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)

Renal and systemic hemodynamics, plasma arginine vasopressin, plasma renin activity, plasma norepinephrine, blood volume and water loading test were studied in 10 patients with falciparum malaria without renal failure. Six patients responded to water load normally, while 4 patients had a decreased response to water load. The patients with a normal water load response had normal renal and systemic hemodynamics and a normal hormonal profile. The patients with a decreased response to water load had hyponatremia, hypervolemia, high cardiac index, low systemic vascular resistance, high plasma arginine vasopressin, high plasma renin activity, high plasma norepinephrine, low creatinine and p-aminohippurate clearances, low urine sodium and high urine osmolality. They had a lower mean arterial pressure during the acute phase of the disease than during the recovery phase. The findings suggest that a decreased response to water load is due to peripheral vasodilatation which results in a decreased effective blood volume leading to the release of vasopressin and norepinephrine, increased renin activity and decreased renal hemodynamics.
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PMID:Renal and systemic hemodynamics, in falciparum malaria. 895 63

Hyponatremia is a common complication after subarachnoid hemorrhage (SAH). Although the mechanism of hyponatremia is still controversial, cerebral salt-wasting syndrome (CSNS) is currently regarded as being more responsible than the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The aim of our study was to assess the plasma volume status of a patient with hyponatremia following subarachnoid hemorrhage. In doing this it may be possible to indirectly differentiate its pathogenesis. Fifty patients with SAH were studied. Twenty patients demonstrated hyponatremia (serum sodium < 135 mEq/L) during day 7 to 13 after subarachnoid hemorrhage. Patients with hyponatremia were categorized on the basis of their daily body weight, and central venous pressure. Group A consisted of patients with hypovolemia (16 patients), with the onset time of hyponatremia being day 7 to 9. Group B included those with hypervolemia (4 patients); hyponatremia was observed during day 10 to 11 and was corrected in all patients within 72 hours after induction of fluid restriction. Our findings suggest that hyponatremia following subarachnoid hemorrhage usually occurs due to CSWS, although SIADH remains as a minor pathogenesis. We conclude that the combination of daily body weight and CVP measurements is a simple and practical method to distinguish promptly SIADH from CSWS.
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PMID:[Differential diagnosis of hyponatremia following subarachnoid hemorrhage]. 963 2

Hypertension is a major risk for cardiovascular complications in dialysis patients. The pathogenesis of hypertension is multifactorial and is not completely understood. Hypervolemia has always been considered a major pathogenetic factor. In addition, a disturbed hormone profile with an activated renin angiotensin system, increased catecholamine, vasopressin and endothelin, and perhaps decreased nitrous oxide activity seem to play a role in the high incidence of hypertension in dialysis patients. The influence of autonomic dysfunction on blood pressure control in hemodialysis patients is not clear. The frequent use of erythropoietin during the last decade may have contributed to the increased incidence of hypertension in the dialysis population. Data from the First Report on Dialysis and Transplant in Sicily showed that hypertension is the cause of end-stage renal disease in 8% of dialysis patients and that the incidence of hypertension, as a cause of end-stage renal disease, increased with age.
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PMID:Hypertension in dialysis patients. 1020 66

Nocturia is a common and troublesome symptom in otherwise healthy elderly men and women. Nocturnal polyuria (an excessive nighttime urine output) has been documented to be a common finding in healthy men with lower urinary tract symptoms. It is also a presenting feature of various medical conditions, such as renal failure, hypercalcemia and diabetes. Fluid balance therapy is an option in those whose nocturia is secondary to nocturnal polyuria. If a reduction in fluid intake fails to reduce nocturnal frequency a variety of drug treatments may be beneficial. Several studies have confirmed the efficacy of intranasal DDAVP, a synthetic analog of antidiuretic hormone, in both healthy patients and those with neuropathic bladders, although fluid overload and hyponatremia are potential side effects. Other drug treatments include early evening diuretics, such as frusemide or bumetanide. More recently imipramine has shown therapeutic benefit in young adults with enuresis, and might prove to be useful in the elderly with nocturnal polyuria.
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PMID:Fluid balance therapy of nocturia in women. 1020 67

The management of heart failure has evolved in parallel with advances in the understanding of the disease process. Inotropes and diuretics are used to combat pump failure and fluid overload. While no convincing data has emerged regarding the long-term safety of inotropes, new exciting data concerning the role of diuretics, especially aldactone, has led to a renewed interest in this class of drug therapy. Angiotensin converting enzyme inhibitors (ACE inhibitors) were noted to not only affect symptomatology but also decrease mortality by interfering with the renin-angiotensin-aldosterone system. Recent research has focused on more complete blockade of the renin-angiotensin system than that achieved with ACE inhibitors alone with the addition of direct angiotensin II receptor blockers. This new class of drugs may become not only a reasonable alternative to ACE inhibitors in patients intolerant of the drug but also a possible addition to ACE inhibitors in the battle to prevent progression of remodelling and disease. beta-blockers are the most exciting new class of drugs used to combat heart failure. They appear not only to combat the remodelling process that occurs in the progression of disease but also other pathological events such as apoptosis and cellular oxidation. New medical therapies currently being investigated include novel agents such as endothelin antagonists, natriuretic peptides, vasopressin antagonists and anticytokine agents--all part of a new era in drug management of heart failure that has evolved with continued advances in the understanding of chronic heart failure (CHF).
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PMID:New advances in the pharmacological management of chronic heart failure. 1124 47

The hepatorenal syndrome (HRS) is a unique form of acute renal failure with entirely normal renal histology in advanced liver disease. Its diagnosis is made by exclusion of all causes of renal failure and by all the five major criteria as set by the International Ascites Club. The presence of hepatomegaly, poor nutritional status, and oesophageal varices at endoscopy are associated with a high risk of HRS. The liver tests, the Child-Pugh score, are of no value in prediction of its occurrence. Contraction of the effective blood volume, which may lead to renal hypoperfusion with preferential renal cortical ischaemia, is proposed pathogenesis of the condition. Because understanding of the pathogenesis of HRS is incomplete, therapy is supportive only. Optimal fluid management is vital as there is almost invariably a reduction in effective arterial blood volume. Dopamine, frusemide and haemofiltration may be helpful in management of fluid overload but do not affect renal function. TIPS has been used successfully in small series of patients. The vasopressin analog also has been used with early excellent response. The treatment of HRS has been discouraging and the only proven cure for HRS is liver transplantation at this point of time.
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PMID:Hepatorenal syndrome: pathophysiology and treatment. 1224 Aug 52

In diabetes insipidus, the amount of water ingested and the quantity and concentration of urine produced needs to be carefully regulated if fluid volume and osmolality are to be maintained within the normal range. One of the principal mechanisms controlling urine output is vasopressin which is released from the posterior pituitary gland and enhances water reabsorption from the renal collecting duct. In diabetes insipidus, the excessive production of dilute urine, and the causes of this clinical picture can be divided into three main groups: the first is primary polydipsia where the amount of fluid ingested is inappropriately large; the second group is cranial diabetes insipidus where the production of vasopressin is abnormally low; and, the third group is nephrogenic diabetes insipidus where the kidney response to vasopressin is impaired. The history and examination may suggest an underlying explanation for diabetes insipidus but a range of baseline and more extensive investigations may be required before a diagnosis can be reached. These investigations are not without risk, and the results need to be interpreted carefully because children do not always segregate neatly into a particular diagnostic category on the basis of one test alone. Children with cranial diabetes insipidus typically respond to arginine vasopressin or its manufactured analogue, desmopressin, with an increase in urine osmolality and an associated reduction in urine output. Such children usually require neuroimaging to look for evidence of evolving CNS pathology, such as an intracranial tumour. Vasopressin "replacement" with desmopressin is the treatment of choice in patients with cranial diabetes insipidus although extreme caution is required when treating babies or small children because of the danger of fluid overload. Abnormal production of other pituitary hormones in children with CNS disease can also influence fluid balance. Nephrogenic diabetes insipidus can be due to abnormal electrolyte concentrations, therefore these should be measured as part of the initial assessment. In a small number of children the defect is a primary abnormality of the vasopressin receptor or one of the water channel proteins (aquaporins) involved in water transport. The treatment of these patients is difficult and typically involves therapy with a diuretic such as chlorothiazide, as well as indomethacin. These agents enhance urine osmolality by their effect on circulating volume and renal solute and water handling. The fluid intake of most young children with primary polydipsia can be safely reduced to a more appropriate level.
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PMID:Diabetes insipidus in children: pathophysiology, diagnosis and management. 1243 Nov 31

RATS HAVE TWO PROMINENT RESPONSES TO DEHYDRATION: secretion of the antidiuretic hormone, vasopressin (VP), and thirst. Many signals directly affect both responses. These include two excitatory signals associated with increased plasma osmolality (pOsm) and two inhibitory signals associated with decreased pOsm (one each from cerebral and visceral osmoreceptors). In addition, both VP secretion and thirst during hypovolemia are stimulated by at least two signals, one neural (from cardiac baroreceptors) and one humoral (i.e., angiotensin II). In contrast to these evident similarities, there are definite dissimilarities in the signals for VP secretion and thirst. For example, acute hypervolemia inhibits VP secretion but not thirst, whereas acute hypertension inhibits thirst but not VP secretion. Thirst and VP secretion in rats each are stimulated by acute arterial hypotension, albeit not by the same signals; water intake is mediated by activation of the renin-angiotensin system but not by a neural signal from arterial baroreceptors, whereas the reverse may be true for the stimulation of VP secretion. These dissimilarities indicate that VP secretion and thirst in rats are neither invariably linked nor controlled by the same mechanisms.
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PMID:Controls of vasopressin secretion and thirst: similarities and dissimilarities in signals. 1252 27

In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), inappropriately elevated secretion of vasopressin can result in a reduction of antidiuretic efficacy: a phenomenon known as 'vasopressin escape'. We compared experimental SIADH with 1-deamino-8-d-arginine vasopressin (dDAVP)-excess rats, where both groups received continuous subcutaneous administration of dDAVP by osmotic minipump but the SIADH rats also received a liquid diet that induced hyponatraemia. The SIADH rats, but not the dDAVP excess rats, showed a marked attenuation of urinary concentrating ability. Vasopressin V(2) receptor binding capacity and mRNA expression were similar between the two groups, but the SIADH rats showed a diminished up-regulation of aquaporin-2 (AQP-2) mRNA and protein expression. These findings indicate the presence of tonicity-response regions in the AQP-2 promoter gene, and that either hypervolemia or hypotonicity may attenuate the postreceptor signalling of vasopressin in renal collecting duct cells in SIADH rats.
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PMID:Pathological role of aquaporin-2 in impaired water excretion and hyponatremia. 1508 64

Vasopressin (AVP), an antidiuretic hormone, is known to induce hypervolemia and to regulate the renal expression of aquaporin-2 (AQP2) water channels, but it is not yet known whether the latter are involved in the pathogenesis of essential hypertension. The aim of the present study was therefore to make a comparative study of blood pressure (BP), urinary volume (UV), urinary osmolarity (uOsm), urinary AQP2 (uAQP2), and plasma AVP levels (PAVP) in male spontaneously hypertensive rats (SHR; n = 30) at 3, 7, and 12 weeks of age and in male Wistar-Kyoto rats (WKY, n = 30), also after the subcutaneous administration of OPC-31260 (OPC), a human AVP V(2) receptor antagonist. At 3 weeks, SHR had markedly higher uOsm and lower UV levels than WKY. At 7 weeks, SHR were hypertensive, showing increased uAQP2, PAVP, and uOsm levels and a decreased UV. At 12 weeks, no significant changes were observed in this condition. At 7 and 12 weeks of age, OPC-treated WKY rats showed significant reduction in BP and uOsm and increase in UV with respect to untreated animals. From 3 weeks of age, OPC-treated SHR presented significantly lower BP levels, higher UV levels, and lower uOsm than untreated animals. In treated WKY and SHR, uAQP2 levels were lower than in untreated animals. The PAVP appeared to be higher in OPC-treated rats from both strains. These findings suggest that AVP and the AQP2 are involved in the pathogenesis of hypertension in SHR.
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PMID:Aquaporin-2 water channels in spontaneously hypertensive rats. 1560 25


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