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 hormonal response to volume depletion by isolated ultrafiltration has been studied in seven non-nephrectomised haemodialysis patients. The mean reduction in blood volume was 14%, and pulmonary artery wedge pressure reduction averaged 77%. No increments in heart rate were observed in any of the patients. Cardiac output decreased while systemic vascular resistance increased. Mean arterial blood pressure remained stable in all but two patients. Significant increments in plasma vasopressin concentration were only found during hypotensive episodes, while in the whole group no significant increase was found. Both plasma renin activity, plasma aldosterone and plasma cortisol increased significantly during isolated ultrafiltration. The moderate increase in systemic vascular resistance indicates that the peripheral sympathetic nervous system - at least partly - was functioning. It was, however, not correlated with changes in any of the measured hormones. Furthermore the adrenal and cardiac response appeared to be absent.
Proc Eur Dial Transplant Assoc 1979
PMID:Hormonal response to volume depletion in non-nephrectomised patients on regular haemodialysis. 39 94

This study was carried out to assess the influence of saralasin (SAR), an angiotensin II-analogue, on peripheral and central angiotensin II-receptors by measurements of plasma renin activity (PRA) and arginine-vasopressin (AVP) release. Before and during i.v. infusion of 10 microgram/kg/min of SAR over a 30 minute period, blood samples were obtained from 15 recumbent hypertensive patients (7 renovascular, 8 essential) to determine hormone activities by radioimmunoassay. In 10 patients with a decrease of blood pressure following SAR, PRA increased significantly whereas AVP levels increased significantly in only 7 of these patients. In the remaining 5 patients without a fall of blood pressure, PRA and AVP remained virtually unchanged. The results indicate that an enhanced AVP release may be due to a hypotensive stimulus induced by SAR in angiotensinogenic hypertension. A direct influence of SAR on central receptors is unlikely under the conditions studied.
Proc Eur Dial Transplant Assoc 1978
PMID:Effect of saralasin on plasma renin activity and arginine-vasopressin in hypertensive man. 74 Jun 74

We describe our observations concerning differences in two groups of young hypertensive patients according to their renin activities after ACE inhibition. Seventeen of these patients (age 26 +/- 7 years), so far untreated, were investigated prospectively for hormone levels (renin, aldosterone, vasopressin), microalbuminuria, renal haemodynamics (inulin and PAH clearance) and signs of organ damage (echocardiography, fundoscopy). Secondary forms of hypertension were excluded by routine methods, including angiography. We differentiated two groups of young hypertensive patients. Group 1 (n = 9) had a false positive captopril test with elevated renin activities after ACE inhibition with captopril (8.4 +/- 5 ng/ml per hour) compared to group 2 (renin activity: 2.2 +/- 1.3 ng/ml per hour) or an increase of greater than 400% of renin activity after ACE inhibition. Baseline renin activities and sodium excretion did not differ between the groups. Group 1 also showed significantly greater GFR, FF, and microalbuminuria, as well as signs of organ damage, with left ventricular hypertrophy and hypertensive changes in fundoscopy. There were no differences between the groups concerning mean arterial blood pressure and duration of hypertension. In conclusion, we were able to demonstrate that patients with highly stimulated renin activities showed signs of visceral organ damage and renal hyperfiltration compared to the normal renin activity group after ACE inhibition. Investigations of the renin-angiotensin-aldosterone system with ACE inhibitors might constitute a helpful indicator of renal changes and organ damages in young hypertensive patients.
Nephrol Dial Transplant 1992
PMID:Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition. 131 92

Plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), plasma renin activity (PRA), and circulatory haemodynamics were studied in five patients with chronic congestive heart failure undergoing ultrafiltration on two consecutive days. The patients were in the New York Heart Association class IV, and were considered candidates for heart transplantation. A mean of 3.3 +/- 0.5 litres of fluid was removed during each ultrafiltration. Plasma ANP concentration remained unchanged during ultrafiltration: 369 +/- 151 pg/ml at start and 316 +/- 116 pg/ml at the end, while plasma ADH concentration and PRA increased from 5.1 +/- 2.1 to 7.5 +/- 3.4 pg/ml (P less than 0.02), and 5.9 +/- 3.0 to 7.7 +/- 3.2 ng/ml (P less than 0.03) respectively (n = 10). After treatment, plasma ADH and PRA declined to baseline values within 1 h. Pulmonary artery, pulmonary capillary wedge, and right atrial pressures decreased significantly, while blood pressure and heart rate remained constant during ultrafiltration. A volume of 3.3 +/- 0.5 litres of fluid was removed, and caused an increase in colloid osmotic pressure from 22.0 +/- 3.0 to 33.7 +/- 3.9 mmHg (P less than 0.02). It was unexpected that plasma ANP concentration did not decline. Due to long-standing severe heart failure the atrial wall may have lost some of its elastic properties, resulting in less ability to adapt to reduced filling pressures. Accordingly, atrial wall stretch remained unchanged, explaining the constant ANP levels. Ultrafiltration treatment caused an increased responsiveness to diuretic therapy, and four patients survived long enough to receive heart transplants.
Nephrol Dial Transplant 1992
PMID:Hormonal changes in patients with severe chronic congestive heart failure treated by ultrafiltration. 131 20

In 39 healthy pregnant women and 45 women with mild or moderate late pregnancy toxaemia (LPT) the influence of head-out water immersion on blood pressure, the renin-aldosterone system, vasopressin and plasma osmolality was examined. Water immersion induced a prompt and marked fall in systolic and diastolic blood pressure, which was significantly higher in LPT women. Simultaneously a significant decrease of plasma renin activity, aldosterone and vasopressin was noted both in healthy and toxaemic pregnant women. In contrast to healthy pregnant women in LPT haemodilution was not observed in the early phase of water immersion.
Proc Eur Dial Transplant Assoc 1983
PMID:Influence of head-out water immersion on plasma renin activity, aldosterone, vasopressin and blood pressure in late pregnancy toxaemia. 636 58

Hemodialyzability of antidiuretic hormone (ADH) was studied in 14 patients undergoing hemodialysis procedure. In addition hemofiltration (dry dialysis) was performed in 8 patients and hemofiltrate samples were collected for ADH assay. The mean values for plasma ADH level in ingoing and outgoing blood were nearly identical. Moreover, no ADH was detectable in the hemofiltrate samples. These findings suggest lack of significant ADH removal by dialysis or hemofiltration.
J Dial 1980
PMID:Hemodialysis studies of antidiuretic hormone. 720 17

Quantative data on plasma levels of antidiuretic hormone (ADH) in renal failure are limited. We measured predialysis plasma ADH levels using a double antibody radioimmunoassay in 14 patients with end-stage renal failure. Plasma ADH was inappropriately elevated in the majority of tested patients despite normal plasma osmolality, moderately elevated blood pressure, and hypervolemia. The etiology of increased plasma ADH in our population is unclear.
J Dial 1980
PMID:Antidiuretic hormone in end-stage renal disease. 744 Aug 45

The basis for hyponatremia is a negative balance for sodium (Na+) plus potassium (K+) and/or a positive balance for water. In patients with normal renal function, vasopressin is needed to prevent the excretion of electrolyte-free water. Vasopressin is not important when there is little residual renal function. If hyponatremia is accompanied by a quantitatively appropriate gain in weight, this implies that a gain of electrolyte-free water was the basis for hyponatremia. In the absence of this weight gain, a loss of salts is to be suspected. If the extracellular fluid (ECF) volume is obviously low, hyponatremia is due to a deficit of NaCl, unless there is a deficit of K+. With a KCl deficit and a contracted ECF volume, there should also be a large shift of Na+ into cells, so metabolic alkalosis would not be an expected finding. In contrast, those patients with no change in weight who have a normal or expanded ECF volume are subdivided into those with a gain of solutes restricted to the ECF compartment (glucose, mannitol), or those with a deficit of solutes of intracellular fluid origin, which implies that a catabolic state (malnutrition) may be present.
Perit Dial Int
PMID:A physiological analysis of hyponatremia: implications for patients on peritoneal dialysis. 1128 Apr 99

Aquaporin (AQP) water channels are important in the function of the kidney. Constitutively expressed AQP1 in the proximal tubule and descending limb is important in normal fluid absorption and in the counter-current multiplication system. The vasopressin-regulated shuttling of AQP2 is essential in antidiuresis and the regulation of water balance. Genetic damage to AQPs, or pathological changes in expression or function, impair renal water handling. The most striking examples of this involve disruption of AQP2 function, which can result in profound nephrogenic diabetes insipidus. Aquaporin 1 is present in capillaries and venules and appears to be important in peritoneal dialysis, where it appears to represent the "ultrasmall pores" of the three-pore model. Decreased expression or function of AQP1 may be responsible for some cases of ultrafiltration failure, but further evidence will be required to establish whether this is the case.
Perit Dial Int
PMID:Aquaporins: roles in renal function and peritoneal dialysis. 1133 May 71

A 61-year-old man had hyponatremia (serum Na 112 mmol/L), which was associated with disturbance of consciousness. Therefore, administration of hypertonic saline was commenced. Eventually he was diagnosed with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Hypertonic saline was continued for 45 days, and plasma Na concentration rose to 138 mmol/L. At that time we were consulted regarding further administration of hypertonic saline. At the time of the consultation marked edema had developed affecting the whole body. The cardiothoracic ratio was increased and pleural effusion was evident on the chest X-ray. Administration of hypertonic saline was discontinued to prevent further worsening of the edema. Furthermore, water restriction (500 mL/day) was started. Body weight decreased by 4.3 kg in 7 days and the edema was diminished. However, plasma Na concentration decreased to 117 mmol/L. At that stage, we needed to balance the treatment of hyponatremia to the increased extracellular fluid volume (ECF). To normalize the ECF, we carried out ultrafiltration (UF) three times. Resolution of edema by using an extracorporeal UF method allowed the control of plasma Na concentration. In this case increased ECF volume hindered the adjustment of plasma Na concentration. The infusion of hypertonic saline is now used commonly by physicians. It is necessary to consider the potential risks of such treatment.
Ther Apher Dial 2007 Aug
PMID:A case report of syndrome of inappropriate secretion of antidiuretic hormone with marked edema due to administration of hypertonic saline. 1766 39


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