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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 989-999 
    ISSN: 1432-1440
    Keywords: Dehydration ; Hemodynamics ; Hypertension ; Vasopressin ; Vasopressin antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 152 (1993), S. 301-305 
    ISSN: 1432-1076
    Keywords: Hyponatraemia ; Syndrome of inappropriate antidiuretic hormone secretion ; Vasopressin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hyponatraemia is one of the most common electrolyte abnormalities in hospitalised children. In a prospective study we tested whether hyponatraemia is associated with sustained release of the antidiuretic hormone arginine vasopressin (AVP). Out of 27 children with persistent hyponatremia (serum sodium 〈130 mmol/l), 25 had measurable plasma concentrations of AVP [median and quartiles 5.0 pg/ml (1.5–8.3)]. Volume contraction as consequence of sodium loss caused hyponatraemia in 16 patients. Hyponatraemia in the presence of extracellular volume expansion and reduced effective arterial blood volume occurred in 5 patients. Only 3 patients had normovolaemic hyponatraemia (so-called syndrome of inappropriate antidiuretic hormone secretion) and 3 suffered from chronic renal failure. It is concluded that plasma AVP concentration is measurable in most children with hyponatraemia. Non-osmotic stimulation of AVP release and lack of suppression of this hormone is an important pathogenetic mechanism of hyponatraemia in children.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Hyponatremia ; Vasopressin ; Thirst ; Diuretics ; Cardiac failure ; Cirrhosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid indake — conditions which have not been addressed sufficiently in published literature — we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Sience a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (〈0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35±0.15 l. In the presence of stimulated vasiopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake. In conclusion, stimulated vasopressin and high fluid intake explain the hyponatremia observed in the present study. This applied similary to diuretictreated and -untreated patients.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 68 (1990), S. 1127-1133 
    ISSN: 1432-1440
    Keywords: Thirst regulation ; Vasopressin ; Renin-angiotensin-system ; Atrial natriuretic peptide ; Endstage renal disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary About 30% of hemodialyzed patients are suffering from chronic fluid overload despite advice to restrict the oral fluid intake. To investigate the cause of the abnormal drinking behaviour a clinical study was performed in 51 non-diabetic patients with endstage renal disease exhibiting lower interdialytic weight gain (〈3 kg,n=17) and increased interdialytic weight gain (〉3 kg,n=34). Blood pressure, body weight self-estimated thirst intensity before and after hemodialysis were analyzed. Biochemical and behavioral variables were measured including hormonal factors of water and sodium metabolism. Significant differences of dry weight, creatinine, urea nitrogen and thirst intensity were found between the two groups. Catecholamines, renin, angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide exhibited a similar pattern in both groups. Atrial natriuretic peptide decreased during hemodialysis in both groups, angiotensin II, however, and norepinephrine showed an exaggerated response to ultrafiltration rate in polydipsic patients. These results suggest that changes in serum osmolality during hemodialysis did not contribute to thirst and drinking behaviour. It seems that postdialytic hypovolaemia together with higher plasma-angiotensin II-levels is responsible for increased oral intake of fluid and excessive weight gain.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-198X
    Keywords: Hydrochlorothiazide ; Indomethacin ; Nephrogenic diabetes insipidus ; Prostaglandins ; Vasopressin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In four boys with congenital nephrogenic diabetes insipidus, plasma arginine-vasopressin (AVP) and urinary excretion of prostaglandins were studied in response to treatment with hydrochlorothiazide and indomethacin. An abnormal relationship between AVP and urine osmolality was demonstrated in all patients. In the first patient, treatment with indomethacin (3 mg/kg per day) resulted in a drop of the inulin and paraminohippurate clearances. In the other three patients urinary excretion of PGE2 was raised, and fell during treatment with hydrochlorothiazide (2 mg/kg per day) and indomethacin (2 mg/kg per day). Urine flow, free water clearance and osmolar clearance decreased during treatment. A combination of both drugs is more effective than hydrochlorothiazide alone and the effect appears to be additive.
    Type of Medium: Electronic Resource
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