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)

Management of postoperative diabetes insipidus (DI) frequently requires intermittent treatment with multiple subcutaneous injections of pituitrin or vasopressin, in doses averaging 20 IU/24 h. Use of a syringe pump for a continuous infusion of ultralow doses of pituitrin produced uniform, constant, and sustained reduction of urinary output, thus facilitating regular fluid replacement. Twelve patients with postoperative DI received iv pituitrin at a dose of 1.6 +/- 0.26 mIU/kg X h (1 to 2 IU/24 h). The antidiuretic effect began at the third hour of treatment, peaked by the sixth hour (diuresis of 37 ml/h, specific gravity of 1.018 +/- 0.002), and was sustained throughout infusion. Polyuria recurred 3 h after the infusion was discontinued; this rapid reversibility is highly advantageous when excessive fluid intake causes overhydration. Pressor effects were not observed during the treatment period.
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PMID:Ultralow doses of vasopressin in the management of diabetes insipidus. 243 34

The involvement of prostaglandin E2 (PGE2), adenosine 3',5'-cyclic monophosphate (cAMP), and vasopressin in lithium-induced polyuria was investigated in rats. Administration of LiCl (4 mmol/kg body wt) for 7 days induced a marked polyuria with a significant excretion of urinary PGE2. Administration of indomethacin (IND, 5 mg/kg body wt) for 4 days to lithium-induced diabetes insipidus (LiDI) rats diminished urine volume by 80% and urinary PGE2 by 85%. The in vitro data of the intact rat kidney showed that lithium stimulated arginine vasopressin (AVP)-induced PGE2 production and suggested that PGE2 suppressed cAMP synthesis in rat renal medulla. The AVP-induced PGE2 synthesis was greater and the AVP-stimulated cAMP production lower in the LiDI rat kidney in vitro. Interference of the vasopressin-associated cAMP system and the increased PGE2 synthesis in the kidney may be involved in the development of LiDI. The reduced cAMP production in the LiDI rat kidney might be partly due to the increased PGE2 synthesis. In LiDI rats plasma vasopressin increased, whereas AVP concentration in the hypothalamus and the neurohypophysis significantly decreased. It is postulated that lithium stimulates vasopressin release from the central nervous system and that elevated plasma vasopressin potentiates PGE2 production in the kidney synergistically with lithium.
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PMID:Involvement of prostaglandin E2, cAMP, and vasopressin in lithium-induced polyuria. 245 89

Rats with mammillary electrolytic lesions show a strong polydipsia and polyuria. This over-consumption may be primary or secondary to the polyuric effect. In this regard, mammillary lesioned rats excrete a greater amount of urine compared with control animals when matched in daily water consumption (partial water deprivation). Moreover, this abnormal water intake is significantly reversed by treatment with Pitressin, a vasopressin analogue. These results suggest that the polydipsia may be determined by the urinary water loss. However, when subjected to the bilateral ureter ligation, the experimental animals still outdrink the control ones, thus also suggesting a primary component of the polydipsia under study. The possible explanation of these components in relation to the mammillary polydipsia is discussed.
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PMID:[Primary/secondary characteristics of polydipsia induced by electrolytic lesion of the mammillary bodies]. 250 36

Sclerosing peritonitis is a serious complication in patients on long-term peritoneal dialysis; it markedly decreases transport of water and solute across the peritoneal membrane. Although the precise mechanism is unknown, organic compounds (i.e., plasticizers) from plastic tubing and dialysis bags have been suggested to be a cause of the syndrome. The effects of three such compounds on water and sodium transport in vitro were studied in the toad bladder. The compounds studied were didodecylphthalate, dioctylphthalate, and benzylbutylphthalate. After 4 hr incubation in vitro, dioctylphthalate and benzylbutylphthalate significantly inhibited vasopressin-stimulated water flow in toad bladder. Basal water flow was not affected by any of the three compounds. Sodium transport, as measured using short-circuit current, was decreased to an equivalent degree by all compounds; inhibition of short-circuit current was dose dependent and was approximately 30% at 10(-3) M. The onset of action was between 3.5 and 4 hr, and the effect on short-circuit current was not reversible. These results demonstrate that the plasticizers (to which patients of all sorts are commonly exposed) inhibit transport across living membranes. In the toad bladder these compounds decrease sodium transport and maximal water flow. Although other evidence suggests that the cumulative toxic effects of these compounds may play a causal role in sclerosing peritonitis in patients on peritoneal dialysis, our study suggests that chronic exposure to the phthalate acid esters in patients with normal renal function may result in sodium wastage, polyuria, and a concentrating defect resistant to AVP.
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PMID:Effect of phthalate acid esters on transport in toad bladder membrane. 255 Jun 21

In two dogs with pituitary-dependent hyperadrenocorticism, adrenocorticolysis with o.p'-DDD led to the disappearance of the signs and symptoms except for the polyuria. After a modified water-deprivation test the osmoregulation of vasopressin release was studied by hypertonic saline infusion. In both dogs the hypertonicity, thus induced, resulted in very minimal responses of the vasopressin secretion.
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PMID:Persistent polyuria in two dogs following adrenocorticolysis for pituitary-dependent hyperadrenocorticism. 255 4

From 1975-1986 6 boys with congenital nephrogenic diabetes insipidus were diagnosed at the age of 3 months to 10 years. Symptoms appeared within the first few weeks of life. The diagnosis was confirmed by polyuria, low urinary osmolality (97-225 mosm/kg H20), hypernatraemia (max. 171 mmol/l) and the missing response to vasopressin. The treatment was variable; 4 boys received only hydrochlorothiazide (2-2.5 mg/kg/d) which lead to a reduction of the daily urinary volume of 26-44%. Hyperelectrolytaemia disappeared and a normal thriving could be achieved. Later an additional treatment with indomethacin (2 mg/kg/d) was necessary in 3 boys because of an increase of polyuria; there was a further reduction of the daily urinary volume of 50-60%. The combination of hydrochlorothiazide and indomethacin in the treatment of the congenital nephrogenic diabetes insipidus was well tolerated and seems to be--especially during the first few years of life--a necessary and effective treatment which allows a normal thriving and psychointellectual development.
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PMID:[Long-term course of 6 boys with congenital nephrogenic diabetes insipidus]. 260 Dec 80

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 28 healthy women either in normal potassium balance (N, n = 14) or after potassium depletion (KD) induced by low potassium dietary intake (less than or equal to 10 meq/d) plus natriuretic treatment according to two different time patterns: two KD groups were obtained with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6). The early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), were significantly different only in D3 as compared to N. Precisely, the LVP-effect to reduce Cc was blunted; moreover a LVP-effect to reduce renal sodium and chloride fractional excretions and a tendentiously enhanced LVP-effect to reduce water fractional excretion were observed. These tubular effects are likely related to the inhibited renal synthesis of prostanoids in the D3 group.
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PMID:[Renal function in experimental potassium depletion. I. Effects of lysine-8-vasopressin in hypotonic polyuria]. 262 31

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 20 healthy women submitted to paired functional explorations in both the absence and presence of indomethacin (100 mg i.m.); the drug effects have been evaluated in both normal potassium balance (N2, n = 6) and in two groups of potassium depletion (KD) with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6), respectively. As regards the early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), the inhibition of prostanoid synthesis with indomethacin produced significant changes: 1) an enhanced reduction in renal chloride excretion in all experimental groups; 2) a reduction in renal sodium and chloride fractional excretions in both KD groups; 3) an enhanced antidiuretic effect in D3 only, i.e. in the experimental condition with inhibition of prostanoid renal synthesis present during the control study.
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PMID:[Renal function in experimental potassium depletion. II. Indomethacin and effects of lysine-8-vasopressin in hypotonic polyuria]. 262 32

Changes in plasma vasopressin, K+, Na levels, osmolality in blood and urine samples, as well as hemodynamic parameters, cardiac output and circulating blood volume including, have been assessed in 38 patients 3, 6, 18 and 48 hours after aortocoronary bypass surgery. It has been found that vasopressin blood level in the postoperative period is considerably (5-7 times) higher than physiological hormone level. The main reasons for vasopressin blood level increase are surgical stress, increase in blood plasma osmolality, hypokalemia, a drop of the arterial blood pressure and central venous pressure elevation. Despite a high vasopressin level and its pronounced impact on the renal excretory function, the first postoperative hours are marked by polyuria, mediated mainly by osmotic diuresis due to infusions of high amounts of osmotically active substances.
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PMID:[Dynamics of the level of plasma vasopressin and its role in the regulation of water-electrolyte metabolism in patients following aortocoronary bypass]. 262 36

The authors discuss about five cases of diabetes insipidus observed in patients affected by traumatic cervical spine fractures and/or dislocations, without either evident lesions of the cerebral structures at CT scan examination, or important craniocerebral trauma. In all patients polyuria and hyperthermia arose some days after the traumatic accident and regressed spontaneously or after exogeneous vasopressin administration. Vasopressin urinary levels confirmed the presence of a true diabetes insipidus, the origin of which is in largely obscure. A central medullary vasopressin mediated pathway, demonstrated only in experimental animals, may be responsible for such a finding.
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PMID:Diencephalic syndrome following cervical spinal cord trauma. 271 4


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