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 renal response of the fetal lamb to repeated complete occlusion of the umbilical cord was studied in nine chronically instrumented animals. Five episodes of occlusion of the umbilical cord, each lasting for two minutes, produced a twofold rise in fetal urine osmolality and sodium, chloride, and potassium concentrations. Output of urine and glomerular filtration rate remained essentially unchanged while free water clearance decreased from a control of +0.10 to -0.02 ml. per kilogram per minute at the end of the fifth episode. Electrolyte concentrations in urine remained elevated for at least two hours following the occlusions. In addition to changes in urine composition, there was a 50- to 200-fold increase in the fetal plasma concentration of vasopressin. These studies indicate that complete interruption of the umbilical circulation, even though of short duration, produces disturbances in fetal renal function that can lead to loss of electrolytes in the urine. They provide an explanation for the low sodium levels reported in asphyxiated newborn infants in renal failure.
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PMID:Renal response of fetal lamb to complete occlusion of umbilical cord. 2 86

The excretion of cyclic AMP in urine has been examined in normal children and in children with nephrogenic diabetes insipidus or moderate renal failure (predominantly defective concentrating ability) under basal conditions and in response to antidiuretic hormone (ADH) and parathyroid hormone (PTH). In contrast to other reported data, we could not confirm an ADH- and (PTH-unresponsiveness in hereditary, congenital nephrogenic diabetes insipidus, but our patients with structural renal disorders characterized by a defective urine concentrating ability did have reduced hormonal responses. It seems necessary to define nephrogenic diabetes insipidus very carefully, and until more data are collected, there appears to be no value in the measurement of urinary cyclic AMP level in the individual patient in the differential diagnosis of disorders due to renal concentrating defects.
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PMID:Basal and hormone-induced urinary cyclic AMP in children with renal disorders. 18 4

In cirrhotic patients without renal failure, salt retention could result from a decreased effective intravascular volume or could be a primary event leading to increased intravascular volume. Clearance of urea and uric acid depend on an effective intravascular volume. In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)--a state of increased intravascular volume--uric acid clearance is increased and that of urea is increased only when salt excretion is low. The intravascular volume of 60 consecutive cirrhotic patients without renal failure was estimated indirectly by studying the relationship between fractional excretion of filtered (FE) sodium, urea, and uric acid. Forty five per cent had a high FE uric acid (> 12%), which could mean a high intravascular volume, and presented with an FE urea that was inversely correlated with FE sodium (r = 0, 62; p < 0.001) as in SIADH, while in the controls the FE urea was positively correlated with FE sodium (r = +0, 46; p < 0.01). In patients who had a normal FE uric acid and low FE sodium (< 0.2%), the FE urea was significantly lower (40 (13)%, n = 20) than in subjects with high FE uric acid and a low FE sodium (61 (9)%, n = 16, p < 0.001); this last group also presented with lower mean blood urea concentrations (3.1 (1.2) mmol/l and 4.0 (1.8) mmol/l; p < 0.05) and a lower supine renin activity (p < 0.01). As observed in the SIADH, cirrhotic patient with high FE uric acid have raised FE urea only when salt excretion is low. It is believed that the low salt excretion is not caused by a decrease in effective intravascular volume and that this is increased in cirrhotic patients with raised FE uric acid.
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PMID:Raised urea clearance in cirrhotic patients with high uric acid clearance is related to low salt excretion. 139 36

Ageing of the kidneys has long been associated with a fall in the number of functioning nephrons resulting in a reduction of renal blood flow and glomerular filtration. This narrow concept of age-related changes in renal function has been developed chiefly during the last few years by Brenner et al. on the basis of experimental studies conducted on rodents. According to these authors, the size and frequency of segmental and focal lesions of glomerulosclerosis increase regularly with age, and in its final phase this pathology results in occlusion of glomerular capillaries. Renal ageing, therefore, can be assimilated to the nephron reduction models obtained by surgical ablation. The hypothesis that hypofiltration in certain nephrons is compensated by hyperfiltration in healthy glomerulis, leading to a vicious circle of self-destruction, was then applied to both ageing and experimental renal impairment: the smaller the number of nephrons, the greater the filtration achieved by the remaining nephrons, a process that accelerates the probability of their destruction. Conversely, any attempt to reduce intracapillary pressure or glomerular filtration slows down the progression of renal failure. This hypothesis is supported by experiments showing that reduction of protein intake or chronic inhibition of angiotensin I-converting enzyme activity are truly capable of limiting the progression of glomerulosclerosis induced in rats by partial renal mass ablation. Similarly, prolonged food restriction increases the life expectancy of rodents and almost totally prevents the occurrence of glomerulosclerosis. The experimental finding that degenerative renal lesions do not necessarily develop with age raises the problem of normal and pathological ageing. With an adequate choice of rats' food, strain and sanitary surroundings it is possible to obtain very old animals devoid of occluded glomerular capillaries and loss of nephron. What about the functional and structural changes due to ageing and not to pathology? This question has given rise to numerous studies which concluded, on the whole, that there exists a normal ageing of the kidneys without loss of nephron and that ageing is expressed by the fact that the kidneys have difficulties in adjusting themselves to disturbances in the inner environment. As regards renal functional reserve, response to the antidiuretic hormone in case of water restriction, or stimulation of the renin-angiotensin system in response to decrease of sodium intake, it is clear that the renal cells responsible for glomerular filtration, tubular transport or synthesis and release of peptidic hormones exhibit functional alterations that are age-related. The cellular and molecular mechanisms underlying these physiological changes are little known.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Normal and pathological renal aging in animals]. 140 79

The negative effect of artificial ventilation with positive pressure on renal function, expresses itself as a decrease of water and sodium excretion, being directly related with the raise of intrathoracic pressure. Factors participating in this process are: lowering in cardiac output, arousal of sympathic nervous system, increase in vasopressin action, activation of renin-angiotensin-aldosterone system and decrease of atrial natriuretic peptide release. This disorder of hydromineral metabolism produces: Impairment of hemodynamic equilibrium, favors the increase of hypoxia and renal failure. The effects of mechanical ventilation on renal function can be attenuated with the adoption of the following measures: a) techniques (use of low levels of PEEP and early disconnection of respirator); b) therapeutic (dopamine 2-3 mcg/kg/min, rational use of diuretics and fluids); y c) monitoring of renal function and hydro-mineral equilibrium.
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PMID:[The kidney in mechanical ventilation]. 148 39

Prominent degrees of hyponatremia are detected in the severe forms of Mediterranean spotted fever and the intensity of this abnormality parallels the severity of the infectious process. In order to determine the incidence, degree and evolution of hyponatremia in 110 patients with Mediterranean spotted fever and to explore the feasible renal mechanism that could lead to this phenomenon, serum and urinary osmolality and levels of urea, creatinine and electrolytes were measured in samples obtained at selected points (up to the fifth week) in the course of the disease, and parameters of renal function were calculated. Mean serum sodium levels of 135.6 +/- 5.5 mEq/l were detected during the acute phase of the infection. At this point, 42 patients (38.2%) had sodium concentrations less than or equal to 135 mEq/l. After recovery, mean serum sodium values were 142.5 +/- 2.5. The analysis of the parameters of renal function indirectly rules out an inappropriate antidiuretic hormone secretion or renal failure as the cause of hyponatremia. As tubular incompetence to reabsorb sodium is also rejected in these patients, a shifting of sodium to the interstitial or intracellular space may account for the phenomenon.
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PMID:Mechanism of low serum sodium levels in Mediterranean spotted fever. 168 72

The clinical course of patients with cirrhosis of the liver is frequently complicated by progressive impairment of renal sodium handling leading to the formation of ascites. The occurrence of ascites is generally accompanied by the activation of several hormones and intrarenal autacoids and a complex derangement of systemic, portal and renal hemodynamics. The earliest "underfilling" theory of sodium retention proposes that ascites formation leads to hypovolemia and secondary sodium retention. According to the "overflow" theory, ascites formation is a secondary event with respect to sodium retention, which occurs as a primary phenomenon in the absence of hypovolemia. A third recently developed theory suggests that peripheral arteriolar vasodilation is the primary event of intravascular underfilling. The major documented site involved in arteriolar vasodilation is the splanchnic circulation. Occurrence of underfilling is not related to a reduction of plasma volume but to the enlargement of the vascular compartment. Vascular underfilling triggers a series of hemodynamic and hormonal compensatory events such as an increase in cardiac output and plasma volume, activation of the renin-angiotensin-aldosterone and sympathetic nervous system and non-osmotic hypersecretion of antidiuretic hormone and sodium retention, all of which aim at refilling the vascular compartment. In patients with compensated cirrhosis, i.e. without ascites, compensatory events maintain blood volume despite vascular underfilling, and so these patients do not develop ascites. In patients with decompensated cirrhosis, vascular underfilling due to arterial vasodilation, together with a reduced oncotic pressure and a severe degree of portal hypertension, favours the development of ascites. Underfilling of the arterial circulation is at its maximum in functional renal failure and the hepatorenal syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ascites in liver diseases. 174 50

In 11 patients with decompensated cirrhosis and deteriorating renal function, the effect of the vasoconstrictor substance 8-ornithin vasopressin (ornipressin; POR 8; Sandoz, Basel, Switzerland) on renal function, hemodynamic parameters, and humoral mediators was studied. Ornipressin was infused at a dose of 6 IU/h over a period of 4 hours. During ornipressin infusion an improvement of renal function was achieved as indicated by significant increases in inulin clearance (+65%), paraaminohippuric acid clearance (+49%), urine volume (+45%), sodium excretion (+259%), and fractional elimination of sodium (+130%). The hyperdynamic circulation was reversed to a nearly normal circulatory state. The increase in systemic vascular resistance (+60%) coincided with a decrease of a previously elevated renal vascular resistance (-27%) and increase in renal blood flow (+44%). The renal fraction of the cardiac output increased from 2.3% to 4.7% (P less than 0.05). A decline of the elevated plasma levels of noradrenaline (2.08-1.13 ng/mL; P less than 0.01) and renin activity (27.6-14.2 ng.mL-1.h-1; P less than 0.01) was achieved. The plasma concentration of the atrial natriuretic factor increased in most of the patients, but slightly decreased in 3 patients. The decrease of renal vascular resistance and the increase of renal blood flow and of the renal fraction of cardiac output play a key role in the beneficial effect of ornipressin on renal failure. These changes develop by an increase in mean arterial pressure, the reduction of the sympathetic activity, and probably of an extenuation of the splanchnic vasodilation. A significant contribution of atrial natriuretic factor is less likely. The present findings implicate that treatment with ornipressin represents an alternative approach to the management of functional renal failure in advanced liver cirrhosis.
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PMID:Ornipressin in the treatment of functional renal failure in decompensated liver cirrhosis. Effects on renal hemodynamics and atrial natriuretic factor. 183 7

In 12 patients with acute non-inflammatory renal failure (ANRF) and in 21 healthy persons the relationship was studied between the activity of the renin-angiotensin-aldosterone (RAA) system and vasopressin secretion. The study was carried out during the so called bed rest test and during water immersion (WI) after captopril-induced blockade of the angiotensin-converting enzyme. The results of these experiments suggest the absence of a close functional relationship between the activity of the RAA system and vasopressin secretion in patients with ANRF and in healthy controls.
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PMID:The activity of the renin-angiotensin-aldosterone (RAA) system and vasopressin secretion in patients with acute non-inflammatory renal failure. 184 99

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


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