of the infection showed an abscess in CSP which showed ring enhancement after contrast media. Therefore, the patient continued to receive intravenous antibiotics to counter the mass effect due to the abscess. The abscess had disappeared on follow-up CT scan obtained ten days later. The patient, however, eventually expired after iatrogenic hypernatremia associated with acute renal failure. The patient was submitted to an autopsy. The authors speculate that the abscess developed through a retrograde cisternal route after infection which had originated from bowel perforation by the peritoneal shunt tube.
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PMID:[A case report: abscess of the cavum septi pellucidi]. 202 72

Two patients treated by chemotherapy for a non-Hodgkin malignant lymphoma developed focal neurological symptoms including disorientation, hemoplegia, and cortical blindness 5 and 15 days after the end of a polychemotherapy course, including methotrexate and vindesine. In both patients ECG and blood pressure were normal. Case 1 had a slight increase of protein level without cells on CSF examination and presented with a paralytic ileus. Case 2 developed an inappropriate antidiuretic hormone secretion (IADHS) syndrome. In both cases, noncontrast CT scans showed bilateral, symmetrical low density areas within the temporooccipital regions. Postcontrast CT images stressed major cortical and subcortical enhancement predominantly over the gray matter. In Case 2 the lesions also affected the right parietal lobe. Magnetic resonance scans 2-3 weeks after the onset of neurological symptoms demonstrated low intensity signal lesions on T1-weighted images and bright signal on T2-weighted images. In Case 1 the visual deficit failed to regress and in Case 2 the patient died 2 months later because of the natural evolution of her lymphoma. The clinical and radiological data suggested that a vascular ischemic process was responsible for the cerebral lesions in these two patients. As Vinca alkaloids and not methotrexate have been implicated as a cause of cortical blindness, and as our two patients presented signs of overdose of vindesine (paralytic ileus and IADHS), we suggest that the neurological and radiological abnormalities in our patients may have been due to neurotoxicity of vindesine.
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PMID:Cortical blindness during chemotherapy: clinical, CT, and MR correlations. 231 56

The anterodorsal part of the third ventricle of conscious ducks was perfused intracerebroventricularly (icv) for 10 min with norepinephrine (NE) or with its agonists phenylephrine (alpha 1, Phe), isoproterenol (beta, Iso), and clonidine (alpha 2, Clo) in artificial CSF (aCSF). Their effects on the plasma level of antidiuretic hormone (AVT, arginine vasotocin in birds), urine excretion, heart rate (HR), and mean arterial pressure (MAP) were investigated in steady-state water diuresis. The correct position of the icv cannula was confirmed by enhanced AVT release and antidiuresis in response to icv perfusion of aCSF made hypertonic (400 mosmol/kgH2O) by adding NaCl. Icv perfusion with hypertonic aCSF and 750 ng/min NE had comparable effects on AVT release and urine excretion, but hypertonic aCSF caused small increases in MAP and HR, whereas NE depressed both MAP and HR. Antidiuresis and circulatory depression caused by NE icv perfusion was dose dependent. Among the adrenergic agonists perfused at similar doses (188 ng/min), only Iso stimulated AVT release. Iso and Phe had small depressive effects on MAP and HR (less than 10%). Clo depressed circulation by greater than 20% for longer than 60 min, and AVT release became significantly reduced 30 min after the start of icv perfusion. The consistent results in ducks contrast with the equivocal data hitherto reported for central stimulations with NE or its agonists in mammals and may be due to the concentric perfusion system used in our study for localized stimulations in the vicinity of the paraventricular nucleus.
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PMID:ADH, renal, and circulatory responses to adrenergic stimulation in anterior third ventricle. 238 40

A 35-year-old man with refractory low grade diffuse centroblastic centrocytic non-Hodgkin's lymphoma was treated accidentally with an overdose of multiple chemotherapeutic agents. He was given adriamycin 50 mg/m2 and cyclophosphamide 350 mg/m2 for 6 days followed by 4 days of vincristine 1 mg/m2 and bleomycin 10 mg/m2. He was transferred when he developed pancytopenia, fever, severe mucositis, ileus and peripheral neuropathy. He was treated with broad spectrum antibiotics, red cell and single donor platelet transfusions and strict parenteral nutrition. In addition, he was given a continuous infusion of 400 micrograms daily human recombinant granulocyte macrophage-colony stimulating factor (rh GM-CSF) for 17 days. Intractable severe bleeding from his oral mucositis necessitated treatment with a continuous infusion of 8-ornithine-vasopressin for 8 days. He recovered and could be discharged home after 36 days of hospitalization with normal blood counts and without severe sequelae.
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PMID:Accidental overdose of multiple chemotherapeutic agents. 248 48

ANF is an exciting, newly discovered hormone that has significant potential for furthering our understanding of the complex interactions involved in fluid and electrolyte balance. In addition to effects on water and salt balance, it is a potent vasodilator, as well as inhibitor of renin, angiotensin II, aldosterone, and vasopressin. ANF is primarily produced in the atria, but production in the brain is suggestive of action as a neuropeptide and as a potential regulator of CSF production. Receptors are found throughout the heart, vascular tree, kidney, adrenal gland, and brain. The stimulus for release appears to be atrial stretch, which may be secondary to intravascular fluid changes. It causes hemoconcentration and may be an important regulator of interstitial fluid distribution as well as capillary permeability. Patients with CHF and renal failure have been found to have elevated levels that decrease in response to treatment. Potentially, it may be useful as a therapeutic agent in acute renal failure, CHF and other fluid disturbances. ANF is a testament to the incredible advances in peptide biology. Within 2 years of the discovery, ANF was sequenced and cloned. Since that time, literally thousands of papers describing its actions have been published. Our knowledge about this hormone grows at an exponential rate. It is clear that this hormone is intimately involved in the regulation of fluid and electrolyte balance, vascular tone, and the pathophysiology of CHF but many questions remain unanswered. Continued research will provide many of the missing pieces to this very complex, new hormone system.
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PMID:Atrial natriuretic factor. 252 98

Thirty-two Sprague-Dawley rats were divided into four groups, eight rats per group. Animals were hypophysectomized with removal of both the pars distalis and the neural lobe of the neurohypophysis. Groups of eight rats were euthanized 1, 2, 4 and 8 weeks following hypophysectomy and prepared for routine scanning electron microscopy (SEM) and correlative immunoelectron microscopy employing antisera against arginine vasopressin (AVP). Eight normal rats served as controls. In experimental rats that survived one to eight weeks posthypophysectomy, remarkable neuroanatomical alterations were notable in the median eminence and adjacent third cerebral ventricular lumen. In contrast to normal control rats, large numbers of neurites were observed with SEM to insinuate from the lateral recess into the cerebral ventricular lumen and as early as one week following hypophysectomy they overgrew the apical surfaces of ependymal cells that constitute the lining of the cerebral ventricle. Immunoelectron microscopy revealed that a significant proportion of these neurites were magnocellular in origin in that they harbored AVP-positive neurosecretory vesicles. In addition to large numbers of invading magnocellular neurites, neuronal perikayria with apparent axosomatic synapses were observed to emerge upon the thick feltwork of invading axons, the latter of which appeared to freely terminate within the ventricular lumen. AVP-positive axon profiles were, in addition, seen to terminate upon the basal lamina of portal perivascular spaces in the zona externa of the median eminence. These data are consistent with the idea that following hypophysectomy (to include high stalk section of the neurohypophyseal system), that there is rapid, and dynamic sprouting and regrowth of AVP-positive axons into the adjacent third cerebral ventricular lumen and to the contact zone of the median eminence as well. This phenomenon may represent a compensatory physiological response to injury of the neurohypophyseal system characterized by a highly plastic neuroanatomical reorganization of magnocellular elements which appear to utilize the CSF of the third cerebral ventricle as a functional terminus for the neurocisternal secretion of AVP which ultimately enters the systemic circulation.
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PMID:Correlative scanning-immunoelectromicroscopic analysis of neuropeptide localization and neuronal plasticity in the endocrine hypothalamus. 270 45


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