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)

This study examined the role of arginine vasopressin in the pressor response to vagal cold block and evaluated a possible interaction between vasopressin and the sympathetic nervous system during vagal block in conscious dogs with (carotid sinus intact) and without (sinoaortic denervated) functional arterial baroreflexes. In both carotid sinus intact and sinoaortic denervated dogs, elimination of the arginine vasopressin pressor system by the specific vasopressin antagonist d(CH2)5Tyr(Me)AVP did not alter the response to vagal block, as evaluated by changes in arterial pressure. Subsequent removal of the sympathetic nervous system by ganglionic blockade abolished the response to vagal block. When ganglionic blockade was induced in the absence of the vasopressin antagonist, the pressor response to vagal block was reduced by only 60%. Arginine vasopressin antagonist after ganglionic blockade reduced the response to vagal block by an amount equivalent to 45% of the original increase in pressure. The effects of blockade of either vasopressin or the sympathetic nervous system on the pressor response to vagal block were significantly greater when the other system had previously been eliminated. Data suggest that both arginine vasopressin and the sympathetic nervous system contribute to the pressor response to vagal block. One interpretation of these results is that vasopressin also interacts centrally to inhibit sympathetic outflow and thus modulates the hemodynamic manifestation of interruption of vagal afferents.
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PMID:The role of vasopressin and the sympathetic nervous system in the cardiovascular response to vagal cold block in the conscious dog. 614 58

These experiments were done to determine the effectiveness of oncotic and oncotic/diuretic ( oncodiuretic ) therapy in dogs with experimental cerebral edema induced by a cold lesion. Dogs were divided into 3 groups and were treated for 6 h with either crystalloid (control group), a 12% hetastarch solution, or a 24% hetastarch solution plus furosemide. The cerebral effects of treatment were evaluated by intracranial pressure (ICP) measurements and by autopsy measurements of brain density and brain water content. The systemic effects were evaluated by measuring fluid balance, wedge pressure, hematocrit, free-water clearance, and serum vasopressin level. Hetastarch and hetastarch /furosemide significantly reduced ICP, increased brain density, and decreased water content of the edematous brain. Hetastarch alone caused a positive fluid balance and marked hemodilution but did not normalize vasopressin levels, whereas hetastarch /furosemide caused a marked diuresis without changing the hematocrits, and normalized vasopressin levels. Oncodiuretic therapy, in contrast to traditional fluid restriction, seems to decrease ICP effectively by causing normovolemic dehydration.
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PMID:Intracranial and systemic effects of hetastarch in experimental cerebral edema. 620 63

When rat posterior pituitary glands were stimulated by a high concentration of potassium, a peak of cyclic AMP and a peak of cyclic GMP were detected after 0.5 min and 1 min, respectively, whereas the rate of release of vasopressin was maximal only after 2 min. When calcium was omitted from the medium, no significant changes in cyclic nucleotide levels were found and the vasopressin release remained at the basal rate. During cold-stimulated (10 degrees C) release of vasopressin, a peak of cyclic AMP was detected after 5 min simultaneously with the maximal rate of vasopressin release. The significance of the cyclic nucleotides in the release of vasopressin is discussed.
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PMID:Cyclic nucleotides and the release of vasopressin from the rat posterior pituitary gland. 628 27

LLC-PK1 is an established porcine renal cell line with epithelial characteristics. Upon hormonal stimulation by vasopressin, LLC-PK1 cells release adenosine 3',5'-cyclic monophosphate (cAMP) into the medium. Release of cAMP is inhibited by the organic anion transport inhibitor probenecid and by cold phosphodiesterase inhibitors and iodoacetate but not by prostaglandins A1 or E1. The kinetics of release are first order, and cAMP analogues do not induce the release of cAMP. When grown on cellulose filters, monolayers of LLC-PK1 have morphological characteristics of transporting epithelia (apical microvilli and intercellular tight junctions) and maintain a transepithelial potential difference. Stimulation of such monolayers by vasopressin elicits probenecid-sensitive release of cAMP into the medium bathing the apical surface. Smaller quantities of cAMP are released from the basolateral surface, but release in this direction is not inhibited by probenecid. In contrast, release of cAMP from the nonepithelial cell line BHK is symmetrical and is symmetrically inhibited by probenecid. Probenecid-sensitive release of cAMP from LLC-PK1 is thus a function of the apical (brush-border) membrane.
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PMID:Release of cAMP from a renal epithelial cell line. 632 92

Activation energies (Ea) for water movement across vasopressin-(ADH) sensitive epithelia have been reported to be about 10 kcal/mol (1, 12). The present study shows that measurements of Ea for osmotic water flow across toad bladders are unreliable, because a temperature change induces marked alterations in membrane permeability to water within a 2.5-min interval. Thus bladders equilibrated with ADH either at room temperature or at 33 degrees C and then suddenly subjected to a lower temperature were found to exhibit a marked increase in membrane permeability to water. This observation suggests that there is a rapid turn-over of water permeability sites and that sudden exposure to cold inhibits the removal more than the induction of sites by ADH. To stabilize ADH-induced water channels for Ea measurements, bladders were exposed to ADH at room temperature, fixed with glutaraldehyde, and subjected to osmotic gradients at different temperatures. The Ea values for osmotic water flow across these ADH-permeabilized, glutaraldehyde-fixed bladders were 5.1 (4-12 degrees C), 4.3 (12-21 degrees C), 3.6 (21-36 degrees C), and 3.6 kcal/mol (30-38 degrees C). Ea values for shear viscosity of water in these temperature ranges were calculated to be 4.7, 4.2, 4.1, and 3.6 kcal/mol, respectively. The close correlation between Ea values for bulk water viscosity and osmotic water flow across the bladder wall suggests that an equivalent number of hydrogen bonds must be broken to achieve an increase in water flow through ADH-induced channels and an increase in fluidity of water in bulk solution.
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PMID:Activation energy for water transport in toad bladder. 640 2

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.
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PMID:Mechanism of cold diuresis in the rat. 640 36

Specific binding sites for vasopressin (AVP) were located in subcellular particulate fractions of rat brain with tritiated vasopressin of high specific activity, 22.5 Ci/mmol. Rat brain tissue was dissected, placed in cold 0.32 M sucrose containing proteolytic inhibitors, homogenized and fractionated into a crude nuclear fraction (1K pellet), crude mitochondrial fractions (12K pellet), and plasma membranes and microsomes (100K pellet). Specific binding of vasopressin was found in the 12K and 100K pellets in the presence of a divalent metal ion with Ni greater than Co greater than Mg greater than Mn greater than no metal ion at pH 7.4 in 50 mM Tris-Maleate buffer. Maximum specific binding of 16 nM AVP was located in the 100K anterior cortex fraction which bound 350 fmoles/mg protein; striatum, midbrain/thalamus, cerebellum, and medulla oblongata and pons bound specifically about 200 fmoles/mg protein and frontal poles and parietal cortex about 100 fmoles/mg protein in the 100K pellet. In all of the brain regions studied, except hippocampus and septum, the 100K pellet bound specifically 2 to 4 times more 3H-AVP than the 12K pellet. In the hippocampus with 16 nM AVP, the 12K pellet bound specifically 150 fmoles/mg protein; the septum, 75 fmoles/mg protein. Little or no binding to the 100K pellet was present in these regions. Bound AVP could be dissociated rapidly from the membranes by the addition of EDTA. The 12K hippocampal pellet was further fractionated into myelin, mitochondria, and synaptosomes; purification was confirmed by marker enzyme assays.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of 3H-AVP binding sites in particulate preparations of rat brain. 641 23

Experiments were carried out to compare the effectiveness of oncotic and osmotic therapy in dogs with experimental cerebral edema caused by a left parietal cold lesion. Animals were divided into five groups and treated for 6 hours with either crystalloid (control group), or mannitol, albumin, furosemide, or albumin/furosemide (treatment groups). The cerebral effects of therapy were evaluated by intracranial pressure (ICP) measurements and by postmortem evaluations of water content, using computerized tomography (CT) density measurements and wet-dry weight measurements. The ICP was significantly reduced by all treatments except albumin alone, and was reduced equally by mannitol, furosemide, and albumin/furosemide. The CT density of the lesion area was significantly increased by all treatments. The density of the contralateral nonlesioned hemisphere was significantly increased by all treatments except albumin. The water content of the lesion area was significantly decreased by all treatments; water content of the opposite hemisphere was not significantly reduced. The systemic effects of therapy were evaluated by measuring net fluid balance, wedge pressures, hematocrits, free water clearance, and vasopressin. Negative fluid balance without an increase in hematocrit or in vasopressin secretion occurred only in dogs treated with albumin/furosemide. Such oncodiuretic therapy seems to cause normovolemic dehydration and to have cerebral effects similar to mannitol and furosemide, without their undesirable systemic effects.
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PMID:Intracranial and systemic effects of osmotic and oncotic therapy in experimental cerebral edema. 642 10

A sensitive and specific radioimmunoassay (RIA) for arginine vasopressin (AVP) has been developed and validated. Synthetic AVP was coupled to bovine serum albumin (BSA) with glutaraldehyde. Antisera against AVP were raised in three rabbits immunized with AVP-BSA complex. After 6 months, at the 16th injection, one of the antisera had a titer high enough to be utilizable for RIA at a final dilution of 1:400,000. The labeling of AVP with 125I Na was performed with the modified chloramine T method, and the purification of iodinated AVP was done with gel filtration chromatography on a Sephadex G-25 fine column (1 X 20 cm) with an elution buffer of 0.01 M acetic acid containing 0.1% BSA. Radioactivities from the Sephadex G-25 were eluted in three peaks. 125I-AVP, which was reactive to the antiserum, was contained in the third peak, and 125I-AVP in the fractions on the down slope of the peak was used for the radioligand in the amount of 1000 cpm. The specific activity of purified 125I-AVP was about 400 muCi/microgram. Diluted antiserum and samples, unlabeled AVP or related peptides were preincubated at 4 degrees C for 24 hr, and then 125I-AVP was added to the mixture and incubated for a further 72 hr. Separation of B and F was done with polyethyleneglycol. The minimal detection limit of AVP, which was 95% of the confidence limit of the mean value of B0, was 0.4 pg/tube. The cross-reactivities with lysine vasopressin, arginine vasotocin, DDAVP and oxytocin were 0.1%, 30%, 1% and 0%, respectively. AVP in plasma was extracted with cold acetone and petroleum ether. The recoveries of synthetic AVP from plasma which was added (2-16 pg) were more than 94%. The intra and inter-assay coefficients of variation determined by plasma of AVP concentration of about 4.8 pg/ml were 8.7% and 11.3%, respectively. The RIA detected AVP of concentration as low as 1 pg/ml following the extraction procedure. AVP immunoreactivity was detected without extraction in urine, and the lyophilized cerebrospinal fluid and acid extract of tissues of the central nervous system, and the reactivities in these samples were demonstrated to be immunologically identical to that of synthetic AVP when diluted serially. The changes of plasma and urinary AVP concentration on water intake, water deprivation and smoking in humans were clearly demonstrated.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A sensitive and specific radioimmunoassay for arginine vasopressin and its validation]. 647 76

Immersing the patient's face in cold water to induce the "diving reflex" is a quick and simple method of treating paroxysmal supraventricular tachycardia. Patients can be trained to perform the "diving reflex" at home. There are many advantages to this method of treatment when compared to many of the other therapies. Polyuria up to 3 L is often noted during the first 90 minutes of a paroxysmal tachycardia. The diuresis is thought to be due to atrial distention with resultant inhibition of antidiuretic hormone secretion.
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PMID:Use of the "diving reflex" in paroxysmal atrial tachycardia. 655 52


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