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)

1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min(-1) kg(-1) for 1 hr into normal, sham-operated and DOCA-salt hypertensive rats. Complete vasopressin/blood pressure dose-response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion. 2. DOCA-salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 +/- SD 3.7 fmol/ml) than either the normal (3.9 +/- 2.3, P less than 0.01) or the sham-operated rats (4.5 +/- 2.4, P less than 0.01). 3. The DOCA-salt hypertensive rats did not have my detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups. 4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min(-1) kg(1), when the plasma concentration was between 30 and 40 fmol/ml. 5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22-23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA- salt hypertensive rats (10.5 +/- 2.3, 14.5 +/- 4.5 and 8.0 +/- 1.6 fmol/ml respectively). 6. These findings suggest that the mechanism of vasopressin involvement in DOCA-salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA-salt hypertension may contribute to the suppression of renin and angiotensin II in this state.
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PMID:Effect of acute vasopressin infusion on blood pressure and plasma angiotensin II in normotensive and DOCA-salt hypertensive rats. 705 14

Arginine vasopressin was measured in the blood and cerebrospinal fluid (CSF) of 42 patients with subarachnoid haemorrhage. Increased concentrations of vasopressin were present in 10 patients, of whom eight had bled from an anterior communicating artery aneurysm. In three patients high blood vasopressin values were associated with gross hyponatraemia. Five patients were found to have increased CSF vasopressin concentrations in the presence of normal plasma values and in all of these the level of consciousness was severely disturbed. It is suggested that an increased secretion of vasopressin into the blood or CSF may be a contributory factor in the worsening condition of some patients with subarachnoid haemorrhage.
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PMID:Vasopressin in plasma and CSF of patients with subarachnoid haemorrhage. 722 44

Single rat neurohypophyses were impaled on a platinum electrode, perifused with isotonic medium and fractions of perifusate collected each minute. Arginine vasopressin content of the fractions was measured by radioimmunoassay. The basal release of arginine vasopressin varied from 50 to 350 pg (0.02-0.14 mU/min) between individual neurohypophyses. Recordings previously obtained from rat supraoptic neurones provided the patterns for electrical stimulation. 8-min segments of a phasically and a continuously firing neurone were selected such that each was firing at a mean rate of 6 spikes/s and possessed very similar overall distributions of interspike intervals. In 15 experiments individual neurohypophyses were stimulated with the phasic pattern, followed by the continuous pattern, or vice versa, separated by an 8-min unstimulated period. In either case, significantly more hormone was released during phasic stimulation than during continuous stimulation. It is concluded that the phasic firing pattern typical of vasopressin neurones is highly efficient for the release of vasopressin from the neurohypophysis, but that its effectiveness does not lie in an increased preponderance of short interspike intervals.
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PMID:Relative efficiency of neural firing patterns for vasopressin release in vitro. 730 Oct 50

Arginine vasopressin (AVP) and oxytocin (OXT) were measured simultaneously in the same sample by specific and sensitive radioimmunoassay (RIAs). The antibodies used did not cross-react to a variety of analogues and related peptides. The extraction procedure using Vycor glass powder resulted in mean recoveries of 84.4% (AVP) and 64.6% (OXT). In both assays, the sensitivity was 1 to 2 pg/ml plasma. A preincubation procedure that depresses plasma levels of both AVP and OXT selectively, provided specific blank values for a given plasma sample. To confirm the validity of the RIAs, dehydration experiments were performed. In rats, the basal levels of plasma AVP and OXT (means: 2.63 pg/ml and 6.80 pg/ml, respectively) are increased significantly after 24 h, 48 h and 72 h of water deprivation. Relationships are presented between both neurohormones in the plasma and neurohypophyses of control and dehydrated animals. As shown in cows, a significant correlation exists between plasma AVP and plasma osmolality but not between plasma OXT and osmolality or plasma AVP and OXT. The conclusion is drawn that basal levels as well as physiological changes in plasma and neurohypophyseal AVP and OXT can be measured by the RIAs described.
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PMID:Simultaneous measurement of arginine vasopressin and oxytocin in plasma and neurohypophyses by radioimmunoassay. 733 24

Arginine vasopressin was measured by RIA in samples of plasma and cerebrospinal fluid (CSF) taken synchronously from 62 patients with proven or suspected disorders of the central nervous system in order to determine the relationship between the secretion of vasopressin into the systemic circulation and that into the CSF. In 12 patients without endocrine or brain disease, mean plasma values (+/- SD) were 2.8 +/- 0.7 pg/ml and CSF values were 2.4 +/- 0.7 pg/ml. Thirty-six patients with various intracranial disorders had plasma and CSF values which were both within the range of 1-4 pg/ml. Eight patients had raised plasma concentrations, but their CSF levels were within the normal range. One patient with posttraumatic diabetes insipidus and 2 patients with subarachnoid hemorrhage had concentrations of CSF vasopressin which were greater than plasma levels. These results indicate that a blood CSF barrier to vasopressin exists in man and that under certain pathological conditions excessive amounts of the hormone can be secreted into the CSF independently of that which is released into the blood, a finding which could have clinical significance in disorders of brain function.
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PMID:Vasopressin in human cerebrospinal fluid. 735 20

Arginine vasopressin (AVP) stimulates renal prostaglandin (PG) production which is thought to inhibit vasopressins' antidiuretic action. Using rat renal medullary cells in culture (RMIC), we compared the ability of the following peptides which possess different biological activities to stimulate prostaglandin biosynthesis: AVP (high antidiuretic and pressor activities); 1-desamino-8-D-arginine vasopressin (a synthetic peptide with high antidiuretic and no pressor activity); and oxytocin (intermediate pressor, low antidiuretic activity). Radiometric thin-layer chromatography of supernatant media from cells incubated with octatritiated or [14C]arachidonic acid revealed only one radiolabeled peak which co-migrated with PGE2. Radioimmunoassay confirmed that PGE2 was the only prostaglandin synthesized by RMIC. Incubation of cells with AVP (1 nM to 3 microM) increased PGE2 synthesis measured by radioimmunoassay in a concentration-dependent fashion up to 2 1/2-fold over control; 1-desamino-8-D-arginine did not increase PGE2 synthesis. Oxytocin stimulated PGE2 synthesis, but was less potent than AVP. Preincubation of RMIC with [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid)-4-valine, 8-D-arginine]vasopressin, a synthetic nonpressor, nonantidiuretic antagonists of AVP's pressor activity, completely blocked the ability of AVP to stimulate PGE2 synthesis. We conclude that the ability of AVP to stimulate PGE2 synthesis in RMIC is related to its pressor, not its antidiuretic, activity.
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PMID:The effect of arginine vasopressin and its analogs on the synthesis of prostaglandin E2 by rat renal medullary interstitial cells in culture. 745 79

Arginine vasopressin (AVP) is a nonapeptide that regulates body fluid and blood pressure homeostasis. We have used expression cloning in the Xenopus laevis oocyte system to identify cDNA clones from a rabbit renal medullary expression library encoding an AVP receptor linked to Ca2+ mobilization. cRNA generated from positive clones conferred upon oocytes the capacity to mobilize intracellular Ca2+ in response to AVP. A cDNA clone encoding a protein of 780 amino acids was isolated, sequenced, and subcloned into an SV40-based expression vector. Expression of the cloned protein [designated the vasopressin-activated, calcium-mobilizing (VACM-1) protein] in COS-1 cells, resulted in increased 125I-labeled AVP binding [dissociation constant (Kd) of approximately 2 nM] and increased AVP-induced mobilization of Ca2+. Importantly, 125I-AVP could be immunoprecipitated both from detergent-solubilized membranes from COS-1 cells expressing VACM-1 protein and from an in vitro translation system, in which VACM-1 protein was synthesized, using antibodies prepared against a synthetic peptide derived from the NH2-terminal sequence of VACM-1. Interestingly, immunohistochemical staining of rabbit kidney sections with this antibody showed specific staining of collecting tubule epithelia. The deduced amino acid sequence is not homologous with any nucleic acid or amino acid sequences reported to date, including those of the V1 and V2 AVP receptors. The VACM-1 protein may represent a novel AVP receptor.
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PMID:Expression cloning of an AVP-activated, calcium-mobilizing receptor from rabbit kidney medulla. 761 60

Arginine vasopressin (AVP) modulates the secretion of ACTH through vasopressin receptor subtype V1b in the pituitary. We recently cloned human V1b, but several inconsistencies were found between the characteristics of this cloned receptor and those of rat pituitary membrane shown by previous workers. To clarify this issue, we report here the molecular cloning and functional expression of the cDNA encoding V1b in rat pituitary. This receptor encodes 425 amino acid protein having the highest identity with the human V1b (81%). Expression of this receptor in COS-1 cells showed pharmacological characteristics of V1b consistent with those of rat pituitary membrane. Northern blot and RT-PCR analyses revealed that mRNA of this receptor was expressed not only in anterior pituitary, but also in other tissues. This finding raises the possibility that V1b may play a role in regulating cell functions of these tissues.
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PMID:Molecular cloning and characterization of rat V1b vasopressin receptor: evidence for its expression in extra-pituitary tissues. 762 8

The area postrema (AP) is a circumventricular organ located on the dorsal surface of the medulla. Substantial evidence suggests that the AP is an important site involved in cardiovascular regulation. Arginine vasopressin (AVP) is thought to act at the AP to increase the sensitivity of the baroreceptor reflex. We have therefore examined the effects of AVP on AP neurons with the use of extracellular single unit recordings in vitro. Coronal medullary brain slices (thickness = 400 microns) were obtained from male Sprague-Dawley rats and maintained in oxygenated artificial cerebrospinal fluid (aCSF). The slices were perfused with AVP (10(-8) to 10(-6) M), and the effect on single AP neurons was recorded. A total of 79 AP neurons was tested of which 50 (63.3%) were excited by AVP and 5 (6.3%) were inhibited, whereas the remaining 24 (30.3%) cells were unaffected. The excitatory effects of AVP were dose dependent: firing rate increased 92.6 +/- 25.8% at 10(-8) M, 289.4 +/- 53.9% at 10(-7) M, and 456.8 +/- 113.1% at 10(-6) M, respectively. We also examined whether these effects of AVP resulted from direct actions of this peptide on AP cells by testing if responses were retained during blockade of synaptic transmission (achieved by perfusion with a low Ca(2+)-high Mg2+ aCSF) in 11 cells excited by AVP. Nine of these cells were excited by AVP during such synaptic blockade. Finally, we demonstrated that the excitatory responses of five AP cells to AVP were all totally abolished by perfusion of slices with aCSF containing the V1 antagonist ([1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid,2-(O-methyl)tyrosine]-Arg8-vasopressin; Peninsula Laboratories, 10(-6) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin actions on area postrema neurons in vitro. 765 71

Antisense oligodeoxynucleotides (AS-ODN) to AT1 receptor mRNA inhibit high blood pressure in Spontaneously Hypertensive Rats (SHR) when injected into the brain. The effect is presumably through inhibition of the actions of brain angiotensin II (Ang II). Central injection of Ang II elicits several physiological responses including release of vasopressin and motivation to drink. The angiotensin II type-I (AT1) receptor is located in brain regions which have been implicated in mediating these effects. Therefore we hypothesized that AS-ODN to AT1 mRNA would inhibit the drinking and AVP response to central administration of Ang II in adult male SHR. AS-ODN were constructed to bases +63 to +77 (15-mer) of the AT1 receptor RNA. 24 h after AS-ODN treatment (50 micrograms/4 microliters) (intracerebroventricularly, i.c.v.), the drinking response to Ang II (50 ng, i.c.v.) was significantly reduced in the SHR (P < 0.05). The drinking response to Ang II (i.c.v.) was also reduced in the Sprague-Dawley rats (P < 0.05). There was no reduction of water intake in the control animals treated with scrambled ODN (SC-ODN). Repeated injection of AS-ODN did not produce a greater reduction in drinking response. Arginine vasopressin (AVP) release to central Ang II was significantly decreased after AS-ODN treatment when compared to vehicle (P < 0.05) and to SC-ODN injections (P < 0.05). Radioligand binding assays of the hypothalamic block after AS-ODN treatment showed a significant decrease of AT1 receptor binding (P < 0.05). The results show that the antisense inhibition of brain AT1 receptor gene expression decreases the Ang II induced drinking and AVP release responses.
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PMID:Antisense oligonucleotide to AT1 receptor mRNA inhibits central angiotensin induced thirst and vasopressin. 771 85


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