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)

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

In the first part of the text the main elements of renal physiology are mentioned as well as the role played by sodium-modulating hormones in the preservation of sodium and water homeostasis. A personal contribution concerns the release as well as the circadian rhythm of atrial natriuretic peptide (ANP) and of the digitalis-like substance (DLS). In the second part, the problem is dealt with from a pathophysiologic point of view, with reference made to the literature, and to our own data. In particular, the problem of essential hypertension with reduced levels of plasma renin activity (PRA) is thoroughly analyzed. As is well known, this kind of hypertension is characterized by normal plasma aldosterone levels associated with reduced kallikrein urinary excretion. The data we gathered not only confirmed these findings but also enabled us to point out other typical features of this particular kind of hypertension: normal values of vasopressin, elevation of ANP and DLS, hyperactivity of Na+/K+ cotransport. The introduction of a single variant in the sodium-modulating systems confirmed that the low PRA patient also behaves distinctively from a dynamic point of view. In fact, prostaglandin inhibition determines hypertension only in these patients, while both oral kallikrein administration and intravenous ANP administration were particularly effective because of a primitive deficit of the natriuretic paracrine systems paralleled by a compensatory increase of ANP. After identifying this group of hypertensive patients we intended to ascertain whether, even in the normal or high PRA patients, it was possible to identify a sub-group of subjects with altered sodium-modulation. The patients we examined were subdivided according to their hormonal and renal response to a saline load, and to angiotensin II, into "modulators" (with normal) and "nonmodulators" (with reduced sodium excretion capacity). An analysis of the hormonal characteristics of non-modulators identified an increased responsiveness of all sodium-modulation systems and not only of the renin-angiotensin-aldosterone system as pointed out by some other authors. The last part of the text is devoted to clinical and therapeutic problems. The behaviour of the daily blood pressure profile in patients with essential hypertension, and then the influence that sodium-modulating systems may have on pressure are discussed. The consequences of a progressive reduction in renal function on the circadian rhythm of arterial pressure are then assessed, and, at the same time, how renal impairment parallels the flattening of the daily pressure rate is observed.
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PMID:The kidney and essential hypertension. 183 73

Blood pressure and heart rate responses to intracerebroventricular (ICV) injections of atrial natriuretic peptide (ANP, 125 ng) arginine vasopressin (AVP, 10 ng), combination of ANP (125 ng) and AVP (10 ng) or artificial cerebrospinal fluid (acsf, 5 microliters) were compared in conscious normotensive (WKY) and spontaneously hypertensive (SHR) rats. In both strains, ICV injection of AVP elicited significant increase of mean blood pressure (MP) and heart rate (HR). Increase of MP but not of HR was significantly greater in SHR than in WKY (p less than 0.05). Injection of acsf or ANP, as well as simultaneous administration of ANP and AVP, did not elicit significant changes of MP either in WKY or in SHR. In SHR, HR was significantly elevated by ICV injections of AVP and ANP + AVP, whereas in WKY HR was increased only after AVP. The data suggest that interaction of ANP and AVP at a central level may result in significant attenuation of central pressor effects of vasopressin.
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PMID:Central ANP attenuates pressor responses to central AVP in WKY and SHR. 183 98

A tomographic method of measuring electrical impedance known as Applied Potential Tomography (APT) has been used to image the impedance changes within the thoraxes of 8 healthy volunteers (4 male, 4 female) during 4-h periods of 6 degrees head-down tilt (HDT). A large decrease in impedance, reflecting an increase in thoracic fluid, was apparent within 1 min of tilting, peaked after 45 min, and was maintained throughout, although during the 4 h there was an 8% return towards baseline resistivity. Resistivity changes were most obvious in the region of the lungs. Simultaneous measurements of the key fluid regulating hormones revealed a significant increase in atrial natriuretic peptide (ANP) and a significant decrease in angiotensin II (AII) and aldosterone. There was no significant difference in plasma antidiuretic hormone level. These results illustrate the dynamic nature of fluid shifts during HDT, the spatial distribution of the fluid within the thorax and the associated endocrine responses.
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PMID:Trans-thoracic fluid shifts and endocrine responses to 6 degrees head-down tilt. 183 13

The renal response to iso-oncotic blood volume expansion with bovine serum albumin was studied in anaesthetized homozygous Brattleboro (DI) rats after acute (1 day) pretreatment with 1 U arginine-vasopressin (AVP) compared to heterozygous controls. In AVP-treated DI (DI + AVP) rats, basal urine flow as well as urinary sodium, chloride, and potassium excretion, were not different from controls. Diuresis and kaliuresis induced by volume expansion were blunted in DI + AVP rats. However, natriuresis and chloruresis were exaggerated in DI + AVP rats. They increased faster, reached a higher maximum, but declined earlier, compared to controls. The blunted diuresis resulted in a positive volume balance by the end of the experiment in DI + AVP rats, whereas the controls showed restoration of normal balance. Significant retention of sodium and chloride was observed in controls, but not in DI + AVP rats, over the time of the experiment. DI + AVP rats lost significantly less potassium than controls during the experiment. As judged from the lithium clearance method, the exaggerated saluresis in DI + AVP rats was mainly due to a reduced proximal sodium reabsorption. Plasma immunoreactivity of atrial natriuretic peptide (ANP) rose during blood volume expansion and fell in the recovery period. It was not different between AVP-treated DI rats and controls at any time of the experiment. Inulin clearance was slightly, but not significantly, lower in DI + AVP rats and increased after blood volume expansion in DI + AVP rats only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal response to blood volume expansion in Brattleboro rats after acute treatment with vasopressin. 183 44

In chronic heart failure, neurohumoral mechanisms play an important role in the regulation of cardiac performance by direct influences on systolic and diastolic function of the myocardium, and indirectly, by modulation of pre- and afterload. Important vasoconstrictor, fluid- and sodium-retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity, and vasopressin; vasodilator, volume, and sodium-eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins like prostacyclin and prostaglandin E2, dopamine, bradykinin, and possibly, endothelial derived relaxing factor (EDRF). There is evidence from experimental and clinical studies that the sympathetic nerve activity is stimulated in the early phase of the disease, as well as is the secretion of atrial natriuretic peptide which increases in relation to a rise in preload. In early or mild heart failure, atrial natriuretic peptide suppresses the activity of the renin-angiotensin-aldosterone system, which may prevent an increase in peripheral vascular resistance and preserve renal blood flow. In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. This is associated with an increased production of vasodilator prostaglandins. In severe heart failure, mostly in connection with hyponatremia, a nonosmolar, inappropriately high secretion of vasopressin can be demonstrated. These findings suggest that early interventions in order to suppress unfavorable neurohumoral mechanisms or to support protective factors like atrial natriuretic peptide may be of particular importance in the treatment of congestive heart failure with the aim of a retardation of the progression of the disease, which would result in an improvement of survival.
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PMID:Role of neuroendocrine mechanisms in the pathogenesis of heart failure. 183 44

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

Three cases of idiopathic edema are reported with the results of water loading tests. Free water clearance and fractional sodium excretion revealed that three cases were different in water and sodium retention both in supine and upright positions. Aldosterone, plasma renin activity and antidiuretic hormone seemed to little to correspond to water and sodium retention; whereas atrial natriuretic peptide markedly increased in the upright position in all the cases. These data suggest that three cases cannot be explained by a single factor, but that enhanced reduction of venous return to the heart in the upright position may be a common feature in all three cases.
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PMID:Water loading tests both in supine and upright positions in three cases of idiopathic edema. 183 3

Hypothalamic osmoreceptor dysfunction resulting in hypodipsia and altered regulation of vasopressin secretion is well established as the pathogenetic mechanism in the syndrome of 'essential hypernatremia'. However, little is known about the secretory pattern of atrial natriuretic peptide (ANP) in this syndrome. Therefore, we assessed ANP regulation by determining ANP concentrations in a patient manifesting this syndrome of essential hypernatremia during several well-established experimental protocols. The serum ANP level was within normal limits despite severe euvolemic hypernatremia (serum Na+ 163 mEq/l) during one of the many admissions and remained unchanged following normalization of serum Na+. Furthermore, a decline in serum ANP instead of an appropriate rise was noted when hypernatremia (serum Na+ 152 mEq/l) was induced by either hypertonic (3%) saline infusion or following a high-Na+ (300 mEq/day) diet for several days (serum Na+ 161 mEq/l). Similarly, exogenous pitressin administration failed to cause a rise in ANP, although an appropriate fall in ANP concentration occurred following fluid deprivation. Therefore, it is apparent that ANP regulation may be significantly altered in essential hypernatremia. However, further studies are required to define whether it plays a role in the pathogenesis of hypernatremia in this syndrome.
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PMID:Altered regulation of atrial natriuretic peptide in essential hypernatremia. 184 Feb 34

This study was conducted to determine the relative importance of efferent muscle sympathetic nerve activity (MSA), vasopressin (ADH) and atrial natriuretic peptide (ANP) in the short-term neurohumoral response to moderate changes in low-pressure cardiopulmonary receptor activity. The low-pressure receptors were stimulated and unloaded, respectively, by autotransfusion of blood (450 ml) and the application of lower body negative pressure (LBNP, -20 mmHg), and in 11 healthy men we measured MSA in the left peroneal nerve, indirect blood pressure, ECG, central venous pressure (CVP) and venous plasma concentrations of ANP and ADH (radioimmunoassay). Total MSA rose by 30% during LBNP and decreased during a rapid autotransfusion of blood, and the changes in MSA were significantly related to changes in CVP. The plasma concentrations of ADH and ANP were not significantly affected by either procedure. It is suggested that during moderate short-term changes in venous return, MSA responded more rapidly and/or at a lower threshold than the ADH and ANP systems.
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PMID:Reflexogenic neuronal and humoral responses to selective stimulation of low-pressure cardiopulmonary receptors in man. 184 20


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