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)

Microalbuminuria is known to increase in various diseases with potential repercussion on the kidneys and indicates an increase in glomerular intracapillary pressure or changes in permeability characteristics. In this study, we measured whether albumin excretion is affected in patients undergoing anesthesia and surgery, which are both known to induce dramatic changes in renal function and in the release of vasoactive substances such as catecholamines, vasopressin, angiotensin, and prostaglandins. Seven patients with normal renal function and physiological microalbuminuria prior to surgery were studied. Urine samples were collected before anesthesia, just before the beginning of surgery, and thereafter 30 min following incision, and 30 min after the end of surgery. Anesthesia induced a significant increase in microalbuminuria, which further increased during surgery. After the end of surgical procedure, microalbuminuria decreased but remained significantly higher than control. This phenomenon may be due to an increase in intracapillary glomerular pressure and/or an alteration in glomerular permeability induced by a direct effect of drugs, or to the action of vasoactive substances on the glomerular structure.
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PMID:Microalbuminuria is acutely increased during anesthesia and surgery. 186 71

The influence of the oxidizing agents (H2O2, KO2 and Vitamin K) on the action of vasopressin to guinea pig hepatocytes was investigated from the view-point of cytoplasmic Ca2+ concentration and protein secretion. 10 nmol/l vasopressin brought about increase in prothrombin secretion along with increase in the cytoplasmic Ca2+ concentration compared to the non-stimulation level. The pretreatment of the cells with 1 mumol/l of the oxidizing agents, however, led to suppression of Ca2+ elevation and inhibited the vasopressin-induced prothrombin secretion completely, while no leak if lactic dehydrogenase (LDH), Na+ and K+ were detected. The same results of the inhibition in fibrinogen and albumin secretion were observed. These results suggested a possibility that the oxidizing agents such as the peroxides act on some site of cellular signal transduction system in cell membrane to reduce the cytoplasmic Ca2+ level and to suppress the vasopressin-induced secretion.
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PMID:Suppression of cytoplasmic Ca2+ response and protein secretion by oxidizing agents. 196 29

Plasma concentrations of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP) and plasma renin activity (PRA) were measured in 15 patients with decompensated cirrhosis of the liver during a control period and subsequently during intravenous administration of albumin. Infusion of hyperoncotic albumin increased diuresis, natriuresis, stimulated ANP secretion and tended to normalize other vasoactive hormone levels in 9 patients (responders), whereas it had no effect in 6 other patients (non-responders). Responders had significantly lower basal levels of ANP and higher ones of PRA, and AVP than non-responders, suggesting that responders had decreased effective intravascular volume. Our data suggest that cirrhotic patients with ascites formation do not represent a homogenous group. In some patients with decompensated cirrhosis a compromised circulatory state with decreased effective circulatory volume induces compensatory changes in several regulatory hormones. It appears that secondary alterations in the plasma concentrations of ANP of cirrhotic patients may occur according to the suspected change of intravascular fluid volume.
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PMID:Atrial natriuretic peptide in patients with decompensated hepatic cirrhosis. 214 34

Studies in vitro have shown that L-histidine increases the hydroosmotic response to vasopressin. We examined whether this phenomenon occurs also in vivo. Homozygous Brattleboro rats (di/di) were fed a regular diet (0.5% histidine) or a diet enriched with histidine and received 1 ng of 1-deamino-8-D-arginine vasopressin (dDAVP) daily. Addition of histidine (1% by weight) increased post-dDAVP urine osmolality to a level higher than that of control (502 +/- 62 vs. 316 +/- 36 mosmol/kg, P less than 0.05). Similar results were seen with 3.0% and 5.5% dietary histidine. There were significant increases in free-water reabsorption and in the ratio of free-water reabsorption to osmolar clearance, but no difference in osmolal clearance. No significant effect was found with supplemental histidine of 0.5% or less. The cause for these findings appears not to be the metabolism of histidine, since the nonmetabolizable D-histidine had a significant, albeit smaller, effect, and the isonitrogenous addition of albumin, alanine, arginine, or glutamine was ineffective. In part, histidine may operate by increasing cAMP since the renal cAMP content in response to vasopressin is increased in histidine-fed rats (13.1 +/- 0.9 vs. 9.8 +/- 0.8 nmol/g dry weight, P less than 0.01). The role of prostaglandins appears less clear. Histidine greatly decreased urinary PGE2 during baseline (1.5 +/- 0.3 vs. 7.0 +/- 2.3 micrograms/mg creatinine, P less than 0.001), but it profoundly augmented urinary prostaglandin excretion after dDAVP stimulation (40.0 +/- 4.2 vs. 7.0 +/- 2.0 micrograms/mg creatinine, P less than 0.001).
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PMID:L-histidine augments the response to 1-deamino-8-D-arginine vasopressin in Brattleboro homozygous (di/di) rats. 215 31

This study has been done to evaluate serum calcium, phosphorus (P), magnesium, parathyroid hormone (PTH), calcitonin (CT), and cyclic adenosine monophosphate (cAMP) in recently diagnosed pulmonary tuberculous patient, (n = 61) and the results were compared with the healthy control group (n = 22). Twenty four hours urine was collected for estimation of these electrolytes as well as cAMP. Nephrogenous cAMP (NcAMP) was calculated. Serum Ca and PTH were significantly reduced in TB groups, but CT was elevated. Serum Mg, P and cAMP as well as urinary Ca and Mg in TB groups were similar to that of the control group. Urinary P, cAMP NcAMP were increased in patient groups compared with the control. The reduced serum Ca could be due to impaired intestinal absorption of Ca, or deficient intake as a result of anorexia, decreased plasma albumin, decreased active metabolites of vitamin D or elevated CT. The rise in serum CT in TB might be due to increased CT secreted from the bronchial K-cells. Increased NcAMP might be due to the associated increase in serum antidiuretic hormone (ADH). The elevated urinary P in TB could be attributed to tissue breakdown, decreased serum PTH or increased CT.
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PMID:Calcium homeostasis in untreated pulmonary tuberculosis. I--Basic study. 216 2

Refractory ascites (or diuretic-resistant ascites), i.e. ascites that cannot be mobilized by medical treatment (low sodium diet and high doses of furosemide and spironolactone) is an infrequent phenomenon in cirrhosis. It usually occurs in patients with functional renal failure as a consequence of alteration in both pharmacokinetics and pharmacodynamics of diuretics. Peritoneovenous shunting, a procedure which improves systemic hemodynamics and renal function and suppresses the plasma levels of renin, aldosterone, norepinephrine and antidiuretic hormone in cirrhotics with ascites, has been proposed as the treatment of choice in patients with refractory ascites. Unfortunately it is associated to a high rate of severe complications and does not prolong the survival of these patients. Moreover, in approximately one third of the patients the shunt becomes occluded within the first year after operation. Recent studies have shown that repeated large volume paracentesis (4-64 per day until disappearance of ascites) or total paracentesis (complete mobilization of ascites in only one paracentesis session) associated to i.v. albumin infusion are an effective and safe therapy of ascites. At present, there is only one controlled trial comparing therapeutic paracentesis versus peritoneo-venous shunt in the management of patients with refractory ascites. In this study, there were no significant difference between both therapeutic groups with respect to survival. However, the incidence of readmission to hospital for the treatment of ascites was higher in the paracentesis group. Therefore, both procedures are valid therapeutic alternatives for that type of patients. Future studies are necessary to investigate if there are subsets of cirrhotics with refractory ascites in which one of these two types of treatment is especially indicated.
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PMID:Diuretic-resistant ascites in cirrhosis. Mechanism and treatment. 226 4

The mechanisms that regulate collagen gene expression in hepatic cells are poorly understood. Accelerated Ca2+ fluxes are associated with inhibiting collagen synthesis selectively in human fibroblasts (Flaherty, M., and Chojkier, M. (1986) J. Biol. Chem. 261, 12060-12065). In suspension cultures of isolated hepatocytes, the Ca2+ agonist vasopressin increases cytosolic levels of free Ca2+ (Thomas, A.P., Marks, J.S., Coll, K.E., and Williamson, J. R. (1983) J. Biol. Chem. 258, 5716-5725). However, whether vasopressin's interactions with plasma membrane V1 receptors attenuate hepatic collagen production is unknown. We investigated this problem by studying vasopressin's effects on collagen synthesis and Ca2+ efflux in long-term primary cultures of differentiated and proliferation-competent adult rat hepatocytes. Twelve-day-old quiescent cultures were exposed to test substances and labeled with [5-3H]proline. Determinations of radioactivity in collagenase-sensitive and collagenase-resistant proteins were used to calculate the relative levels of collagen production. Synthetic [8-arg]vasopressin stimulated 45Ca2+ efflux within 1 min and inhibited hepatocyte collagen production within 3 h by 50%; overall rates of protein synthesis were not affected significantly. In cultures labeled with [35S]methionine, vasopressin also decreased the levels of newly synthesized and secreted albumin, but not fibrinogen, detected in specific immunoprecipitates analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Northern blot analyses using specific [32P]cDNA probes revealed 70% decreases in hybridizable levels of collagen alpha 1(I) mRNA in hepatocyte cultures treated with either vasopressin or Ca2+ ionophore A23187; hybridizable levels of albumin mRNA also fell approximately 50% following vasopressin treatment. Vasopressin did not affect collagen production in quiescent cultures of mouse Swiss 3T3, human myofibroblast or rat smooth muscle cells; and hepatocyte collagen production was unaffected by treatment with glucagon or dibutyryl cAMP. Thus, accelerated Ca2+ fluxes induced by vasopressin are associated with decreased production of hepatocyte collagen and albumin in primary cultures that simulate quiescent adult rat liver.
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PMID:Vasopressin inhibits type-I collagen and albumin gene expression in primary cultures of adult rat hepatocytes. 254 14

The role of intra- and extrarenal factors in oedema formation in children with nephrotic syndrome is reviewed. Oedema reflects an abnormal accumulation of fluid within the interstitial tissue. At the capillary level oedema develops when increased lymph flow is no longer effective for the removal of interstitial fluid and the maintenance of intravascular volume. Alterations of intrarenal haemodynamics and tubular sodium reabsorption contribute to sodium retention. Recent studies suggest that during oedema formation reduced effective circulatory volume triggers changes in various hormonal systems, such as renin-angiotensin-aldosterone, noradrenaline, dopamine, vasopressin, prostaglandins and natriuretic factors, which contribute to sodium and water retention. It appears that the release of atrial natriuretic peptide following central volume expansion is responsible for the increased urine flow and natriuresis after intravenous administration of albumin.
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PMID:Intra- and extrarenal factors of oedema formation in the nephrotic syndrome. 270 97

The contiguous three lobe of the pituitary gland have different endocrine functions and vascular bed. This study was designed to investigate the effects of dehydration, which stimulates the secretion of vasopressin, on the pituitary microcirculation. Male Sprague-Dawley rats, weighing 300-380 g, were divided into two groups. Twenty three rats were allowed free access to food and water, and 24 rats had free access to food but were deprived of water for 5 days. Capillary solute transfer (K), plasma volume (Vp) and erythrocyte volume (Ve) in each pituitary lobe were determined for both control and dehydrated rats. Quantitative autoradiographic techniques were used to measure the K with 14C-alpha-aminoisobutyric acid (AIB, a small neutral amino acid), the Vp with 125I-albumin and the Ve with 51Cr-erythrocytes. Body weight was lower (-23%) and the arterial hematocrit was higher (+22%) in the dehydrated rats. In the lobes of the control pituitary gland, the order of K from the highest to the lowest was posterior much greater than anterior greater than intermediate lobe. K was increased by several folds only in the posterior lobe in dehydrated rats (p less than 0.05). Even under normal hydrated conditions, K for AIB in the posterior lobe was several hundreds times greater than in cerebral gray matter structures. The rank of Vp and Ve in each lobe of normal animals was about the same order and anterior greater than posterior much greater than intermediate. Normal microvascular Vp in the anterior and posterior lobes was 5-10 times larger than in cerebral gray matter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of dehydration of the pituitary microcirculation in rats]. 280 38

The mechanisms underlying the vascular responses of superficial fibular nerve stimulation (SFNS) have not been defined. Right hindpaws of anesthetized heparinized dogs were vascularly and neurally isolated, enclosed in a volume recorder, and perfused with controlled pressure. Vascular volume (VV) (131I-labeled albumin) and rate of tissue volume changes (VT) (plethysmography) were determined. SFNS increased blood flow resistance, reduced capillary filtration coefficient (CFC) and permeability-surface area product (PS) of 86Rb, increased VV, and reduced 131I-albumin recovery. VT increased at the rate of 3.35 +/- 0.45 ml/min. SFNS during terbutaline increased resistance, CFC, PS, and VV were unchanged, 131I-albumin recovery was complete, and VT increased at one-fourth the control rate. Phentolamine and yohimbine blocked all responses to SFNS. Prazosin with SFNS attenuated hemodynamic changes and VT increased to two-thirds of control, decreased VV, albumin, and Rb recovery but not PS and CFC. SFNS during pyrilamine maleate reduced VT increase to two-thirds of control rate and blocked decreases in PS and CFC. Metiamide did not change the SFNS responses, except to reduce vascular volume and VT. The combined histamine H1 and H2 blockers reduced VT increase to one-third of control and attenuated albumin loss, prevented histamine dilation, attenuated vasopressin and norepinephrine but not angiotensin constriction. SFNS stimulation increased precapillary resistance by alpha 1- and alpha 2-receptors and venous resistance by alpha 2-receptors and increased permeability by histamine release from endothelium.
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PMID:Adrenergic and histaminergic neural interactions in dog paws. 290 Dec 31


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