Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antihypertensive effects of a novel adenosine A2 receptor agonist, 2-octynyl adenosine (YT-146), were evaluated in Dahl salt-sensitive rats. After rats were fed a high-salt (8% NaCl) diet for 2 or 3 weeks, they received oral YT-146 (0.1 or 1.0 mg/kg) or vehicle as a single dose (acute study) or once daily for 10 days (chronic study). In the acute study, tail-cuff blood pressure (BP) and pulse rate (PR) were measured before and 3, 6, and 24 h after administration, and blood samples were collected 3 h after administration. In the chronic study, BP and PR were measured 3 and 24 h after administration and urine was collected for 24 h on day 9. Blood samples were also collected 3 h after administration on day 10. BP was significantly lowered by 1.0 mg/kg of YT-146 in either the acute study (from 184 +/- 3 to 152 +/- 5 mm Hg, P < .01) or the chronic study (from 226 +/- 4 to 201 +/- 2 mm Hg, P < .01), while an increase in PR was not observed (acute study: from 382 +/- 8 to 366 +/- 3 beats/min; chronic study: from 420 +/- 8 to 411 +/- 8 beats/min). YT-146 had no effect on plasma renin activity (PRA), plasma aldosterone, vasopressin (ADH), and atrial natriuretic peptide (ANP) in the acute study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antihypertensive effects of 2-octynyladenosine (YT-146), a selective adenosine A2 receptor agonist, in Dahl salt-sensitive rats. 784 25

The restricted environmental stimulation technique or REST is a method of relaxation where the level of environmental sensory inputs is kept very low. A particular REST technique called tank flotation, or flotation REST, consists of 1 h sessions in a tank containing water with a high salt content and maintained at 35.5 degrees C. In this protocol, five normal subjects were studied before and during 2 h after a 60 min flotation REST session and a control session of 60 min in a supine position on a bed. Cortisol, thyreostimulating hormone (TSH), thyroxine (T4), prolactin, melatonin, luteinizing hormone (LH), growth hormone (GH), beta-endorphin, vasopressin (ADH), gamma-aminobutyric acid (GABA) and homovanillic acid (HVA) were measured in plasma. HVA, 5-hydroxy-indoleacetic acid (5-HIAA) and vanylmandelic acid (VMA) were measured in urine. There were no changes in hormones concentrations that could be attributed to flotation REST. The urinary excretion of VMA was lower after the flotation REST session. The psychological consequences of flotation REST were more easily demonstrated than the neuroendocrine changes that are assumed to reflect the state of relaxation. Flotation REST increased subjective levels of sedation and euphoria. The possible mechanisms by which flotation REST induces relaxation are discussed.
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PMID:Neuroendocrine and psychological effects of restricted environmental stimulation technique in a flotation tank. 800 91

The results of experiments on white rats, consuming different quantities of NaCl, show that excessive sodium chloride load increases osmolarity of blood plasma mainly due to excessive accumulation of Cl- in the blood. At the same time urine osmolarity increases by a factor of 10 due to the rise of water reabsorption and a fall in reabsorption of osmotical active substances such as sodium, potassium, chlorides, phosphates and other ions showing tendency to the glomerulus filtration rate rise. This testifies to the priority of osmoregulation over ionoregulation. NaCl injection causes a fall in difference of Na+ and Cl- concentrations in the blood plasma due to Na+ deposition by tissues, which leads to extracellular metabolic acidosis. Kidneys respond to it by a decrease of the urine pH and increase of excretion of hydrogen ions in the form of titrated acids and ammonium, as well as by removal of chloride ions which are not connected with sodium. The conclusion is made that kidneys' function of acid-excretion depends first of all on the acid-base status of extracellular fluids and not on intracellular pH. Concentration of corticotropin in the blood increases in the case of sodium deficiency as well as in the excess of sodium. Deficiency of Na+ intensifies activity of the renin-angiotensin-aldosterone system and decreases ADH secretion, while salt load produces just the opposite effect. The role of the hormones in kidneys' compensatory reaction to excessive NaCl load is discussed.
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PMID:[Response and endocrine mechanisms in the kidney effected by sodium chloride]. 804 19

The pathophysiology of dehydration is reviewed. The normal response to dehydration, i.e. decreased effective arterial blood volume or effective circulating volume is described. Due to water retention and drinking following stimulation of ADH secretion and thirst, osmoregulation is overruled by volume conservatory mechanisms, which lead to hyponatremia. Only patients with impaired mental function or those who are unable to drink will develop a progressive water deficit--with or without salt depletion--recognizable by hypernatremia. Decreased effective arterial blood volume and hypernatremia affect cerebral function in a way that perception of external stimuli as well as perception of pain will be impaired. Alert dehydrated patients are disturbed mainly by thirst and dryness of the mouth. Both symptoms are perceived more intensely by young than by elderly persons. Dryness of the mouth increase thirst on its own. Distress by thirst and oral dryness increases as a function of the level and the rapidity of developing hypernatremia. The simple act of filling the oral cavity with fluid and swallowing alleviates thirst in the absence of any change in plasma sodium concentration. Thirst quenching efficacy is increased by administering chilled hypotonic fluid with lemon or other fruit acid added (for stimulation of salivation).
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PMID:[Pathophysiology of dehydration]. 836 27

We report the case of a patient with an idiopathic syndrome of inappropriate secretion of ADH for more than 6 years. Water restriction was effective only during hospital care but was socially difficult to maintain at home, so that the patient presented frequent symptoms of water intoxication. Normal natremia was also obtained with a high salt intake (9 g/day) but this induced leg edema mild dyspnea and gastric intolerance. The patient was however successfully treated for more than 5 years without any side effects with oral urea (30 g/day) allowing her a normal fluid intake (1-1.5 liters/day). Oral urea, even during long periods, is a safe and effective therapeutic approach for patients with chronic SIADH which is not controlled by water restriction alone.
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PMID:5-year treatment of the chronic syndrome of inappropriate secretion of ADH with oral urea. 845 86

A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism, presenting severe hyponatremia, is described. A 57-year-old man complaining of nausea, vomiting and fatigability was admitted to our hospital because of hyponatremia (114 mEq/I). The low levels of serum cortisol and urinary 17-OHCS suggested glucocorticoid deficiency, and that the glucocorticoid deficiency was due to isolated ACTH deficiency was confirmed by a continuous ACTH loading test and pituitary gland stimulation tests. Although the low level of serum sodium was normalized after the administration of cortisone acetate (50 mg/day) combined with an increase in oral salt intake, urinary sodium loss persisted by the results of hypertonic saline infusion test. Treatment led to improvement of impairment of water diuresis due to hypersecretion of ADH. Hyporeninemic hypoaldosteronism persisted after treatment. We have shown that severe hyponatremia that occurs with combined deficiency of glucocorticoids and mineralocorticoids can be corrected with high salt intake and glucocorticoid replacement without correcting mineralocorticoid deficiency.
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PMID:A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism. 877 60

Creatinine clearance decreases with age by 1 ml/min/year after 40 years of age, although serum creatinine remains constant because of reduction of muscle mass. Reduction of water intake may occur in the elderly because of a reduced sensation of thirst; this is associated with a tendency to lose water with urine. The capacity to respond to sodium load is impaired in aged kidneys, thereby leading to ECV expansion and hypertension. But there is also, in the elderly, a reduced capacity for retaining sodium (FENa is higher than in young subjects), making old subjects sensitive to salt depletion and ECV contraction. Hypernatraemia (Nas > 150 mmol/l) is not infrequent in the elderly (1%) and is usually due to water deficiency (old subjects should be forced to drink), and rarely to iatrogenic excess of sodium. It is the abrupt occurrence of severe hypernatraemia that causes neurological symptoms due to dehydration and brain shrinking, which may lead to cerebral haemorrhage and death. Hyponatraemia (Nas < 130 mmol/l) is frequent among the elderly (7-11%) and is mainly due to water overload, which is usually iatrogenic. Hypovolaemic hyponatraemia occurs when salt depletion causes ECV contraction > 10%, and is due to water retention in an attempt to normalize ECV. Hypervolaemic hyponatraemia is due to ADH hypersecretion because of a decrease in 'effective' circulating blood volume. 'Pseudohyponatraemia' may occur because of hyperlipidaemia or hyperproteinaemia. It is the abrupt occurrence of severe hyponatraemia that causes neurological symptoms (water intoxication), secondary to the oedomatous swelling of the brain within the skull. While rapidly occurring hyponatraemia may be lethal, slowly occurring hyponatraemia is usually asymptomatic. Rapid correction of hyponatraemia may cause cerebral dehydration and 'osmotic demyelination syndrome' ('central pontine myelinosis'). Decrease (e.g. by diuretics) or increase (e.g. by ACE-inhibitors, non-steroidal anti-inflammatory drugs, beta-blockers) or serum potassium may occur in the elderly. Diuretics should be used with caution in elderly subjects to avoid salt depletion, hypotension and renal function impairment.
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PMID:Some sodium, potassium and water changes in the elderly and their treatment. 905 29

Head-out water immersion (HOI) induces various renal functional changes, such as diuresis, natriuresis, and kaliuresis. The present study was undertaken 1) to characterize the renal response to HOI in Koreans who routinely ingest high salt diet and 2) to evaluate the impact of exercise on the renal response to HOI. Six healthy male subjects (average Na+ intake of 232 mEq.day-1) were immersed upto the neck in 34.5 degrees C water and rested in a seated position or exercised on a bicycle ergometer for 3 hours. In resting subjects, we observed a reversible increase in urine flow and a decrease in urine osmolality, with no changes in creatinine clearance. The peak urine flow observed during the second hour of immersion was 4-fold greater than the pre-immersion level. The excretion of total osmotic substances rose progressively during the 3-hour immersion, which was accompanied by a similar change in Na+ excretion. The K+ excretion was slightly elevated. The major component of the immersion diuresis was a water diuresis in the early phase and an osmotic diuresis in the late phase of immersion. In exercising subjects, the diuretic and natriuretic responses to HOI were attenuated and the kaliuretic response was potentiated. Blood hemoglobin concentration and plasma levels of renin, ADH, and aldosterone decreased during immersion-rest, but they remained unchanged or increased during immersion-exercise. These results suggest that 1) the cardiac mechanoreceptor-mediated renal responses to HOI are not changed by chronic high salt diet, and 2) excessive urinary sodium and water losses are prevented by exercise during immersion.
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PMID:Effect of physical exercise on renal response to head-out water immersion. 908 96

A young male sustained very serious head and soft tissue injuries in a motor vehicle accident (MVA). Three interesting problems developed in the sodium (Na) and water area in the second week in hospital. First, on day 11 after the MVA, his urine output increased to 3 liters per day; the urine osmolality was 1000 mOsm/kg H2O and Na and Cl were the principal urine osmoles. There appeared to be a salt wasting syndrome because he had a very large natriuresis (close to 900 mmol/24 hr) at a time when his central venous pressure was low. To help identify the nephron site responsible for a natriuresis with a high urine osmolality, additional studies were carried out in normal volunteers who took a loop or a thiazide diuretic on different occasions while ADH was acting. The pattern of natriuresis in the patient was similar to that after the thiazide but not the loop diuretic. The second problem concerned his hypernatremia (153 mM) because his urine was hypertonic and his intravenous therapy was isotonic saline. To explain hypernatremia while receiving more electrolyte-free water, we speculated that there was a water shift into cells resulting from particles generated and retained in his intracellular fluid. Given the large shift of water required, a lesion in muscle was suspected, a form of rhabdomyolysis. The third problem concerned the rate of catabolism of lean body mass. The metabolic consequences of generating these intracellular particles and the large amount of urea that was excreted could reflect a large degree of protein catabolism.
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PMID:Profound natriuresis, extracellular fluid volume contraction, and hypernatremia with hypertonic losses following trauma. 942 5

Low-temperature stress induces the expression of a variety of genes in plants. However, the signal transduction pathway(s) that activates gene expression under cold stress is poorly understood. Mutants defective in cold signaling should facilitate molecular analysis of plant responses to low temperature and eventually lead to the identification and cloning of a cold stress receptor(s) and intracellular signaling components. In this study, we characterize a plant mutant affected in its response to low temperatures. The Arabidopsis hos1-1 mutation identified by luciferase imaging causes superinduction of cold-responsive genes, such as RD29A, COR47, COR15A, KIN1, and ADH. Although these genes are also induced by abscisic acid, high salt, or polyethylene glycol in addition to cold, the hos1-1 mutation only enhances their expression under cold stress. Genetic analysis revealed that hos1-1 is a single recessive mutation in a nuclear gene. Our studies using the firefly luciferase reporter gene under the control of the cold-responsive RD29A promoter have indicated that cold-responsive genes can be induced by temperatures as high as 19 degrees C in hos1-1 plants. In contrast, wild-type plants do not express the luciferase reporter at 10 degrees C or higher. Compared with the wild type, hos1-1 plants are l ess cold hardy. Nonetheless, after 2 days of cold acclimation, hos1-1 plants acquired the same degree of freezing tolerance as did the wild type. The hos1-1 plants flowered earlier than did the wild-type plants and appeared constitutively vernalized. Taken together, our findings show that the HOS1 locus is an important negative regulator of cold signal transduction in plant cells and that it plays critical roles in controlling gene expression under cold stress, freezing tolerance, and flowering time.
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PMID:HOS1, a genetic locus involved in cold-responsive gene expression in arabidopsis. 966 34


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