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)

We prepared nine analogues (1-9) of MCPA-D-Phe-Phe-Ile-Asn-Cys-Pro-Arg-Gly-NH2, [MCPA1, D-Phe2, Phe3, Ile4, Arg8]oxytocin (MCPA = beta-mercapto-beta,beta-pentamethylenepropionic acid), a potent antagonist of the rat uterotonic action of oxytocin (OT). We replaced D-Phe with D-Trp and made [MCPA1,D-Trp2,Phe3,Ile4,Arg8]OT (1), which had OT pA2 of 7.51, somewhat higher than that of the D-Phe2 antagonist which has OT pA2 = 7.35 in our rat uterotonic assay. Both compounds are equipotent as antagonists of [Arg8]vasopressin in the rat antidiuretic assay, with pA2 = 8.1. Other substitutions gave [MCPA1,D-Trp2,4-Cl-Phe3,Ile4,Arg8]OT, (2), OT pA2 7.44; [MCPA1,D-Trp2,Phe3,Ile4,3,4-dehydro-Pro7,Arg8]OT (3), OT pA2 = 7.42; [MCPA1,D-Trp2,Phe3,Arg8]OT (4), OT pA2 = 7.58; [MCPA1,D-Trp2,Phe3,Arg8,Gly9-NHEt]OT (5), OT pA2 = 7.49; [MCPA1,D-Trp2,Ile4,Arg8]OT (6), OT pA2 = 7.46; [MCPA1,D-Trp2,Val4,Arg8]OT (7), OT pA2 = 7.58; [MCPA1,D-Trp2,Thr4,Arg8]OT (8), OT pA2 = 7.48; and finally, [MCPA1,D-Trp2,Arg8]OT (9), which was a more potent and more selective OT antagonist, with OT pA2 = 7.77 in the uterotonic assay and ADH pA2 less than 5.9 in the antidiuretic assay and hence is an important lead for the design of OT antagonists.
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PMID:Design of potent oxytocin antagonists featuring D-tryptophan at position 2. 199 88

We report a patient with squamous cell carcinoma of bronchus who developed the syndrome of inappropriate antidiuretic hormone secretion (SIADH) after receiving cisplatinum (CDDP) and vindesine (VDS). The 75-year-old man developed right chest pain and was found to have a squamous cell carcinoma of bronchus (stage IIIA, T3N1M0). He was treated by CDDP and VDS. The serum sodium concentration decreased from 136 mEq/l to 120 mEq/l after drug administration. SIADH was diagnosed on the basis of hyponatremia with corresponding serum hypoosmolality and an inappropriately high urinary osmolality due to continued sodium excretion. In our case, SI-ADH was probably induced by CDDP or VDS. Fluid restriction and sodium supplement resulted in a progressive rise in the serum sodium level to 134 mEq/l in 4 days.
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PMID:[Syndrome of inappropriate antidiuretic hormone secretion following cisplatinum and vindesine administration in a patient with squamous cell carcinoma of the lung]. 205 80

We reported an 11-year-old boy who suffered from transient hypernatremia, hypothermia, and circadian rhythm disturbances of sleep-wakefulness and body temperature from the age of 4 years, as sequelae of acute subdural hematoma. T1-weighted magnetic resonance imaging (MRI) of the brain revealed low intensity consistent with necrotic change in the whole left cerebral hemisphere, hypothalamic region, and the right-sided brain stem including tegmentum, while the pituitary structure was well preserved. Anterior pituitary function was almost normal. ADH (antidiuretic hormone) was neither stimulated by hyperosmolality nor suppressed by hyposmolality but continued to be secreted at almost constant level approximating the normal basal state. This pattern seemed to be due to complete destruction of the osmoreceptor located in the anterior hypothalamus. He exhibited a dispersed-type sleep with differentiated stages of NREM (non-rapid eye movement), although the percentage of sleep was higher at night than in the daytime. It is suggested that circadian rhythm of sleep-wakefulness and differentiation of NREM sleep stages are regulated by different neuromechanisms. Brain stem lesion on MRI may be connected with the pathogenesis of the dispersed-type sleep with special respect to amplitude reduction of sleep-waking circadian rhythm. Circadian rhythm of body temperature (BT) was irregular in amplitude, phase, and period without synchronization with sleep-wakefulness rhythm. Hypothermia was also demonstrated at the basal state, while BT increased when he suffered from respiratory infection. It is likely that hypothermia in our case is caused by the BT shift to the lower side due to malfunction of BT integrating system including preoptic area and anterior hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sodium regulation disorder, hypothermia, and circadian rhythm disturbances of the body temperature and sleep-wakefulness as sequelae of acute subdural hematoma]. 205 28

The authors report the favorable evolution of one case of inappropriate antidiuretic hormone secretion after a cerebral hemorrhage limited to the caudate nucleus. The limitation of the lesions explains the transient desinhibition of ADH producing centers.
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PMID:[Inappropriate antidiuretic hormone secretion by hematoma of the caudate nucleus]. 209 39

We monitored the plasma and urine osmolalities, fractional excretion of sodium, fractional excretion of chloride, plasma levels of antidiuretic hormone (ADH, AVP), aldosterone and atrial natriuretic peptide (ANP) before and after acute water ingestion in 12 patients with overt hypothyroidism. The ability of the patients to dilute and concentrate urine was found impaired and the ability of excretion of water load decreased and delayed. Acute water load test was proved to be effective in evaluating the urinary excreting function for the patients. We hypothesize that inappropriate secretion of anti-diuretic hormone and elevated plasma ANP may be homeostatic factors for abnormal urinary excretion in patients with hypothyroidism.
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PMID:Effect of acute water loading on plasma levels of antidiuretic hormone AVP aldosterone, ANP fractional excretion of sodium and plasma and urine osmolalities in myxedema. 214 45

In a strain of mice called DI +/+ Severe, nephrogenic (or vasopressin-resistant) diabetes insipidus is caused by an inability of the antidiuretic hormone (ADH, or vasopressin) to increase the water permeability of the renal collecting system. That inability, in turn, arises from abnormally high activity of the enzyme cAMP-phosphodiesterase, specifically of the isozyme type III (PDE-III), which hydrolyzes cAMP and prevents the intracellular buildup of this second messenger. Two rather specific inhibitors of PDE-III, rolipram and cilostamide, used either in vitro or in vivo, reverse the deficiencies in DI +/+ Severe mice by increasing intracellular cAMP and water permeability toward or to their normal values. These results have implications for the treatment of nephrogenic diabetes insipidus in human patients.
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PMID:Causes of the urinary concentrating defect in mice with nephrogenic diabetes insipidus. 216 65

The role of antidiuretic hormone in the organism ability to resist against considerable salt shifts, was studied in Wistar (1st group) and Brattleboro rats--heterozygotes (2nd group). 5% NaCl solution was infused into animals' stomach (30-50-70-100 ml/kg). An increase in diuresis especially at 7-10% load, and a decrease in Na and K excretion occurred in Brattleboro rats. A decrease in tissue cation accumulation was found in Brattleboro rats as compared to Wistar ones. The Brattleboro rats with a partial defect of ADH synthesis revealed a decrease in the reserve possibilities of the system regulating the water-salt metabolism. As a result, 100% of Brattleboro rats died after 100 ml/kg salt load whereas the mortality in Wistar rats was only 22.2%.
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PMID:[The effect of hypertonic saline solutions on water-salt metabolism in Brattleboro rats]. 217 Jan 83

To evaluate the incidence and causes of hyponatremia in intensive care unit (ICU) patients, retrospective and prospective studies were done. Hyponatremia was defined as a serum sodium concentration equal to or less than 134 mmol/l (134 mEq/l). Prospectively, 29.6% of patients displayed hyponatremia. Relevant data were obtained in twelve patients. Two patients did not have serum hypoosmolality. In the ten patients with serum hypoosmolality, urine osmolality was not maximally dilute and urine sodium concentration was greater than 30 mmol/l (30 mEq/l) suggesting inappropriate antidiuretic hormone secretion (SIADH). However, three patients exhibited suppressed ADH levels despite absence of maximal urinary dilution. The data suggest that hyponatremia is common in ICU patients and that renal diluting defects are frequent. Therefore, hypotonic fluid should be administered cautiously.
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PMID:Incidence and etiology of hyponatremia in an intensive care unit. 225 2

Human vasopressin (arginine-vasopressin, AVP, antidiuretic hormone, ADH) was estimated, after protein precipitation and extraction in ethanol, using a new radioimmunoassay from Immuno Technology Service, Wijchen, Netherlands. Concentrations in human seminal plasma were 1.84 +/- 1.23 (0.6-4.1) pg/ml, estimated in good duplicates in all 20 samples, where 1 pg = 0.410 uIU/ml WHO 1st 77/501. This is about the same concentration as in blood serum, for which levels up to 8 pg/ml are found by the same kit. In contrast, only trace amounts of vasopressin were found in amniotic fluid at 16-22 weeks of gestation, with zero values in 8 of 19 samples, while another 9 samples showed zero in one duplicate and up to 0.46 pg/ml in the other duplicate, and one sample showed 0.09 pg/ml in good duplicates.
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PMID:Vasopressin: another pregnancy protein in human seminal plasma. 226 24

We reported two infants with hydranencephaly and chronic hypernatremia. Their plasma sodium concentration gradually increased during the first week and remained between 150-160 mEq/L thereafter. They showed no signs of thirst. A water deprivation test demonstrated low urine osmolality and low plasma ADH concentration despite markedly elevated plasma osmolality in both cases. Urine was significantly concentrated when vasopressin was given. Thus, it was concluded that both thirst mechanism and ADH secretion were disturbed in these two cases. ADH producing cells, the thirst center and the osmoreceptor are all located in the hypothalamus. Radiographic measures showed dysplasia of the hypothalamus, providing the anatomical basis for their dysfunction.
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PMID:[Endocrinological analysis of chronic hypernatremia in two cases of hydranencephaly]. 229 50


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