Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The purpose of the present study was to measure plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction without heart failure, and also to assess the temporal sequence of changes of plasma ANP during the first hours of recovery from myocardial infarction. The study was performed in 22 patients who were admitted to the Intensive Care Unit with the diagnosis of acute myocardial ischaemia that had an evolution of less than 6 h. Blood samples were drawn on admission and at 1, 8, and 24 h, and plasma concentrations of ANP, renin, aldosterone, epinephrine, norepinephrine and vasopressin were measured. Compared with control subjects, on admission patients showed increased plasma levels of ANP, as well as increased plasma renin activity (PRA), aldosterone, norepinephrine, epinephrine, dopamine, and antidiuretic hormone (ADH). ANP, but not renin or aldosterone plasma values, decreased with time, and there was a significant correlation between ANP and time after onset of pain. No increase in plasma creatinine was observed during the hospital stay, and the patients showed a negative fluid balance. No relationship was found between the location or extension of the infarction, or morphine treatment and ANP plasma levels. The high levels of ANP seem to counteract the haemodynamic and fluid-retention effects of the vasoconstrictive factors released after myocardial infarction.
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PMID:Atrial natriuretic peptide in patients with acute myocardial infarction without functional heart failure. 182 81

When men are exposed to a hyperbaric environment, urine flow increases. In order to elucidate the mechanism of this hyperbaric diuresis, a dry saturation dive experiment was carried out. Five male subjects were exposed to a 16-21 ATA (atmospheric pressure absolute) helium-oxygen (He-O2) environment for 4 days. Five blood samples were obtained in the early morning (0600-0630 h): once at predive 1 ATA air, 3 times at 16-21 ATA He-O2, and once at postdive 1 ATA air. Eight-hour timed urine samples, 0600-1400 h, 1400-2200 h, and 2200-0600 h (night urine), were collected throughout the experimental period. Urine flow markedly increased by the exposure to hyperbaria in the presence of constant creatinine clearance. The increase was mostly attributable to the urine flow during 2200-0600 h. The secretion of antidiuretic hormone (ADH) was suppressed at daytime and night during the exposure. On the other hand, the secretion of atrial natriuretic polypeptide (ANP) increased solely at night during hyperbaria and correlated with the increases of both the nocturnal urine flow and the nocturnal urinary excretion of sodium. These results suggest that both suppressed ADH secretion and stimulated ANP secretion cause hyperbaric diuresis.
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PMID:Hyperbaric diuresis is associated with decreased antidiuretic hormone and increased atrial natriuretic polypeptide in humans. 183 Mar 48

Neuroendocrine activity in normal subjects was compared to patients with chronic renal failure on maintenance hemodialysis (CRF-HD) and to cyclosporine-treated renal transplantation (RT) recipients in an effort to further define the mechanisms underlying their associated fluid, electrolyte, and hemodynamic abnormalities. To evaluate neuroendocrine function in CRF and RT patients, plasma levels of angiotensin II (A-II), vasopressin (AVP), atrial natriuretic peptide (ANP), neuropeptide Y, neuropeptide Y (NPY), epinephrine (E), and norepinephrine (NE) were measured before and after HD and RT. Plasma concentrations of A-II, AVP, ANP, and NPY were significantly elevated in patients with CRF. HD did not produce a significant change in plasma concentrations of AVP, ANP, NPY, E, or NE. NE plasma levels, but not E levels, increased pre- and post-HD. A-II plasma levels were elevated basally in CRF patients and significantly increased following HD. Following RT, plasma levels of A-II, AVP, NPY, and creatinine decreased significantly over the first week, but AVP and NPY did not normalize. Plasma levels of ANP were elevated during the first month, then decreased to normal levels in RT patients. NE levels, but not E levels, were elevated both pre- and post-RT. Despite antihypertensive treatment, the group mean arterial pressure increased post-RT from 100 +/- 4.4 to 116 +/- 3.7 mmHg by POD 6.
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PMID:Neuroendocrinology of chronic renal failure and renal transplantation. 183 95

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).
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PMID:The electrolytes in hyponatremia. 183 86

The effect of partial (50 ml/min/kg) left heart bypass (LHBP) on renal function, plasma renin activity (PRA), aldosterone, arginine vasopressin and atrial natriuretic peptide (ANP) response was studied in ten anesthetized, open-chested mongrel dogs (weight 23-50 kg) over a period of 6 h. Standard equipment with systemic heparinization (control), initially 300 IU/kg, was employed in five dogs, and heparin-coated equipment without additional heparin in the other five (heparin coated). Urine was continuously collected through a transurethral catheter. Urine samples and pulmonary artery blood samples for hormonal assays were taken at preset intervals before and during LHBP. The results in each group were summarized as median (25th-75th) and compared using the Mann-Whitney U test. In the control group higher blood loss required higher volume substitution. Urine output was maintained in heparin coated and slightly decreased at 3-4 h in control LHBP. Creatinine clearance at 3-5 h and free-water clearance at 3-6 h were significantly higher with heparin-coated LHBP. PRA, aldosterone and vasopressin peaked at 1-2 h of LHBP similarly in both groups, not exceeding the values before perfusion. PRA and aldosterone response was sustained during 6 h and the percentage changes corrected for hemodilution indicated a stronger response with standard equipment. Vasopressin concentrations were slightly but significantly higher in the control group at 1 and 6 h of perfusion. Corrected for hemodilution, vasopressin percentage changes were not different in the two groups. ANP, despite atrial unloading, rose similarly in both groups. There was a tendency to poorly sustained ANP response (control greater than heparin-coated) after 6 h of perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin-coated left heart bypass: renal function and hormonal response. 183 57

We evaluated 38 newborns with acute renal failure (plasma creatinine (Pcr) concentration greater than = 1.5 mg/dl), measured between the 2nd and 5th days. We used renal ultrasound to exclude the possibility of congenital renal anomalies, obstructive pathology or vascular disorders. We calculated the glomerular filtration rate (GFR) using Schwartz' formula and the maximal concentrating capacity using intranasal administration of desamino-cis-1-D-arginine-8-vasopressin (DDAVP test). Two newborns were treated with peritoneal dialysis and died during the first month of life. Thirty-six had a follow-up blood sample drawn: 24 preterm babies between 1 and 12 months, and 12 full-term babies between 1 and 36 months of life. From this sampling 4 babies (11.1%) showed defective maximal concentrating ability. Our data reveal the persistence of altered concentrating ability in newborns affected by renal failure and shows that this problem needs a longitudinal study and further diagnostic investigations.
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PMID:The prognostic significance of acute neonatal renal failure. 186 76

Endogenous opioids may be involved in the pathogenesis of ascites and edema in patients with liver cirrhosis. We administered the opioid antagonist naloxone (5 mg bolus followed by a 0.06 mg/min infusion) to eight male patients with alcoholic cirrhosis and ascites and to five healthy age- and sex-matched control subjects and determined the effects of naloxone on water and electrolyte excretion after a nonsustained water load (20 ml/kg). In comparison with saline vehicle infusion carried out in the same subjects, naloxone administration resulted in a 50% increase in urine output and creatinine clearance and twofold increases in sodium and potassium excretion in patients with cirrhosis. Fractional sodium and potassium excretion, minimal urinary osmolality, plasma vasopressin and aldosterone levels, arterial blood pressure, and heart rate were not affected by naloxone treatment. The diuretic effect of naloxone was not observed in control subjects. Plasma naloxone levels were about six times higher in patients with cirrhosis than in control subjects (probably because of impaired metabolism of the drug) but only a weak correlation was found between drug levels and the degree of diuresis observed. The diuretic effect of naloxone may be related to an increase in glomerular filtration rate, possibly in conjunction with altered tubular reabsorption.
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PMID:Naloxone increases water and electrolyte excretion after water loading in patients with cirrhosis and ascites. 194 May 89

HFRS-related oliguria brings about hyperactivity of the system hypothalamus-hypophysis-adrenals and hyperfunction of the pancreas; glucose, urea and creatinine plasma levels are elevated. Prednisolone treatment leads to diminution of ACTH and cortisol levels, elevation of glucose, insulin and C-peptide concentrations in plasma compared to prednisolone-untreated patients, producing insignificant effect on plasma levels of STH, vasopressin, aldosterone, area and creatinine. Therefore, a course administration of glucocorticoids to HFRS patients is justified only in severe collapses and hypopituitary coma confirmed by the laboratory methods.
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PMID:[Effect of glucocorticoid hormones on the status of the hypothalamo-hypophyseal-adrenal system and endocrine function of the pancreas in patients with hemorrhagic fever with renal syndrome]. 197 53

The present study was designed to test the possible role of vasopressin in the renal response to dietary protein. This possibility was suggested by the similarity of effects on renal function and morphology of chronic high-protein intake and chronic stimulation of urine concentration. Adult male Brattleboro rats, genetically unable to produce vasopressin, were fed high-protein (32% casein = HP, n = 8) or low-protein (10% casein = LP, n = 9) diet for 7 wk. Renal function was evaluated by clearance techniques based on 24-h urine collections in metabolic cages. The response to a single injection of the vasopressin analogue 1-desamino-8-D-arginine vasopressin (DDAVP) was also tested. Kidney weight and height of the different renal zones were assessed at the end of the study. HP diet increased urea excretion nearly sevenfold. Water intake increased by 57% (P less than 0.001) and urine flow rate by 71% (P less than 0.01). Urine osmolality rose from 104 to 181 mosmol/kgH2O (P less than 0.001). At variance with what occurs in rats with endogenous vasopressin (Sprague-Dawley; Bouby, N., et al. Kidney Int 34: 4-12, 1988), HP diet increased creatinine clearance per unit body weight by only 14% and did not change free water clearance, renal mass, and height of inner stripe of outer medulla. However, the rise in urine osmolality and drop in free water clearance after DDAVP were significantly greater in HP- than in LP-fed Brattleboro rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin is involved in renal effects of high-protein diet: study in homozygous Brattleboro rats. 199 84

Heat-stressed pregnant ewes deliver intrauterine growth-retarded lambs. Selected maternal and fetal changes were investigated during acute heat stress in order to elucidate the mechanism for this growth retardation. Uterine blood flow decreased 20 to 30% in pregnant ewes during 1 degree C increases in core temperature. The decreases were accompanied by 60 and 100% increases in serum oxytocin and antidiuretic hormone, respectively. These effects were mimicked by salt loading or injections of antidiuretic hormone or oxytocin, suggesting a role for either or both hormones in regulating uterine blood flow during pregnancy. Chronically heat-stressed pregnant ewes were delivered by Caesarean section. Their fetuses were approximately 20% smaller than thermoneutral controls. Within each pair of heat-stressed twins, one fetus weighted one-third less than its litter mate. No difference in weights were observed within the control twins. The livers and brains of the heat-stressed fetuses were disproportionate in size. The livers from the small heat-stressed twins contained only one-half the protein of the controls and one-fourth the protein of their litter mates. Muscle protein was decreased in the heat-stressed fetuses, and liver and muscle glycogen were elevated as were liver arginase, glutamate-pyruvate transaminase and muscle creatinine. These results are consistent with the following hypothesis: heat stress stimulates the release of maternal antidiuretic hormone or oxytocin, which reduces uterine blood flow and causes a shift in fetal metabolism from anabolic to catabolic pathways; one fetus of heat-stressed twins is more severely affected than its litter mate.
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PMID:Maternal endocrine and fetal metabolic responses to heat stress. 203 Jan 75


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