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)

Impaired water excretion has been described in stable, nonedematous patients with chronic obstructive lung disease (COLD). To elucidate the mechanism involved, we measured basal glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and water, sodium, and solute excretion for 4 hours after water loading (20 ml. per kilogram orally or as D5W intravenously) in two groups of 10 age-matched, hypoxic, stable, nonedematous COLD normocapneic and hypercapneic patients (PCO2 less than or greater than 45 mm. Hg, respectively). In 5 patients of each group, additional measurements of plasma and urine osmolality and plasma vasopressin were made at 30-minute intervals after oral water loading and the results compared to those obtained in 10 normal control subjects. Hypoxic (PO2 61 plus or minus 2 mm. Hg), normocapneic (PCO2 39 plus or minus 1 mm. Hg) patients had normal GFR (114 plus or minus 5 ml. per minute) and ERPF (517 plus or minus 31 ml. per minute) and excreted the load normally (101 plus or minus 5 per cent of oral or intravenous water per 4-hours). This was associated with a normal rate of sodium excretion (34 plus or minus 5 mEq. per 4-hours) and low-normal plasma vasopressin (1.9 plus or minus 0.7 pg. per milliliter) which was suppressed appropriately with water loading. Hypercapneic (PCO2' 62 plus or minus 5), hypoxic (PCO2' 57 plus or minus 2) patients had normal GFR (106 plus or minus 7), low baseline vasopressin (1.1 plus or minus 0.2) which was suppressed appropriately, and decreased (p less than 0.05) 4-hour water excretion (63 plus or minus 8 per cent), 4-hour sodium excretion (15 plus or minus 9), and ERPF (394 plus or minus 31). A significant correlation was observed between impaired water and impaired sodium excretion (p less than 0.05). These studies indicate that in COLD patients: (1) hypercapnia but not hypoxemia is related to the abnormal water handling and to the increased reabsorption of sodium by the renal tubule; (2) the defect in water excretion is not related to abnormal vasopressin secretion or metabolism; (3) the alteration in sodium excretion may be due to hypercapneic-induced increase in renal bicarbonate reabsorption and/or abnormal renal blood flow.
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PMID:Impaired water handling in chronic obstructive lung disease. 114 29

In this paper, we present examples of some of the several behaviors which have been taken to indicate the reinforcing efficacy of drugs, including ethanol. Efforts to identify the genetic determinants of these behaviors have employed diverse pharmacogenetic methods. For example, we have used selective breeding to develop mice selected for severe or attenuated ethanol withdrawal and have found that Withdrawal Seizure Prone mice show a greater conditioned preference for ethanol-associated locations than the selected Withdrawal Seizure Resistant line. Similarly, HOT mice, selected for insensitivity to ethanol-induced hypothermia, had greater conditioned place preference after ethanol training than COLD mice, selected for ethanol hypothermic sensitivity. We have also developed selected mouse lines responsive or unresponsive to ethanol-stimulated locomotor activity. These FAST and SLOW lines develop sensitization rather than tolerance to ethanol-induced activity. Using inbred strains of mice, others had shown that strains differed in preference for drinking ethanol solutions. We found that these strains also differed in acceptance of ethanol. Single-gene techniques have been used to show that preference drinking is significantly altered in mutant rodent strains lacking hypothalamic vasopressin, or with nephrogenic diabetes insipidus. In a specific panel of Recombinant Inbred mouse strains, we found that a single gene appeared to control a significant portion of the variance in preference drinking. These examples show that traits putatively related to drug reinforcement show substantial genetic control. Specifically, single-gene methods show promise of identification and mapping of genes related to drug reinforcement.
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PMID:Genetic determinants of ethanol reinforcement. 163 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

Terlipressin (Glypressin) is a "pro-hormone"; after intravenous injection the glycyl radicals are slowly cleaved by enzymatic action, liberating vasopressin. We have assessed the efficacy of terlipressin in the treatment of severe hemoptysis. The study was performed on 20 patients: in 5 cases there was very copious hemoptysis and in 15 cases there was repeated hemoptysis of lesser volume. The cause was distributed as follows: 6 cases of neoplasms, 5 were sequelae of tuberculosis, bronchial dilatation 2 cases, pneumonia with abscess 2 cases, chronic airflow obstruction (COPD) 2 cases and 3 cases of silicosis. The treatment consisted of a slow intravenous injection of 2 mgm 4 times per day (9 patients), then in 11 patients an injection of 2 mgm at the time of acute episodes followed by 1 mgm every 6 hours. The patients received an average of between 15 and 20 mgm of the product for a treatment lasting over 5 days at the maximum. The results were as follows: total success 12 cases; partial success (a reduction to at least one-third of the initial hemoptysis): 5 cases; failure: 3 cases. The failures were linked in two cases to neoplastic disease and in one case there was an intolerance to the drug which did not allow the treatment to be pursued.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of severe hemoptysis with terlipressin. Study of the efficacy and tolerance of this product]. 279 45

Ten clinically stable, hypercapneic patients with advanced chronic obstructive pulmonary disease were studied to assess the effect of angiotensin-converting enzyme blockade on their inability to excrete a sodium load. Renal, hormonal, and cardiovascular responses to sodium loading were determined during two 5.5-h studies: control day, placebo; and experimental day, captopril. At baseline, compared with control subjects, patients displayed a decrease in urinary sodium associated with low effective renal plasma flow and high plasma level of aldosterone. Captopril, given before sodium loading, produced a significant increase in urinary sodium without increasing effective renal plasma flow and without suppressing plasma aldosterone more than sodium loading alone. Thus, the mechanism by which angiotensin-converting enzyme inhibition induces an acute sodium diuresis in these patients remains to be elucidated. The blockade of angiotensin with captopril also affected the osmotic regulation of vasopressin: for a given increase in plasma osmolality, the increase in plasma vasopressin was subnormal, a finding consistent with the hypothesis that angiotensin II contributes to the regulation of vasopressin secretion.
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PMID:The effects of angiotensin-converting enzyme inhibition on sodium handling in patients with advanced chronic obstructive pulmonary disease. 331 Jul 71

The pathogenesis of edema and hyponatremia associated with chronic obstructive lung disease (COLD) is poorly understood. In ten edematous COLD patients with acute respiratory failure (ARF), we monitored plasma renin activity (PRA), aldosterone (PA), and antidiuretic hormone (arginine vasopressin, AVP) for six days. Six patients receiving supplemental oxygen and antibiotics had near normal PRA, PA, and AVP, and diuresed Na+ and H2O and lost weight; only one patient was hyponatremic (PNa+ less than 130 mEq/L). On the same therapy, nonresponders (n = 4), with persistently elevated PRA, PA, and AVP, demonstrated no loss of Na+, H2O, or weight; three patients were hyponatremic. The PRA and PA correlated inversely with sodium loss; AVP correlated inversely with free water clearance. These studies suggest that in patients with COLD, edema, and ARF (1) lack of sodium diuresis may be contributed to by secondary hyperaldosteronism; and (2) hyponatremia can be explained by inappropriately elevated plasma AVP.
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PMID:Hormonal abnormalities affecting sodium and water balance in acute respiratory failure due to chronic obstructive lung disease. 669 Feb 51

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.
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PMID:Effect of acute hypercapnia on alpha atrial natriuretic peptide, renin, angiotensin II, aldosterone, and vasopressin plasma levels in patients with COPD. 787 53

Chronic obstructive pulmonary disease (COPD) is associated with right heart failure and salt and water retention. The possible roles of haemodynamically active hormones in the early stages of COPD have not previously been described. Adrenaline, noradrenaline, renin activity, aldosterone, vasopressin, cortisol, growth hormone, prolactin and atrial natriuretic peptide (ANP) were measured during right heart catheterization in mixed venous blood and in a peripheral artery, in the supine and standing position, in two groups of patients with COPD: Group A with arterial oxygen tension (Pa,O2) < 8.0 kPa (60 mmHg) and Group B with Pa,O2 > 8.0 kPa (60 mmHg). A group of 15 control subjects was studied to obtain control hormonal measurements with a venous blood sample only. Haemodynamic and blood gas values and hormone levels were measured in the supine and standing positions to record changes in the various parameters in COPD patients, and the relationship between pulmonary haemodynamics and hormone levels. No differences were found in hormonal samples between peripheral artery and mixed venous blood. In comparison with the control group, both groups of COPD patients showed a significant reduction in cortisol (p < 0.0001) and in vasopressin (p < 0.005), and an increase in ANP (p < 0.05) and growth hormone (p < 0.05). A marked, but not significant, increase in renin activity, and aldosterone was also found. After standing the increment of adrenaline was significantly higher in COPD patients (p < 0.02). A significant inverse relationship was recorded between forced expiratory volume in one second (FEV1) and noradrenaline (p < 0.02). There is a complex hormonal response even in the early phase of chronic obstructive pulmonary disease. An increase of plasma levels of atrial natriuretic peptide appears to be the earliest neuroendocrine response in these patients.
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PMID:Plasma hormone levels and haemodynamics in patients with chronic obstructive lung disease. 900 25

There is evidence that changes in arterial P(CO(2)) (P(a,CO(2))), as well as P(O(2)), influence neuroendocrine function. The hyponatraemia and fluid retention (cor pumonale) seen in chronic obstructive pulmonary disease (COPD) and type II respiratory failure is associated with increased vasopressin release. This study examines the specific effects of altered P(a,CO(2)) on hormone release from the posterior and anterior pituitary. The study was performed in 20 ventilated ICU patients in the late recovery phase of their illness. None had primary respiratory disease. Control blood samples were taken and the alveolar ventilation was then adjusted to allow the P(a,CO(2)) increase or decrease for a period of 3 h, during which time further blood samples were taken for the determination, by radioimmmunoassy of vasopressin, oxytocin, growth hormone and cortisol. Urine output and electrolyte concentrations were also measured. Circulating concentrations of growth hormone and oxytocin increased with increasing P(a,CO(2)). Vasopressin release showed a similar pattern up to a P(a,CO(2)) of approximately 6.0 kPa, above which vasopressin concentrations were inversely related to P(a,CO(2)). There was no significant effect on cortisol concentrations. No significant effects were established in urinary parameters during the short period of this study. Thus an increase in CO(2) is associated with stimulated pituitary hormone release. The effect on the neurohypophysial hormones may account for the fluid retention and hyponatraemia seen in COPD and hence provide a rationale for treatment.
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PMID:The effect of changes in arterial PCO2 on neuroendocrine function in man. 1512 64

Water retention and hyponatraemia are typically observed in the final stages of Chronic Obstructive Pulmonary Disease (COPD) and the onset of edema is a poor prognostic factor. For several years the pathogenesis of edema in COPD patients was attributed to heart impairment because of pulmonary hypertension, but the evidence that cardiac output is often adequate for the metabolic demands has suggested, since 1960, that the pathogenesis of edema in these patients would be correlated with gas exchange impairment and in particular with carbon dioxide (CO2) retention. The gas exchange impairment induces, in these patients several hormonal abnormalities: renin (Rn), angiotensin II (AnII), aldosterone (Ald), atrial natriuretic peptide (ANP), vasopressin (ADH) and endothelial factors are some of the factors involved. The systemic response to hypercapnia has the effect of reducing the renal blood flow and, as a result, increasing water and sodium retention with the final effect of edema and hyponatraemia. The aim of this brief review is to highlight the current knowledge on renal/hormonal abnormalities in COPD and their therapeutic implications.
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PMID:Water and sodium imbalance in COPD patients. 1551 Jul 11


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