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)

Specific, homologous human neurophysin I and II radioimmunoassays were established and used to measure the individual, immunoreactive neurophysin concentrations in human plasma. Circulating levels of human neurophysin I in normal individuals were less than 1 ng/ml and neurophysin II levels were 1-2 ng/ml. During dehydration, there was a significant rise in plasma neurophysin I, together with an increase in neurophysin II. Haemorrhage also was associated with a rise in plasma neurophysin I and II, but the percent increase was greater for I than II. In two subjects in whom nicotine inhalation caused a rise in plasma neurophysin I, there was no detectable increase in plasma neurophysin II. These stimuli which have been reported to release vasopressin from the posterior pituitary also are associated with the differential release of neurophysin I. Plasma neurophysin II levels could more clearly be shown to rise independently of plasma neurophysin I during events thought to be related to oxytocin release. Plasma neurophysin II levels were significantly elevated in women taking oral contraceptives. Similarly during pregnancy there was a progressive rise in plasma neurophysin II concentration which was proportional to the period of gestation. Plasma neurophysin II concentrations in seven of fifteen nursing women rose significantly during suckling. There was no detectable change in plasma neurophysin I concentrations during any of these events. Plasma neurophysin I and II levels were both significantly elevated in fourteen patients with chronic renal failure and rose over haemodialysis, suggesting that the kidney may be the major route of clearance of the neurophysins. In humans the independent release of neurophysin II was associated with stimuli thought to release oxytocin, but neurophysin I showed only a differential release compared to neurophysin II in vasopressin stimulated events.
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PMID:Individual neurophysin concentrations in the pituitary and circulation of humans. 45 40

Plasma vasopressin (VP) was determined in 28 patients with chronic renal failure undergoing hemodialysis. Plasma VP levels were significantly higher in the patients than in the normal subjects. It was also observed that plasma VP levels did not fall significantly despite a marked decrease of effective plasma osmolality following hemodialysis, and that no correlation was obtained between the plasma VP levels and effective plasma osmolality, both before and after hemodialysis. By analyzing the changes in blood volume and blood pressure in addition to plasma osmolality in each case, a dysfunction of VP release in response to osmotic stimulus was found in 5 out of 28 patients.
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PMID:A study of plasma vasopressin in patients undergoing chronic hemodialysis. 91 76

U-Deamino-8-D-arginine-vasopressin (DDAVP) is a new synthetic antidiuretic hormone with prolonged action. 0.02 mg given intranasally to 38 patients with far advanced chronic renal failure effected an instantaneous decrease in urine volume as well as an augmentation of U/P-inulin ratio, fraction of filtered sodium and chloride excreted and of the absolute elimination of these ions. These findings suggest an improvement of permeability at the descending limb of Henle, too, the latter and a diminution of circulation in the renal medulla being responsible for the increase in renal salt loss after DDAVP. A rise of blood pressure or other side effects could not be observed.
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PMID:[Effect of 1-desamino-8-D-arginine-vasopressin in limited renal function]. 117 46

The original observation by de Bold et al. (1981) of a rapid, massive, and short-lasting diuretic and natriuretic effect following injection of rat atrial extracts into intact rats, led to the identification, isolation and purification of the atrial natriuretic factor (ANF). ANF is stored in atrial myocytes and released into the blood stream by atrial distension. Available data suggest that the mechanism of ANF-induced natriuresis involves either renal hemodynamic effects, such as the increase in glomerular filtration rate and reduction of medullary tonicity, or direct effect on sodium transport in the medullary collecting ducts. ANF induces relaxation of vascular smooth muscle, decreases blood pressure and cardiac output. All these effects displayed by ANF are associated to the an inhibition of aldosterone, renin and vasopressin release. Most of these actions are mediated by specific high affinity receptors, which are coupled to a particulate guanylate cyclase. Although ANF levels are increased in some disorders, such as severe heart failure, hypertension, chronic renal failure, the role of the peptide is uncertain. To better define the potential physiopathological role and the possible therapeutic implications of this new hormonal system in conditions of disturbed body fluid and sodium homeostasis, further experimental and clinical data must be awaited.
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PMID:[The physiopathological aspects of the atrial natriuretic factor]. 131 27

Diuretics have long been used to lower blood pressure in hypertensive patients or to control body fluid and electrolyte homeostasis in diseases such as congestive heart failure, chronic renal failure or cirrhosis. The initial response to diuretics is a negative sodium and fluid balance. The diuretic-induced loss of salt and water activates several hormonal systems such as vasopressin, the renin-angiotensin-aldosterone system or the sympathetic nervous system which tend to compensate for the changes in sodium and water balance. This neurohormonal response may have important clinical implications. Thus, the activation of the renin-angiotensin-aldosterone cascade appears to be partially responsible for the flat dose-blood pressure response curve of thiazides in hypertensive patients. It may also be responsible for the difference between responders and non-responders to diuretic therapy and for the development of side-effects such as hypokalaemia, metabolic alkalosis or hyponatraemia. There are several ways to prevent the undesirable consequences of the neurohormonal responses to diuretics. The first is to use low doses of these agents. It is also possible to combine them with agents that block the activity of the renin-angiotensin-aldosterone system such as ACE inhibitors or in combination with drugs that reduce aldosterone secretion such as calcium antagonists. The development of drugs able to enhance urinary sodium excretion and to reduce simultaneously the activity of the renin-angiotensin-aldosterone system may offer a new interesting alternative. This might perhaps be achieved in the future with the administration of neutral endopeptidase inhibitors which interfere with the enzymatic degradation of atrial natriuretic peptide.
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PMID:Neurohormonal consequences of diuretics in different cardiovascular syndromes. 136 43

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients. 145 6

The present study has aimed to answer the following questions: 1) to what extent does the profile of volume related hormones in patients with chronic renal failure (CRF) differ from that of healthy subjects, and 2) do volume related hormones influence the electrolyte composition of thermal sweat? Twelve hemodialyzed patients with CRF and 20 healthy subjects were examined before and after one hour exposition to humid heat. In all examined subjects the following parameters were assessed before and after thermal dehydration: plasma renin activity (PRA) and plasma aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations. In addition sodium, potassium, and chloride were estimated in thermal sweat collected after 15 and 45 minutes respectively of thermal exposition. Patients with CRF showed significantly higher values of PRA, Ald, AVP and ANP before thermal dehydration. After one hour of heat exposition a significant increase in PRA, Ald and AVP but a significant decrease of plasma ANP level were noticed in both healthy subjects and patients with CRF. The magnitude of plasma Ald and ANP alterations induced by thermal dehydration was significantly more marked in patients than in healthy subjects. A similar electrolyte composition of thermal sweat was found in both examined groups. No significant correlation was found between the plasma profile of volume related hormones and electrolyte composition of sweat both in patients and normals. Results presented in this paper suggest, that volume related hormones do not influence the electrolyte composition of thermal sweat both in healthy subjects and patients with CRF.
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PMID:[Influence of thermal dehydration on blood values of hormones which regulate volume and composition of electrolytes in sweat of patients with ic renal failure treated with hemodialysis]. 181 85

Neuroendocrine activity in normal subjects was compared to patients with chronic renal failure on maintenance hemodialysis (CRF-HD) and to cyclosporine-treated renal transplantation (RT) recipients in an effort to further define the mechanisms underlying their associated fluid, electrolyte, and hemodynamic abnormalities. To evaluate neuroendocrine function in CRF and RT patients, plasma levels of angiotensin II (A-II), vasopressin (AVP), atrial natriuretic peptide (ANP), neuropeptide Y, neuropeptide Y (NPY), epinephrine (E), and norepinephrine (NE) were measured before and after HD and RT. Plasma concentrations of A-II, AVP, ANP, and NPY were significantly elevated in patients with CRF. HD did not produce a significant change in plasma concentrations of AVP, ANP, NPY, E, or NE. NE plasma levels, but not E levels, increased pre- and post-HD. A-II plasma levels were elevated basally in CRF patients and significantly increased following HD. Following RT, plasma levels of A-II, AVP, NPY, and creatinine decreased significantly over the first week, but AVP and NPY did not normalize. Plasma levels of ANP were elevated during the first month, then decreased to normal levels in RT patients. NE levels, but not E levels, were elevated both pre- and post-RT. Despite antihypertensive treatment, the group mean arterial pressure increased post-RT from 100 +/- 4.4 to 116 +/- 3.7 mmHg by POD 6.
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PMID:Neuroendocrinology of chronic renal failure and renal transplantation. 183 95

Influence of blockade converting enzyme on plasma renin activity (PRA), aldosterone and vasopressin secretion in 12 hemodialyzed patients with chronic renal failure and in 21 healthy subjects was observed. Our observation were provided during bed rest and water immersion tests. We didn't observe statistically significant influence PRA (increase after converting enzyme blockade) on vasopressin secretion in patients with chronic renal failure and in healthy subjects. Correlation between PRA and vasopressin secretion was absent.
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PMID:[Renin-angiotensin-aldosterone system (RAA) and vasopressin secretion in patients with chronic renal failure]. 189 92

Water immersion (WI) induced alterations of plasma vasopressin (AVP), plasma osmolality, plasma volume (PV) and plasma sodium and potassium concentration were examined in 12 patients with noninflammatory acute renal failure (NARF) at the anuric/oliguric phase, 20 patients with chronic renal failure (CRF) and 15 healthy persons. In all examined groups a significant increase of PV and decrease of plasma osmolality and AVP after WI was observed. In patients with NARF the increase of PV was significantly greater than in CRF and in healthy persons. In patients with NARF a significantly greater decrease of plasma sodium concentration after WI was also noted than in patients with CRF and in healthy persons. Only in healthy persons, but not in patients with acute or chronic renal failure a significant correlation between PV or decrease of plasma osmolality and WI induced decrease of plasma AVP level was stated. We conclude that patients with NARF and CRF are characterized by an inappropriate volumetric and osmotic regulation of AVP secretion.
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PMID:Water immersion (WI) induced alterations of plasma vasopressin (AVP) levels in patients with noninflammatory acute renal failure (NARF) and in patients with chronic renal failure (CRF). 213 33


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