Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VASOPRESSIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1988

Neonatal vasopressin antagonist treatment facilitates adult copulatory behavior in female rats and increases hypothalamic vasopressin content.

This study confirms that i.c.v. administration of Arg-vasopressin (AVP, 20 ng) inhibits copulatory behavior in female rats (lordosis response, LR) and demonstrates that this inhibitory effect is blocked by the vasopressin antagonist (3-mercapto-3-methylbutyryl-Tyr-[Me])arginine vasopressin (dPTyr(Me)AVP, 20 ng, i.c.v.). The effects of neonatal AVP antagonist treatment on adult female copulatory behavior, hypothalamic content of AVP and AVP-like immunoreactive (AVP-ir) neurons were examined. dPTyr(Me)AVP was given to female rats 1 microgram/animal/day s.c. from day 1 through to day 7 (day 0 = day of birth). The females were ovariectomized as adults and sexual receptivity activated by submaximal doses of estradiol plus progesterone. The LR was significantly facilitated in the neonatally dPTyr(Me)AVP treated females who also showed a higher content and an increased number of AVP-ir neurons in the suprachiasmatic nucleus compared to saline controls. Functional, biochemical and immunocytochemical evidence is provided that neonatal exposure to an AVP antagonist induces persistent changes in central vasopressinergic neuronal mechanisms.

Animals↗
PubMed1991

Comparative effects of arginine vasopressin, [pGlu4,Cyt6]arginine vasopressin-(4-9) and nerve growth factor on maintenance of functional tolerance to ethanol in mice.

Previous work has demonstrated that arginine vasopressin (AVP), acting in the CNS, can maintain functional tolerance to ethanol. We now show that the AVP metabolite peptide, [pGlu4,Cyt6]arginine vasopressin-(4-9), also maintains ethanol tolerance, with a potency similar to that of arginine vasopressin, while nerve growth factor has only a marginal effect. The effects of these peptides on ethanol tolerance correlate with their previously described ability to induce expression of the proto-oncogene, c-fos, in the septum, a putative mechanism underlying peptide effects on neuroadaptive processes.

Animals↗
PubMed1983

Biochemical characterization of a vasopressin-like neuropeptide in Locusta migratoria. Evidence of high molecular weight protein encoding vasopressin sequence.

The biochemical characterization of a diuretic neurohormone, immunologically related to the mammalian vasopressin (AVP) and present in Locusta migratoria has been performed. The results have been obtained using an AVP radioimmunoassay as method of detection and quantification. The "AVP like" molecule exhibits the same C terminal moiety: the tetrapeptide 1/2 Cys-PrO-Arg-Gly NH2. 125I-radiolabelling allows us to demonstrate the presence of a tyrosyl residue. The molecular weight of this molecule is estimated by gel filtration to 2500 +/- 400 Daltons. The isoelectric point is 7.5 and the electrophoretic migration lead to conclude to the presence of amino acid residues lacking in the vasopressin hormone. We have demonstrated the presence of a vasopressin sequence included in high molecular weight protein which have been quantified in suboesophageal ganglion (biosynthetic site) and in the nervous ventral cord (release site).

Amino Acid Sequence↗
PubMed1981

Arginine vasopressin and a vasopressin antagonist peptide: opposite effects on extinction of active avoidance in rats.

Systemic injection or arginine vasopressin (AVP) (1 micrograms/rat) significantly prolonged extinction of a pole-jump, active avoidance response in rats; lateral ventricular injection of 1000-fold less AVP (1 ng/rat) produced similar results. A new AVP analogue, [1-deaminopenicillamine-2-(O-methyl)tyrosine]arginine vasopressin (dPTyr-(Me)AVP), is known to antagonize behavioral and vascular effects of exogenous AVP at molar ratios of 5 : 1. At a dose of 100 micrograms/rat (subcutaneously) dPTyr-(Me)AVP produces, by itself, a behavioral effect opposite to that of exogenous AVP, namely a facilitation of extinction. Injections of dPTyr-(Me)AVP into the lateral ventricle were ineffective except at a dose of 10 micrograms/rat. These results confirm previous reports of the effect of vasopressin on delaying extinction of avoidance behavior, but suggest a site of action distant from the lateral ventricle.

Animals↗
PubMed1985

Vasopressin pressor antagonist injected centrally reverses behavioral effects of peripheral injection of vasopressin, but only at doses that reverse increase in blood pressure.

Previous work in rats (Ader, R. and De Wied, D., Psychon. Sci., 29 (1972) 46-48) has established that subcutaneously (s.c.) injected arginine vasopressin (AVP) prolongs extinction of active avoidance and that this effect could be prevented by pretreatment with the vasopressin antagonist analog [1-deaminopenicillamine, 2-(O-methyl)tyrosine]-beta-arginine vasopressin (dPtyr(Me)AVP). The purpose of the present study was to determine if peripherally administered AVP acts via a peripheral blood pressure effect or by a direct action in the central nervous system. We therefore tested the effects of the antagonist injected intracerebroventricularly (i.c.v.) on the prolongation of active avoidance and on blood pressure effects of s.c. injected AVP. The antagonist (i.c.v.) blocked the behavioral effects of systemically injected AVP only at dose sufficient to block the peripherally mediated pressor response of systemically administered AVP. The results show that peripherally injected AVP acts on peripheral systems and support our hypothesis that the peripheral visceral action of AVP contributed significantly to its behavioral action.

Animals↗
PubMedDate not supplied

Vasopressin(1-8) (des-glycinamide9-[Arg8]vasopressin) is an endogenous peptide present in rat plasma.

Using a radioimmunoassay for [Arg8]vasopressin(1-8) (des-glycinamide9-[Arg8]vasopressin; DGAVP) endogenous immunoreactive DGAVP (IR-DGAVP) was detected in extracts of plasma prepared from trunk blood of male Wistar rats. The IR-DGAVP was further characterized by reversed-phase high pressure liquid chromatography (HPLC). One of the two immunoreactive peaks obtained by HPLC coeluted with synthetic DGAVP and did not cross-react in a radioimmunoassay specific for [Arg8]vasopressin(1-9) (AVP). The other showed the chromatographical and radioimmunological characteristics of AVP. Analysis by HPLC of plasma prepared from fresh blood spiked with 3H-AVP indicated that under the experimental conditions employed no DGAVP was formed during extraction. The results indicate that DGAVP is present in rat plasma, possibly as an endogenous metabolite of AVP.

Animals↗
PubMed1993

Increased loss of brain DNA in the neonatal vasopressin-deficient Brattleboro rat, but not in normal rat treated with vasopressin antagonist.

In order to establish whether vasopressin (VP) influences brain cell survival, [3H]thymidine was injected in 10-day-old vasopressin-deficient Brattleboro rat pups, as well as in Wistar pups treated, neonatally, with the VP antagonist dP[Tyr(Me)2]VP followed by subsequent measurement of [3H]DNA in olfactory bulbs and cerebellum days and weeks thereafter. Results show, first of all, that the incorporation of [3H]thymidine into DNA was enhanced in the homozygous (HOM) Brattleboro, when compared with the heterozygous (HET; non-vasopressin-deficient) controls. The difference is due to the greater and prolonged tissue availability of [3H]thymidine, possibly pointing to an altered thymidine uptake and/or metabolism. Between postnatal days 25 and 39 no differences were seen in [3H]DNA content of the brain parts of the HET and Wistar control rats. For the HOM rats, however, a loss of [3H]DNA was seen (up to 8%), indicating that increased postnatal brain cell death might occur in the mutant. The antagonist treatment in Wistar rat up to 21 days of age failed to show a similar effect. It is proposed that general growth impairments, rather than VP receptor-mediated effects, lead to the brain cell loss.

Aging↗
PubMed1984

Potent and selective antagonists of the antidiuretic responses to arginine-vasopressin based on modifications of [1-(beta-mercapto-beta,beta-pentamethylenepropionic acid),2-D-isoleucine,4- valine]arginine-vasopressin at position 4.

As part of a program in which we are attempting (a) to obtain more potent and/or more selective antagonists of the antidiuretic responses to arginine-vasopressin (AVP) and (b) to delineate the structural features at positions 1-9 required for antidiuretic antagonism, we have synthesized 13 new analogues of the antidiuretic antagonist [1-(beta-mercapto-beta,beta-pentamethylenepropionic acid),2-D-isoleucine,4- valine]arginine-vasopressin [d(CH2)5[D-Ile2]VAVP] in which the valine residue at position 4 has been replaced by the L-amino acids Abu, Ile, Thr, Ala, Ser, Nva, Gln, Leu, Lys, Cha, Asn, Orn, and Phe and two new analogues of the antidiuretic antagonist [1-(beta-mercapto-beta,beta-pentamethylenepropionic acid),2-D-phenylalanine,4- valine]arginine-vasopressin [d(CH2)5[D-Phe2]VAVP] with the Val4 residue replaced by Ser and Orn. These analogues are 1, d(CH2)5[D-Ile2,Abu4]AVP; 2, d(CH2)5[D-Ile2,Ile4]AVP; 3, d(CH2)5[D-Ile2,Thr4]AVP; 4, d(CH2)5[D-Ile2,Ala4]AVP; 5, d(CH2)5[D-Ile2,Ser4]AVP; 6, d(CH2)5[D-Ile2,Nva4]AVP; 7, d(CH2)5[D-Ile2]AVP; 8, d(CH2)5[D-Ile2,Leu4]AVP; 9, d(CH2)5[D-Ile2,Lys4]AVP; 10, d(CH2)5[D-Ile2,Cha4]AVP; 11, d(CH2)5[D-Ile2,Asn4]AVP; 12, d(CH2)5[D-Ile2,Orn4]AVP; 13, d(CH2)5[D-Ile2,Phe4]AVP; 14, d(CH2)5[D-Phe2,Ser4]AVP; and 15, d(CH2)5[D-Phe2,Orn4]AVP. The protected peptide precursors for these peptides were prepared by the solid-phase method, followed by ammonolytic cleavage. The free peptides 1-15 were obtained by deblocking with Na in NH3, oxidation of the resultant disulfhydryl compounds with dilute K3[Fe(CN)6], and purification on Sephadex G-15 in a two-step procedure with 50% HOAc and 0.2 M HOAc as eluants. Analogues 1-15 were tested in rats for agonistic and antagonistic activities by antidiuretic, vasopressor, and oxytocic assays.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Probes for vasopressin receptors. Attachment of affinity and fluorescent groups in vasopressin.

Fluorescent, photoreactive, and biotinylated analogs of vasopressin have been prepared in which one of these three groups has been attached to a reactive amino group in either position 4 or position 7. Using solid phase methodology, we have synthesized two active parent compounds, [1-desamino,4-lysine,7-hydroxyproline]arginine vasopressin and [1-desamino,7-aminoproline]arginine vasopressin, and acylated them to obtain biotinyl, azidobenzoyl, and fluoresceinyl derivatives. We have also prepared analogs in which a "spacer arm" was inserted between lysine in position 4 and the marker group. Some of these derivatives have good antidiuretic activity and could be valuable probes in studying hormone-receptor interaction and in receptor visualization and purification.

Affinity Labels↗
PubMed1988

The vasopressin mRNA poly(A) tract is unusually long and increases during stimulation of vasopressin gene expression in vivo.

We developed a method, termed an H-blot, by which the poly(A) tract of any specific mRNA may be detected by RNA filter hybridization after its removal from the body of the mRNA by a RNase H-catalyzed endonucleolytic cleavage in the 3' untranslated region. Using this method, we studied the modulation of the length of the poly(A) tract of rat vasopressin mRNA in vivo during changes in the levels of this mRNA resulting from a physiologic stimulus, osmotic stress. The poly(A) tract of hypothalamic vasopressin mRNA in hydrated rats was, quite remarkably, approximately 250 nucleotides in length, in contrast to that of somatostatin mRNA, which was approximately 30 nucleotides long. Vasopressin mRNA poly(A) tail length increased progressively from approximately 250 to approximately 400 nucleotides with the application of the hyperosmotic stimulus and declined to base line after its removal; somatostatin mRNA poly(A) tail length did not change during osmotic stress. The poly(A) tract length of total hypothalamic mRNA was between 35 and 140 nucleotides and also did not change with osmotic stress. Modulation of poly(A) tract length of specific mRNAs during stimulation of gene expression may provide an additional level of genetic regulation.

Animals↗
PubMed1992

Effect of vasopressin on brain swelling at the cellular level: do astrocytes exhibit a furosemide--vasopressin-sensitive mechanism for volume regulation?

Two sets of new observations are reported: (i) astrocytes in primary cultures show an increased potassium-induced swelling in the presence of 1-100 x 10(-12) M vasopressin, whereas no similar phenomenon is found in primary cultures of neurons, and (ii) the furosemide-sensitive cotransport system for uptake of K+, Na+, and Cl-, which is known to exist in astrocytes, is absent in neurons. On the basis of these findings and observations by other investigators on transport of ions and water in the brain in vivo, a novel mechanism is suggested, according to which all boundaries of brain parenchymal tissue (perivascular astrocytic end-feet, glia limitans, and ependyma) in the absence of vasopressin are capable of performing a net uptake of K+, Na+, and Cl- without uptake of water, and that the resulting hyperosmolarity in the presence of vasopressin leads to water uptake (cell swelling), which causes a reduction in the amount of water in the interstitial fluid and thus an increase in extracellular concentrations of ions.

Animals↗
PubMed1996

Rat renal arcade segment expresses vasopressin-regulated water channel and vasopressin V2 receptor.

The arcades are long, branched renal tubules which connect deep and mid-cortical nephrons to cortical collecting ducts in the renal cortex. Because they are inaccessible by standard physiological techniques, their functions are poorly understood. In this paper, we demonstrate that the arcades are a site of expression of two proteins, aquaporin-2 (the vasopressin-regulated water channel) and the V2 vasopressin receptor, that are important to regulated water transport in the kidney. Using a peptide-derived polyclonal antibody to aquaporin-2, quantitative ELISA in microdissected segments showed that aquaporin-2 is highly expressed in arcades and that the expression is increased in response to restriction of fluid intake. Immunocytochemistry revealed abundant aquaporin-2 labeling of structures in the cortical labyrinth in a pattern similar to that of the Na(+)-Ca2+ exchanger and kallikrein, marker proteins expressed in arcades but not in cortical collecting ducts. RT-PCR experiments demonstrated substantial aquaporin-2 and V2 receptor mRNA in microdissected arcades. In situ hybridization, using 35S-labeled antisense cRNA probes for the V2 receptor demonstrated strong labeling of both arcades and cortical collecting ducts. Thus, these results indicate that the arcades contain the specific proteins associated with vasopressin-regulated water transport, and may be a heretofore unrecognized site of free water absorption.

Animals↗
PubMed1978

[Effect of vasopressin on the lower esophageal sphincter. Study on the action mechanism of vasopressin in bleeding esophageal varices].

The effect of vasopressin on the lower esophageal sphincter has been investigated in 12 healthy volunteers. Peripheral infusion of 0.2 U/min resulted in a significant (p less than 0.05) decrease in sphincter pressure. Accordingly, vasopressin-induced myogenic compression of bleeding varices has been ruled out as a potential additional hemostatic mechanism of vasopressin.

Esophageal and Gastric Varices↗
PubMedDate not supplied

Vasopressin and vasopressin-antagonists applied to neonatal Wistar rats: effects on body and brain development and water metabolism.

Neonatal Wistar rats were continuously treated with the vasopressin-antagonists d(CH2)5[Tyr(Me)2]AVP, d(CH2)5DAVP or d(CH2)5[D-Ile2,Ala4]AVP, which have high anti-vasopressor or anti-anti-diuretic activity. The treatments were performed to test the hypothesis that arginine-vasopressin (AVP) might have a stimulatory effect on brain development, which is based upon the disturbed brain development of the AVP-deficient Brattleboro rat. None of the treatments with antagonists, either being given via a small drug-delivery device or by twice daily injections, inhibited body or brain development, though d(CH2)5[Tyr(Me)2]AVP treatment even had some stimulatory effect on cerebellar weight as measured at one month of age. Similar drug-delivery treatment with AVP or oxytocin (OX), or injections with 250 ng AVP, lysine-vasopressin (LVP), arginine-vasotocin (AVT) or OX had no stimulatory developmental effect. However injections with 2.5 micrograms of these peptides reduced body development, albeit transiently, of the neonatal Wistar rats. Moreover in this latter group not only the known lasting effects of AVP and LVP on body water metabolism were seen but also such effects were present after AVT and OX treatment.

Animals↗
PubMed1987

Histochemical and ultrastructural study of renal cortical necrosis in rats treated with oestrone + vasopressin, and its prevention with a vasopressin antagonist.

Renal cortical necrosis was induced by the administration of vasopressin to oestrogen-pretreated rats. Histochemical (succinic dehydrogenase, trichrome, perjod acid Schiff) and electronmicroscopic methods were applied to examine how the vasopressin antagonist d(CH2)5Tyr(Met)AVP influences the development of this renal cortical necrosis. The experiments revealed that vasopressin did not induce hypoxia or necrosis in the renal tubules if the antagonist was administered simultaneously, even after oestrogen pretreatment. The conclusion is drawn that this pressor antagonist may be of value for the prevention of renal cortical necrosis in rats or in human beings.

Animals↗
PubMed2000

Characterization of a novel nonpeptide vasopressin V(2)-agonist, OPC-51803, in cells transfected human vasopressin receptor subtypes.

We discovered the first nonpeptide arginine-vasopressin (AVP) V(2)-receptor agonist, OPC-51803. Pharmacological properties of OPC-51803 were elucidated using HeLa cells expressing human AVP receptor subtypes (V(2), V(1a) and V(1b)) and compared with those of 1-desamino-8-D-arginine vasopressin (dDAVP), a peptide V(2)-receptor agonist. OPC-51803 and dDAVP displaced [(3)H]-AVP binding to human V(2)- and V(1a)-receptors with K(i) values of 91.9+/-10.8 nM (n = 6) and 3.12+/-0.38 nM (n = 6) for V(2)-receptors, and 819+/-39 nM (n = 6) and 41.5+/-9.9 nM (n = 6) for V(1a)-receptors, indicating that OPC-51803 was about nine times more selective for V(2)-receptors, similar to the selectivity of dDAVP. OPC-51803 scarcely displaced [(3)H]-AVP binding to human V(1b)-receptors even at 10(-4) M, while dDAVP showed potent affinity to human V(1b)-receptors with the K(i) value of 13.7+/-3.2 nM (n = 4). OPC-51803 concentration-dependently increased cyclic adenosine 3', 5'-monophosphate (cyclic AMP) production in HeLa cells expressing human V(2)-receptors with an EC(50) value of 189+/-14 nM (n = 6). The concentration-response curve for cyclic AMP production induced by OPC-51803 was shifted to the right in the presence of a V(2)-antagonist, OPC-31260. At 10(-5) M, OPC-51803 did not increase the intracellular Ca(2+) concentration ([Ca(2+)](i)) in HeLa cells expressing human V(1a)-receptors. On the other hand, dDAVP increased [Ca(2+)](i) in HeLa cells expressing human V(1a)- and V(1b)-receptors in a concentration-dependent fashion. From these results, OPC-51803 has been confirmed to be the first nonpeptide agonist for human AVP V(2)-receptors without agonistic activities for V(1a)- and V(1b)-receptors. OPC-51803 may be useful for the treatment of AVP-deficient pathophysiological states and as a tool for AVP researches.

Arginine Vasopressin↗
PubMed1984

Vasopressin antagonists block peripheral as well as central vasopressin receptors.

The aim of the present study was to differentiate between the postulated central behavioral effects of vasopressin and its pressor response, which is mainly mediated by peripheral vascular receptors. Thus, the interaction between the vasopressor antagonists dPTyr(Me)AVP (AAVPa) and d(CH2)5Tyr(Me)AVP (AAVPb) with the effects of [Arg8]vasopressin (AVP-(1-9)) and [pGlu4,Cyt6]AVP-(4-8) (referred to as AVP-(4-8)) was examined using passive avoidance behavior and the pressor response as parameters. AVP-(4-8) was approximately 4 and 200 times more potent than AVP-(1-9) in facilitating passive avoidance behavior after subcutaneous (SC) or intracerebroventricular (ICV) administration respectively. This effect of SC injected AVP-(1-9) and AVP-(4-8) could be prevented by both vasopressor antagonists following SC treatment. A similar antagonistic action was found when AVP-(1-9) or AVP-(4-8) and the antagonist AAVPb were administered ICV. SC injection of AAVPb prevented the behavioral effect of ICV administered AVP-(1-9) while ICV treatment with the antagonist blocked the behavioral action of systemically injected AVP-(1-9) and AVP-(4-8). In contrast to SC injected AVP-(1-9) which dose-dependently increased blood pressure and decreased heart rate, AVP-(4-8) injected SC in identical doses did not affect blood pressure and heart rate, neither did AVP-(1-9) and AVP-(4-8) when injected ICV in behaviorally active doses. A SC, but not an ICV injection of the antagonist AAVPb could prevent the blood pressure increase and bradycardia induced by SC AVP-(1-9).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Solid phase synthesis and some pharmacological properties of 8-D-homoarginine-vasopressin and 1-deamino-8-D-homoarginine-vasopressin.

Fully protected 8-D-lysine-vasopresin and 1-deamino-8-D-lysine-vasopressin were synthesized by the solid phase method. Selective removal of the lysine protection and reaction with 1-guanyl-3,5-dimethylpyrazole converted D-lysine into D-homoarginine. The title compounds were then obtained by treatment with sodium in liquid ammonia and oxidation in dilute aqueous solution. Although the antidiuretic activities are lower than for the corresponding D-argining derivatives, the even lower pressor effects make the new analogues highly specific antidiuretic agents. The A/P ratios for 8-D-homoarginine-vasopressin and its 1-deamino derivative are 100 and 3,300, respectively.

Animals↗