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)

Previous reports have described 5-20% prevalence of hyponatremia in extended care facilities, due largely to drugs or inappropriate antidiuretic hormone secretion. In our 400 bed VA extended care facility, 15 men with organic brain syndrome (Alzheimer's, multi-infarct dementia, anoxic encephalopathy or alcoholism) currently receive Isocal via gastrostomy as the sole source of nutrition. We noted intermittent hyponatremia in about half of these patients, and conducted a chart review to investigate the cause. Mean age was 68 yr (range 46-92); tube feeding duration was 3 mo.-3 yr; 266 Na concentrations were obtained from the charts. Simultaneous with these Na analyses, one of three diets prevailed: (A) mixed foods (3-6 g Na/day) orally before gastrostomy; (B) Isocal supplemented with NaCl to give 2 g Na/day; (C) unsupplemented Isocal providing 1 g Na/day. (B) and (C) had been randomly varied by rotating physicians. Serum Na was directly related to Na intake. On (A), Na was within normal range (135-145 mEq/l) in all men. One patient was hyponatremic during diet (B). During (C), eight patients were hyponatremic. Na was less than 135 mEq/l in 40% of all samples during diet (C) and less than 130 mEq/l in 14%. Changing from diet (A) or (B) to diet (C) caused nearly equivalent declines in Na and Cl; K and HCO-3 were unaffected. No hyponatremic patient took drugs known to cause hyponatremia, or had congestive heart failure, hypoalbuminemia, lipemia or fasting hyperglycemia. At the end of the study, four hyponatremic men were changed from (C) to (B); serum Na became normal in all four patients, without edema or hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremia in tube-fed elderly men. 308 Apr 61

Angiotensin II (AII), aldosterone (Aldo) and arginine vasopressin (AVP) in plasma were determined during basal conditions in seventeen patients with congestive heart failure and in seventeen control subjects. The same parameters were measured before and 1, 2 and 3 h after an oral water load of 20 ml (kg body weight)-1 together with urine volume (V) and free water clearance (CH2O) in seven patients with congestive heart failure and in seven control subjects. AII, Aldo and AVP were significantly higher in heart failure than in control subjects (AII:81 and 12 pmol l(-1) (medians), P less than 0.01; Aldo: 411 and 103 pmol l(-1), P less than 0.01; AVP: 5.3 and 2.0 pmol l)-1), P less than 0.01). AVP was positively correlated to Aldo in both heart failure (p = 0.593, n = 17, P less than 0.02) and control subjects (p = 0.511, n = 17, P less than 0.05), but in neither of the groups to AII. V and CH2O were significantly lower in heart failure when compared to control subjects (maximum increase in CH2O 3.55 and 5.86 ml min-1, P less than 0.02), but did not correlate directly with either A II, Aldo or AVP. Creatinine clearance was reduced in heart failure. It is concluded that the activity of both the renin-angiotensin-aldosterone system and the osmoregulatory system is enhanced in congestive heart failure, presumably as a compensatory phenomenon in order to maintain arterial blood pressure. It is suggested that the decrease in free water clearance may be attributed to both an elevated level of vasopressin and a reduced glomerular filtration rate.
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PMID:Angiotensin II, aldosterone and arginine vasopressin in plasma in congestive heart failure. 308 74

The pathogenesis of hyponatremia remains debated; therefore, we determined the roles of plasma vasopressin, fluid intake and renal free water excretion in hyponatremic medical patients. We evaluated 100 consecutive hypo-osmolar hyponatremic patients (PNa = 127 +/- 0.7 mM l-1) in a prospective manner. We observed: hyponatremia was often found in association with advanced congestive cardiac failure (twenty-five of 100 patients), liver cirrhosis (16%) and primary volume contraction (29%). There was a 17% in-hospital mortality of hyponatremic patients. This was primarily related to the severity of underlying illnesses rather than to hyponatremia per se. The most consistently observed laboratory finding of hyponatremia was non-osmotic vasopressin stimulation; mean observed PADH was 4.7 +/- 0.7 pg ml-1 and vasopressin was detectable by radioimmunoassay (RIA) in 91% of all patients. In addition to vasopressin stimulation we also found evidence of advanced 'circulatory underfilling' in most hyponatremic patients. Mean urinary osmolality was hypertonic to plasma (441 +/- 17.4 m0sm kg H2O-1). This applied to patients with hyponatremic cardiac failure, liver cirrhosis and volume contraction. Almost all of these patients received high ceiling diuretics. (v) Spontaneous mean daily fluid intake was 2.4 +/- 0.2 l. In summary, our findings suggest that disturbances of vasopressin, fluid intake and renal free water excretion co-operate in the pathogenesis of hyponatremia. In clinical states of advanced circulatory underfilling the occurrence of hyponatremia indicates a poor prognosis of the patient.
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PMID:Pathogenesis of clinical hyponatremia: observations of vasopressin and fluid intake in 100 hyponatremic medical patients. 310 2

Arginine vasopressin is elevated in congestive heart failure. To determine the effect of arginine vasopressin upon systemic hemodynamics and regional blood flows, we administered the specific inhibitor of the vascular action of vasopressin [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)-tyrosine]-arginine vasopressin [d(CH2)5Tyr(Me)AVP] to 15 dogs with chronic right-heart failure produced by tricuspid avulsion and progressive pulmonary artery constriction. The animals exhibited increased plasma arginine vasopressin and norepinephrine levels. Vasopressin inhibition increased cardiac output and left ventricular dP/dt and dP/dt/P, and it decreased total peripheral vascular resistance, whereas mean aortic pressure did not change significantly. Simultaneously, blood flow increased to skeletal muscle, kidneys, skin, and right and left ventricular myocardium. Plasma catecholamines also increased. Pretreatment with propranolol and prazosin abolished the increases in cardiac output and left ventricular function produced by vasopressin inhibition. Pretreatment also led to a decrease in mean aortic pressure after vasopressor inhibition. In contrast, administration of d(CH)2)5Tyr(Me)AVP to 11 sham-operated animals or administration of normal saline to nine sham-operated and eight heart-failure dogs was without effect either in the absence or in the presence of adrenergic receptor blockade. Thus, arginine vasopressin participates in the control of the circulation in right-sided congestive heart failure, with both a direct constrictor action on blood vessels and an indirect action by inhibition of the sympathetic nervous system.
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PMID:Short-term hemodynamic effects of vasopressin V1-receptor inhibition in chronic right-sided congestive heart failure. 318 Mar 81

A case of a 69-year-old woman with postpartum hypopituitarism (Sheehan's syndrome) associated with congestive heart failure and severe hyponatremia is reported. She developed congestive heart failure after cholecystectomy, and marked improvement was noted by treatment with oxygen, digoxin, furosemide, and dopamine. Two weeks after surgery, she became confused, and hyponatremia, 106 mEq/l, was detected. She was referred to us. Past history revealed postpartum hemorrhage at the age of 34, followed by a failure to lactate, menoschesis, and loss of pubic hair and axillary hair. Hypertonic saline (1.5%) infusion and water restriction increased her serum sodium concentration into the low normal range. Despite hyponatremia, serum vasopressin was not suppressed. Basal levels of pituitary hormones were low, and they did not respond to provocation tests. Marked impairment of water excretion was noted, and plasma vasopressin was not suppressed during a water-loading test. These results suggest that inappropriately increased vasopressin played an important role in impaired water excretion, and this defect could have been responsible for the development of hyponatremia and congestive heart failure in this patient.
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PMID:A case of postpartum hypopituitarism (Sheehan's syndrome) associated with severe hyponatremia and congestive heart failure. 326 36

Congestive heart failure is a complex clinical syndrome characterized by a number of neuroendocrine responses. These responses are probably an evolutionary vestige of mechanisms designed to defend volume and maintain circulatory homeostasis. Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and the release of vasopressin have been clearly documented in patients with heart failure. Unlike the normal ventricle, the failing ventricle responds to peripheral vasoconstriction and sodium retention with further hemodynamic embarrassment and circulatory congestion. Certain vasorelaxant natriuretic substances are also released during heart failure, perhaps in an attempt to offset excessive peripheral constriction and sodium retention. Prostaglandin E2, atrial natriuretic peptide (or atrial natriuretic factor) and plasma dopamine are found to be increased in some patients with heart failure. However, peripheral constriction and sodium retention appear to be dominant, particularly in the advanced stages of heart failure. An understanding of these neuroendocrine responses has led to new developments in therapy. Angiotensin-converting enzyme inhibitors have emerged as distinctly useful drugs in the treatment of heart failure. Agents designed to block excessive sympathetic drive and inhibit vasopressin are under investigation. Infusion of atrial natriuretic factors and the use of selective dopamine agonists are also undergoing clinical trials in patients with heart failure. Increased knowledge of the neuroendocrine responses will likely result in even newer and more imaginative therapy.
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PMID:Neuroendocrine manifestations of congestive heart failure. 329 96

A review of the history of our knowledge and understanding of the peripheral oedema of congestive cardiac failure points to the conclusion that an inability of the heart to maintain the arterial pressure is of central importance in this condition. Although the function of the circulation is to perfuse the tissues, the body monitors the adequacy of its perfusion, not not through metabolic messengers carried from the tissues in the blood stream, but by sensing the arterial pressure; and the mechanisms evoked act to maintain the arterial pressure. In the short term this is achieved by autonomic regulation of the heart and blood vessels; in the longer term the arterial pressure is maintained through an increase in the blood volume by a retention of salt and water by the kidney. To support the latter process, intrinsic renal mechanisms are successively magnified by the renin-angiotensin-aldosterone system and by the activities of the sympathetic system and vasopressin. The natriuretic influence mediated through volume receptors and the release of atrial peptide is overruled by the arterial baroreceptors, so that the body maintains the arterial pressure at the expense of an increase in blood volume. In these ways the syndrome of congestive cardiac failure may be regarded as one which arises when the heart becomes chronically unable to maintain an appropriate arterial pressure without support.
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PMID:Congestive cardiac failure: central role of the arterial blood pressure. 331 Oct 96

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.
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PMID:Variable arginine vasopressin levels in neonatal congestive heart failure. 334 66

We measured systemic hemodynamics, regional blood flow, and neurohormonal parameters in 13 patients with severe chronic congestive heart failure before and after 1 month of therapy with oral milrinone, a bipyridine cardiotonic agent. After milrinone there were significant reductions in pulmonary wedge pressure (27 +/- 2 to 19 +/- 3 mm Hg; P less than 0.02) and systemic vascular resistance (1866 +/- 152 to 1393 +/- 93 dyne X sec/cm5; P less than 0.05) that were associated with increases in cardiac index (1.85 +/- 0.15 to 2.47 +/- 0.20 L/min/m2; P less than 0.02). There was a marked improvement in forearm blood flow (1.98 +/- 0.14 to 3.02 +/- 0.16 ml/min/dl; P less than 0.01) and a reduction in forearm vascular resistance (45 +/- 3 to 30 +/- 3 U; P less than 0.01). Overall there was no significant change in renal blow flow, renal vascular resistance, or glomerular filtration rate. However, there was a heterogeneous response of renal blood flow and glomerular filtration rate, such that both were directly correlated with the magnitude of increase of cardiac index (r = 0.587 [P less than 0.05] and r = 0.721 [P less than 0.01], respectively). After milrinone there were no significant overall or subgroup changes in urinary sodium excretion, blood volume, plasma renin activity, urinary aldosterone levels, plasma or platelet vasopressin levels, or plasma norepinephrine levels. Thus 1 month of therapy with milrinone improves systemic and forearm hemodynamics, but its effects on renal blood flow and function were heterogeneous. These heterogeneous effects on regional blood flow may depend on the relative vasodilator and inotropic effects of milrinone.
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PMID:Regional blood flow and neurohormonal responses to milrinone in congestive heart failure. 351 Jul 99

Fifty patients with congestive heart failure received, by infusion, 15 ml/kg body weight water load, and systemic hemodynamic, renal function, and neurohumoral parameters values were measured before, 2 days, and 1 month after randomly allocating patients to prazosin or captopril therapy. Both prazosin and captopril caused similar and persistent hemodynamic changes, but important differences existed between their renal and neurohumoral effects. After 1 month of continuous therapy, captopril increased creatinine clearance from 71 to 84 ml/min/1.73(2) (p less than .05), increased the water load excreted in 5 hr from 50% to 71% (p less than .005), and increased 5 hr sodium excreted from 6.8 to 14.7 meq (p less than .005), Captopril also caused a decrease in plasma norepinephrine from 568 to 448 pg/ml (p less than .005), in plasma epinephrine from 94 to 73 pg/ml (p less than .05), and in plasma aldosterone from 57 to 28 ng/dl (p less than .005), without changing plasma vasopressin. These beneficial effects were greater after 1 month of therapy than after 2 days. The only beneficial effect of prazosin was to increase water excretion from 49% to 59% (p less than .05). The long-term response to captopril was similar in patients with higher (greater than 2.5 ng/ml/hr) and lower renin levels. However, in patients with lower renin levels, prazosin decreased pulmonary capillary wedge pressure (24.8 to 21.8 mm Hg, p less than .05), decreased plasma arginine vasopressin (1.16 to 0.75 pg/ml, p less than .05), increased water excretion (62% to 85%, p less than .005), and decreased plasma epinephrine (81 to 46 pg/ml, p less than .05), while in patients with higher renin levels none of these beneficial effects were noted. We conclude that captopril produces long-term beneficial renal and neurohumoral effects that prazosin does not despite similar hemodynamic changes with the two drugs, that these effects are at least partially dependent on the initial neurohumoral and hemodynamic status of the patient, and that through hemodynamic improvement vasodilators may chronically interrupt vasopressin overstimulation.
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PMID:Differential long-term intrarenal and neurohormonal effects of captopril and prazosin in patients with chronic congestive heart failure: importance of initial plasma renin activity. 351 21


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