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)

Hyponatremia with simultaneous renal sodium loss was associated with the inappropriate secretion of antidiuretic hormone in a dog with heartworm disease. Antidiuresis caused expansion of extracellular fluid volume, which induced renal salt wasting and a negative sodium balance. The combination of water retention, salt wasting, and inactivation of intracellular solute contributes to the decrease in serum sodium concentration. Water intoxication due to hypotonicity of body gluids induced anorexia, depression, weakness, and incoordination.
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PMID:Inappropriate secretion of antidiuretic hormone in a dog. 50 Apr 39

The incidence of new cases of extrapulmonary tuberculosis has remained constant, despite the decline in new cases of active pulmonary tuberculosis. This might be due to a delay in recognition, and particularly a lack of consideration of tuberculosis when the presenting symptoms are other than respiratory. Extrapulmonary tuberculosis should be considered in the differential diagnosis of bone, joint, genitourinary tract and central nervous system (CNS) diseases. To determine factors that might delay recognition and identification, 62 patients having extrapulmonary tuberculosis during 1969-1972 at the Los Angeles County-University of Southern California Medical Center were studied.Three quarters of these patients had had CNS, skeletal or genitourinary tuberculosis in equal distribution or 25 percent each. CNS involvement was seen frequently in the disseminated form. Presenting symptoms were protean and not specific, such as fever, anorexia, weight loss, cough, lymphadenopathy and neurologic abnormalities. Roentgenograms of the chest were abnormal in most. When a roentgenogram of the chest suggests pulmonary tuberculosis, signs and symptoms in other body systems should suggest extrapulmonary tuberculosis. If no abnormalities are seen on a roentgenogram of the chest, however, this does not preclude the diagnosis of extrapulmonary tuberculosis. Neither does a negative tuberculin skin test exclude the condition. Abnormal laboratory findings are common, especially in disseminated tuberculosis. These include various anemias, bone marrow disorders, hyponatremia due to inappropriate antidiuretic hormone syndrome. Analyses of pleural, peritoneal, pericardial and joint fluid usually show an exudate high in lymphocytes and occasionally low in glucose. Similar findings are seen in spinal fluid. The histological features of caseous or noncaseous granulomas are suggestive of but not specific for tuberculosis. Only culture of mycobacteria from sputum, urine, spinal fluid, pleural and other effusions and tissue biopsy specimens will yield a definitive diagnosis. Physicians must have a high index of suspicion to diagnose extrapulmonary tuberculosis, as it can resemble any disease in any organ system. Immediate therapy in the disseminated variety, sometimes even before a definite diagnosis can be made, may be lifesaving.
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PMID:The spectrum of extrapulmonary tuberculosis. 85 17

The present experiments investigated the effect of vasopressin (VP) on food intake in rats under various conditions. VP (1.25-10 micrograms/kg body weight = b.wt.) injected intraperitoneally (IP) at the onset of the dark phase of the lighting cycle inhibited feeding in a dose-dependent manner. The suppression of feeding induced by VP was primarily due to a delayed onset of the first meal after injection and was reversed by a V1-receptor antagonist (7 micrograms/kg b.wt., IP), by the Ca(++)-channel blocker verapamil (5 mg/kg b.wt., IP) and by the alpha-adrenergic receptor antagonist phentolamine (500 micrograms/kg b.wt.), but not by dissection of the hepatic branch of the vagus. In further experiments VP inhibited gastric emptying. This effect was not reversed by phentolamine. VP had also an aversive effect, but this effect was weaker than that of LiCl and probably not involved in VP-induced hypophagia. The results suggest that VP reduces feeding through a V1-receptor-mediated activation of an alpha-adrenergic mechanism. The inhibition of gastric emptying or a possible stimulation of hepatic oxidative metabolism by VP seems to be not essential for VP's effect on feeding. The results are consistent with a role of VP in stress-induced anorexia in rats.
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PMID:Mechanisms of vasopressin's anorectic effect. 182 89

A 63-year-old white woman with a history of hypertension and chronic obstructive pulmonary disease presented to the emergency room with worsening shortness of breath, anorexia, coughing, increased thirst, and leg edema of two weeks' duration. Medications included lisinopril 10 mg/d, which had been started six weeks earlier, sustained-release theophylline 300 mg q12h, and an albuterol inhaler. The lisinopril was discontinued on admission. Serum sodium concentration was 109 mmol/L; the osmolality of the blood and of the urine were 253 mOsmol and 438 mOsmol, respectively, with a specific gravity of 1.025 and a urine sodium of 17 mmol/L. The hyponatremia initially was considered to be the syndrome of inappropriate antidiuretic hormone secretion in response to the patient's suspected pneumonia. Due to worsening blood pressure, lisinopril was restarted and the serum sodium concentration dropped from 134 to 126 mmol/L. Evaluation of the patient's hyponatremia included assessment of thyroid, adrenal, hepatic, and cardiac function that were within normal limits. The patient was discharged on the following medications: sustained-release theophylline 300 mg tid, prednisone 10 mg/d, albuterol inhaler 2 puffs q6h, and sustained-release verapamil 240 mg/d for blood pressure control. Her serum sodium concentration has remained between 135 and 140 mmol/L during hospitalizations for exacerbations of chronic obstructive pulmonary disease and for pneumonias 10 and 12 months after discharge.
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PMID:Severe hyponatremia: an association with lisinopril? 165 42

This study has been done to evaluate serum calcium, phosphorus (P), magnesium, parathyroid hormone (PTH), calcitonin (CT), and cyclic adenosine monophosphate (cAMP) in recently diagnosed pulmonary tuberculous patient, (n = 61) and the results were compared with the healthy control group (n = 22). Twenty four hours urine was collected for estimation of these electrolytes as well as cAMP. Nephrogenous cAMP (NcAMP) was calculated. Serum Ca and PTH were significantly reduced in TB groups, but CT was elevated. Serum Mg, P and cAMP as well as urinary Ca and Mg in TB groups were similar to that of the control group. Urinary P, cAMP NcAMP were increased in patient groups compared with the control. The reduced serum Ca could be due to impaired intestinal absorption of Ca, or deficient intake as a result of anorexia, decreased plasma albumin, decreased active metabolites of vitamin D or elevated CT. The rise in serum CT in TB might be due to increased CT secreted from the bronchial K-cells. Increased NcAMP might be due to the associated increase in serum antidiuretic hormone (ADH). The elevated urinary P in TB could be attributed to tissue breakdown, decreased serum PTH or increased CT.
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PMID:Calcium homeostasis in untreated pulmonary tuberculosis. I--Basic study. 216 2

Amelioration of cisplatin (CDDP)-induced vomiting and anorexia by methylprednisolone (MP) was studied using conscious dogs. The incidence of vomiting was 88.9% and the mean number of emetic episodes was 8.22 +/- 1.25/dog during 5 hours after i.v. administration of 1.5 mg/kg CDDP in 9 dogs. In control dogs, food intake on the day after administration of CDDP was markedly reduced to 60 +/- 22.4 g/day from 461 +/- 23 g. Continuous high-dose infusion of MP (10 mg/kg, 10 min before the start of CDDP infusion and 50 mg/kg/h for 5 h) markedly reduced the incidence (33%) and mean number of vomiting episodes (2.00 +/- 1.51/dog) and also mitigated the reduction of food intake (350 +/- 30.6 g/day). However, continuous low-dose infusion of MP (5 mg/kg, 10 min before CDDP infusion and 16.6 mg/kg/h for 5 h) showed a little effect on CDDP-induced vomiting. Plasma MP levels after the high-dose and the low-dose regimens were 6.20 +/- 0.628 micrograms/ml and 4.66 +/- 1.72 micrograms/ml, respectively, 30 min after CDDP infusion. In both cases, MP levels gradually increased and reached to those more than twice 5 hours after CDDP infusion. Bolus administrations of MP (30 mg/kg, each time) 2 hr and 30 min before CDDP infusion also significantly reduced the mean number of emetic episodes (3.22 +/- 1.33/dog) and mitigated the reduction of food intake (325 +/- 37.3 g/day). No significant changes in catecholamines, prostaglandins, vasopressin, plasma renin activity, Na+, K+, Mg++ and osmolality in peripheral blood were noted after administration of CDDP and/or MP. The results suggest that administration of MP was effective against CDDP-induced vomiting and anorexia in dogs.
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PMID:[Amelioration of cisplatin-induced vomiting and anorexia by methylprednisolone]. 271 80

Rats bearing the Walker-256 (W-256) tumor display an anorexic profile which resembles that of normal animals forced to drink 2% NaCl [2,24], a regimen which depletes neurohypophyseal dynorphin-A (DYN) [3,9]. As expected, the naloxone reversible feeding induced by 2-deoxy-D-glucose (2-DG) was attenuated (36%) in the W-256 tumor bearing rats (TBR). Interestingly, immunoreactive (ir) levels of dynorphin-A 1-17 (DYN-17) and its postulated breakdown product, dynorphin-A 1-18 (DYN-8), were also reduced in the neurohypophysis of W-256 TBR by 42 and 50%, respectively. However, ir-DYN levels were not reduced in TBR in those brain regions which are probably involved in the regulation of appetite (e.g., hypothalamus). 2-DG itself did not consistently affect ir-DYN levels in any tissue for either controls or TBR. The ratio of DYN-8 to DYN-17 did not change in response to any treatment, including the depletion of both peptides from the NIL of TBR. In summary, the present data do not support DYN depletion as being a factor which contributes to the anorexia of the W-256 TBR.
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PMID:Assessment of dynorphin-A depletion in the anorexia of Walker-256 tumor bearing rats. 286 63

One of the important factors in outer space is the absence of gravity (OG). During longterm missions, this factor is responsible for the larger number of anatomical and physiological changes that astronauts experience. The cardiovascular system undergoes these changes with severe intensity, which is part of an adaptation process to the new environmental conditions. The modifications observed in both the anatomy of the cardiovascular system and its hemodynamics occur in two phases. The first phase begins when the astronauts enter into Earth orbit or in interplanetary trajectory and extends until the second or fourth day of the mission. It is characterized by an important shifting of fluids from the lower extremities to the cephalic regions which produces an increase of the venous return and the preload, the heart rate is increased, the blood volume in the thorax is also increased, the cardiac chambers become dilated, and by reflex action, the antidiuretic hormone diminishes, diuresis increases and leads to a virtual state of dehydration. Clinically, the first stage is manifested by headache, dizziness, space disorientation, nausea, anorexia, projectile vomiting, sweating and pallor. This constalation of data is known as "The Space Adaptation Syndrome". The second phase begins at the end of the first phase and finishes toward the fortieth or fiftieth day of the mission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Behavior of the cardiovascular system in outer space]. 295 26

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.
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PMID:Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy. 365 42


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