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PubMed2005

Downregulation of the vasopressin type 2 receptor after vasopressin-induced internalization: involvement of a lysosomal degradation pathway.

Vasopressin (VP) increases urinary concentration by signaling through the vasopressin receptor (V2R) in collecting duct principal cells. After downregulation, V2R reappears at the cell surface via an unusually slow (several hours) "recycling" pathway. To examine this pathway, we expressed V2R-green fluorescent protein (GFP) in LLC-PK1a cells. V2R-GFP showed characteristics similar to those of wild-type V2R, including high affinity for VP and adenylyl cyclase stimulation. V2R-GFP was located mainly in the plasma membrane in unstimulated cells, but it colocalized with the lysosomal marker Lysotracker after VP-induced internalization. Western blot analysis of V2R-GFP showed a broad 57- to 68-kDa band and a doublet at 46 and 52 kDa before VP treatment. After 4-h VP exposure, the 57- to 68-kDa band lost 50% of its intensity, whereas the lower 46-kDa band increased by 200%. The lysosomal inhibitor chloroquine abolished this VP effect, whereas lactacystin, a proteasome inhibitor, had no effect. Incubating cells at 20 degrees C to block trafficking from the trans-Golgi network reduced V2R membrane fluorescence, and a perinuclear patch developed. Cycloheximide reduced the intensity of this patch, showing that newly synthesized V2R-GFP contributed significantly to its appearance. Cycloheximide also inhibited the reappearance of cell surface V2R after downregulation. We conclude that after downregulation, V2R-GFP is delivered to lysosomes and degraded. Reappearance of V2R at the cell surface depends on new protein synthesis, partially explaining the long time lag needed to fully reestablish V2R at the cell surface after downregulation. This degradative pathway may be an adaptive response to allow receptor-ligand association in the hypertonic and acidic environment of the renal medulla.

Animals↗
PubMed1989

Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.

Arginine vasopressin (AVP) is a potent vasopressor and antidiuretic neurohormone. However, when administered intravenously to humans, AVP causes forearm vasodilation. This effect has been attributed to sympathetic withdrawal, secondary to AVP-induced sensitization of baroreceptors. The possibility that AVP also causes forearm vasodilation directly has not been examined. Accordingly, the direct effect of AVP was determined by studying the forearm blood flow (FBF) response to intraarterial (IA) AVP infusion (0.01-1.0 ng/kg per min). Infusion of IA AVP increased FBF (96%) in the infused arm, but not the control arm, in a dose-dependent manner. The role of specific AVP V1 receptors in mediating this FBF response was determined before and after pretreatment with a V1 antagonist (AVP-A). AVP-A alone had no effect on FBF, but coadministration of AVP and AVP-A potentiated the vasodilatory response (223%). IA infusion of the V2 agonist, 1-desamino[8-D-arginine] vasopressin, caused a dose-dependent increase in FBF. These findings suggest that AVP causes direct, dose-dependent vasodilation in the human forearm that may be mediated by V2 vasopressinergic receptors. In contrast, AVP infusion caused digital vasoconstriction that was blocked by AVP-A, whereas dDAVP did not affect digital blood flow. Thus, AVP induces regionally selective vascular effects, with concurrent forearm vasodilation and digital vasoconstriction.

Adult↗
PubMed1976

Metabolic clearance of immunoreactive vasopressin and immunoreactive [131I]iodo vasopressin in the hypophysectomized dog.

Fourteen acutely hypophysectomized, anesthetized dogs were given a constant infusion of arginine vasopressin (AVP) and 131I-labeled arginine vasopressin ([131I]AVP). After 90 min, 3 blood samples were collected at 15 min intervals for determination of total body clearances of immunoreactive AVP and immunoreactive [131I]AVP. Seven dogs were then nephrectomized. Ninety minutes later, a second set of 3 blood samples was collected at 15 min intervals for clearance measurements in these and the 7 time-control dogs. Prenephrectomy AVP clearance averaged 5.1+/-1.0 ml/min-kg (mean +/- SE, n=7), and the 210-240 min postnephrectomy AVP clearance average 4.9+/-0.8. The 90-120 min average clearance in the time-control dogs was 6.1+/-0.9 ml/min-kg (n=7) and AVP clearance in these dogs increased (P less than 0.01) with time to 7.3+/-0.9 ml/min-kg during the 210-240 min period of constant infusion. Although the postnephrectomy AVP clearance was not significantly changed from prenephrectomy levels, it was significantly lower (P less than 0.05) than the 210-240 min average clearance in the time-controls. Clearance of [131I]AVP was 3.3+/-0.2 ml/min-kg (n=7) before nephrectomy and 2.9+/-0.2 ml/min-kg after nephrectomy. This was a significant 12% reduction (P less than 0.01). [131I]AVP clearance in the time control dogs was 3.9+/-0.3 during 90-120 min of infusion and 3.9+/-0.4 during 210-240 min of infusion. [131I]AVP clearance before nephrectomy was 79+/-12% of AVP clearance (P less than 0.005) and afther nephrectomy was 74+/-16% of AVP clearance (P less than 0.05). Although these results might suggest that [131I]AVP clearance is at least a qualitative indicator of AVP clearance, there was no significant correlation (P less than 0.20) between AVP clearance and [131I]AVP clearance.

Animals↗
PubMed1985

Resistance of 1-deamino-[8-D-arginine]-vasopressin to in vitro degradation as compared with arginine vasopressin.

In order to elucidate the mechanism(s) responsible for the prolonged antidiuretic activity of 1-deamino-[8-D-arginine]-vasopressin (dDAVP), antidiuretic activities of dDAVP and arginine vasopressin (AVP) were determined in the rat following either oral administration or incubation with AVP-degrading enzymes and reagents. Oral administration of dDAVP to conscious water-loaded rats resulted in significant antidiuresis while AVP resulted in slight and transient antidiuresis. In the ethanol anesthetized water-loaded rats, antidiuretic activities of 136pg of AVP and 50pg of dDAVP, which were found to be equipotent, were compared after incubation with digestive enzymes (pepsin, trypsin, alpha-chymotrypsin), late pregnancy plasma, or sodium thioglycollate. The antidiuretic activity of AVP was completely destroyed by 30-min incubation with trypsin, alpha-chymotrypsin, or late pregnancy plasma and almost all AVP was inactivated by 0.2 M sodium thioglycollate. On the other hand, the antidiuretic activity of dDAVP was not destroyed by trypsin or pregnancy plasma but was partly destroyed by alpha-chymotrypsin and sodium thioglycollate. Neither the antidiuretic activity of AVP nor that of dDAVP was affected by pepsin. Thus, the antidiuresis observed after oral administration of dDAVP might be brought about by the resistance to digestive enzymes. Furthermore, the resistance of dDAVP to digestive enzymes, late pregnancy plasma and sodium thioglycollate might be responsible for the prolonged antidiuretic action of dDAVP in vivo.

Animals↗
PubMed1992

Effect of 1-desamino-8-D-arginine vasopressin (DDAVP) on vasopressin release and blood pressure during hemorrhage.

Whether or not 1-desamino-8-D-arginine-vasopressin (DDAVP) reduces blood pressure or affects the release of arginine vasopressin (AVP) and renin is controversial, although evidence suggests AVP and renin are important in maintaining blood pressure during hemorrhage. We therefore investigated the effect of DDAVP on endogenous release of AVP and renin and on blood pressure during hemorrhage in dogs. In the control group the hemorrhage was performed at a rate of 0.4 ml.kg-1.min-1 for 40 min from the femoral artery. The plasma AVP concentration and renin activity (PRA) increased progressively in response to the hemorrhage, from 7.5 +/- 0.5 to 40.3 +/- 7.3 pg.ml-1, and from 11.8 +/- 1.5 to 20.5 +/- 4.2 ng.ml-1.h-1, respectively, while blood pressure decreased slightly. In the DDAVP group, intravenous infusion of DDAVP (2.5 ng.kg-1.min-1 for 40 min) and hemorrhage were simultaneously performed. The plasma DDAVP concentration increased progressively to 218 +/- 21.0 pg.ml-1. There was no significant difference, however, between the control and DDAVP groups in the response of AVP, PRA and blood pressure. The results suggested that DDAVP may not affect the release of AVP and renin or blood pressure during hemorrhage.

Aldosterone↗
PubMed1988

Elevated serum oxytocin of the vasopressin-deficient Brattleboro rat is present throughout life and is not sensitive to treatment with vasopressin.

The postnatal developmental course of the enhanced OT serum level of the vasopressin-deficient (homozygous) Brattleboro rat was investigated radioimmunochemically together with the response to treatment with Pitressin tannate. Compared with heterozygous Brattleboro (control) pups, in which serum OT appeared to have an adult value from birth onwards (about 10 pmol/l), homozygous rats had approximately 2-fold enhanced OT serum level throughout early development. Between day 55 and adulthood the levels of OT rose further to 40-50 pmol/l. A 3-day treatment with Pitressin tannate both in the period before or after the age (day 16) at which the polyuria of the homozygous Brattleboro mutant can be revealed, failed to reduce the serum OT. It was therefore concluded that the high OT serum levels in the vasopressin-deficient Brattleboro rat are not induced by osmotic imbalance, but probably originates from functional teratological aspects of the mutation.

Animals↗
PubMed1982

Blood-cerebrospinal fluid barrier to arginine-vasopressin, desmopressin and desglycinamide arginine-vasopressin in the dog.

The passage of 125I-labelled arginine-vasopressin (AVP) and its analogues desmopressin (DDAVP) and desglycinamide arginine-vasopressin (DGAVP) into cerebrospinal fluid (CSF) has been studied in the dog. After intravenous injection or infusion of these peptides radioactive substances were found in the CSF in amounts ranging from 0.5 to 1.4% of the total plasma radioactivity. However, only DDAVP could be identified in the CSF as the unmetabolized peptide. This observation may be related to the long plasma half-life of DDAVP which was found to be 50 min, compared with a half-life of 13 min for AVP and 8 min for DGAVP. After the intranasal administration of either [3H]AVP or 125I-labelled AVP similar results were obtained. Radioactivity was again present in the CSF but no AVP could be identified. These observations showed that the intranasal route of administration provides no increased access to the CSF. The existence of a blood-CSF barrier to AVP is confirmed and indicates that the concentrations of the hormone normally found in CSF arise from sources other than the blood.

Administration, Intranasal↗
PubMed1976

Synthesis of peptides by fragment condensation on a solid support. II. A scheme for preparation of 4,8-disubstituted vasopressins evaluated on 8-arginine-vasopressin.

A convenient scheme for the synthesis of 4,8-disubstituted vasopressins has been designed and its usefulness evaluated in the preparation of one of the parent hormones, 8-arginine-vasopressin. The main feature of the scheme involves preparation of two protected tripeptide fragments, Z-Cys(Bzl)-Tyr(Bzl)-Phe and Boc-Asn(Mbh)-Cys(Bzl)-Pro which are incorporated in a synthesis on a solid support. Both tripeptides were prepared conventionally with the carboxyl groups protected as benzyl esters. The benzyl-ester groups were removed by transesterification with 2-dimethylaminoethanol and subsequent hydrolysis. To avoid racemization in the coupling step with the fragment containing a C-terminal phenylalanine, N-hydroxysuccinimide was added. After removal of the peptide from the resin, deprotection, oxidation and desalting, final purification was effected by ion-exchange chromatography. Apart from the main product, which exhibited full pressor activity, only small amounts of impurities could be isolated.

Arginine Vasopressin↗
PubMed1994

Normal acid-base equilibrium in acute hyponatremia and mixed alkalosis in chronic hyponatremia induced by arginine vasopressin or 1-deamino-8-D-arginine vasopressin in rats.

The effects of acute and chronic water intoxication induced by the administration of oral water and arginine vasopressin (AVP) or 1-deamino-8-D-arginine-vasopressin (DDAVP) on blood acid-base equilibrium and aldosterone, corticosterone, and thyroxine secretion were studied in rats. Acute hyponatremia (3 hours) was associated with normal bicarbonate and blood acid-base equilibrium and a decrease in aldosterone and thyroxine concentrations, while corticosterone was increased. When similar levels of hyponatremia (serum sodium 110 mEq/L) were maintained for 24 or 72 hours, a normal serum bicarbonate concentration was observed, but blood acid-base equilibrium showed a mixed respiratory and metabolic alkalosis. Blood pH was negatively correlated with serum sodium concentration (R = -0.65; p < 0.001), as was the metabolic alkalosis (base excess; R = -0.64; p < 0.001) and the aldosterone concentration (R = -0.52; p < 0.01), while the PCO2 was positively correlated (R = +0.49; p < 0.01). Hyperaldosteronism was similar whether hyponatremia was induced with AVP or DDAVP and was observed even for mild hyponatremia. When hyponatremia was induced by a high water and salt intake (2.5% D-glucose, 0.45% NaCl; 15% body weight), aldosterone concentration was as high (about three times control values) as in rats with similar levels of hyponatremia but with a salt-free diet. The high salt intake was associated with a more severe metabolic alkalosis (base excess +5,5 mEq/L). In chronic hyponatremia, corticosterone and thyroxine values were normal. In hyponatremia related to syndrome of inappropriate secretion of antidiuretic hormone, the normal serum bicarbonate level is an expected observation; as in acute water intoxication, it stays normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

Dual duplication of neurohypophysial hormones in an Australian marsupial: mesotocin, oxytocin, lysine vasopressin and arginine vasopressin in a single gland of the northern bandicoot (Isoodon macrourus).

Neurohypophysial hormones of an Australian marsupial, the Northern bandicoot (Isoodon macrourus), have been identified by their retention times in high-pressure reverse-phase liquid chromatography using two solvent systems and by their molar pressor or uterotonic activities. Two pressor peptides, arginine vasopressin and lysipressin, and two uterotonic peptides, mesotocin and oxytocin, have been characterized. Because mesotocin and arginine vasopressin have been identified in three other Australian marsupial families, it is assumed that a duplication of each ancestral gene occurred in Peramelidae and subsequent mutations in one copy led to the additional oxytocin and lysipressin. A similar dual duplication of neurohypophysial hormones has previously been discovered in the North-American opossum (Didelphis virginiana) so that the duplication propensity seems peculiar to marsupials in contrast to placental mammals.

Animals↗
PubMed1992

Potent antagonistic action of OPC-31260, a vasopressin V2 receptor antagonist, on [Arg8]vasopressin-induced vasoconstriction in isolated simian femoral arteries.

Using a perfusion technique with isolated vessels, we investigated the effect of OPC-21268 (a selective V1 receptor antagonist) and OPC-31260 (a V2 receptor antagonist) on arginine vasopressin (AVP)- or norepinephrine (NE)-induced vasoconstrictions of isolated simian femoral arteries. The dose-response curve for AVP was shifted to the right in parallel by OPC-31260 but not by OPC-21268. Neither antagonist significantly modified the NE-induced vasoconstriction. On the basis of these results, there are functionally constrictory vasopressin V2 receptors but no V1 receptors in isolated simian femoral arteries.

Animals↗
PubMed1984

Antagonism of effects of vasopressin (AVP) on inhibitory avoidance by a vasopressin antagonist peptide [dPtyr(Me)AVP].

After training in two different passive avoidance tasks, the platform box of Ader and De Wied (1972) and the Jarvik box of Jarvik and Kopp (1967), rats injected with vasopressin immediately following the training trial showed a significant enhancement of retention 24 hours later. This vasopressin effect was reversed by high doses of the vasopressor antagonist, dPtyr(Me) AVP. These results support the hypothesis that the visceral afferent signals may be involved in the apparent memory-enhancing effects of AVP, but the high doses of antagonist required suggest that factors other than a simple reversal of the pressor effects of AVP may be important.

Animals↗
PubMed1992

Potentiometric and spectroscopic studies of the Cu(II) complexes of Ala-Arg8-vasopressin and oxytocin: two vasopressin-like peptides.

The results are reported of a potentiometric and spectroscopic study of the H+ and Cu2+ complexes of Ala-Arg8-vasopressin (Ala-AVP) and oxytocin at 25 degrees C and an ionic strength of 0.10 mol dm-3 (KNO3). The coordination chemistry of oxytocin and Cu(II) has been shown to be virtually identical to that of Arg8-vasotocin, forming unusually stable complexes with four nitrogen coordination (4N complexes) below pH 7. Spectroscopic evidence suggests weak interaction between Cu(II) and the sulphur atom of the -Cys6- residue in the 2N species (pH congruent to 6) but this is absent in the 4N complex. Evidence is also presented for perturbation of electronic transitions within the aromatic ring of the Tyr residue by Cu(II). While the physiological potency of Ala-AVP is very high, its coordination chemistry differs significantly from that of Arg8-vasopressin. With Cu(II) it forms complexes of similar stability to those with tetraglycine, demonstrating that the addition of an alanyl residue to the amino-terminal of the peptide destroys the conformation which is particularly favorable for rapid 4N coordination.

Amino Acid Sequence↗
PubMed1988

Vasopressin and amphetamine, but not desglycinamide vasopressin, impair positively reinforced visual attention performance in rats.

Rats were trained to respond to the lever above which a light stimulus was briefly (0.5 s) presented at unpredictable times. Once the task had been learned to criterion, subjects were injected, intra-peritoneally, with arginine8-vasopressin, desglycinamide arginine8-vasopressin (AVP or DGAVP: 0, 5, 10 or 20 micrograms/kg) or D-amphetamine (AMP: 0, 0.75, 1.5 or 3 mg/kg) prior to test. Attention performance was assessed using several different indices, including percent corrects, sensitivity and responsivity measures derived from signal detection theory, the recently described probability of (response) repetition and switching, and latency to respond. AVP had a disruptive effect on percent corrects at the highest dose and increased response latencies, but DGAVP, which lacks pressor activity, had no behavioral effects. AMP markedly impaired most aspects of performance, and was the only substance to alter response strategies by inducing bias and repetitive responding. It is concluded that (1) contrary to some recent reports, visual attention is disrupted, not improved, by peripherally injected AVP, (2) these effects reflect pressor potency, (3) the disruption induced by AMP reflects response alterations, while the peptide probably affects more cognitive mechanisms, and (4) certain recently described indices are more sensitive than others in detecting response bias.

Animals↗
PubMedDate not supplied

Vasopressin in aged rats: longitudinal studies of vasopressin excretion in Sprague-Dawley and Fischer 344 strains.

In order to provide physiological baseline values for future experimental procedures, indices of vasopressin secretion were assessed in male Sprague-Dawley (SD) and Fischer 344 (F344) rats at 3 and 20 months of age. Daily water intake, urine volume, urine osmolality, and urinary vasopressin excretion were monitored in SD rats for 30 days, and in F344 rats for 60 days. In the SD strain, daily water and urine volumes, expressed as ml/24 hr/100 g b.wt., were consistently lower in aged animals, as was a calculation of water balance (water intake-urine output volumes/24 hr). Although mean VP concentration in urine appeared higher in aged rats (33.9 +/- 20.4 pg/ml) than in young (16.3 +/- 7.7 pg/ml), total daily VP excretion was comparable for both ages when expressed as a function of body weight [80.6 +/- 37.3 pg for 3 months old (m.o.) and 81.9 +/- 47.2 pg/24 hr/100 g b.wt. for 3 and 20 m.o. respectively]. Young and old F344 males showed comparable daily drinking and urine volumes, and water balance, during two months of monitoring, but VP excretion was lower (p less than 0.025) in aged rats (83.8 +/- 19.0 pg/24 hr/100 g b.wt.) than in 3 m.o. rats (213.0 +/- 48.1 pg/24 hr/100 g b.wt.). Urine VP concentration was comparable (69.6 +/- 20.6 for 3 m.o.; 59.8 +/- 25.6 pg/ml for 20 m.o.). Mean urine osmolality was not significantly different among groups. Urine osmolality and daily urine volumes showed a significant correlation with daily VP excretion among young, but not aged, rats of both strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Vasopressin and vasopressin analogues for treatment of memory disorders in clinical practice.

1. Beyond its antidiuretic and vasopressor effects, vasopressin has central nervous system effects, first described in rats by David de Wied in 1965. 2. Its first clinical use in humans, in 1978, confirmed its stimulant action in normal individuals, especially in middle-aged male subjects. 3. Its utility in mnemic problems is also worht considering when the pathology is relatively recent (less than 2 years prior) and unaccompanied by major neurological lesions. Behavioral modifications, such as improvement of "sociability", "mood" improvement, independent of its effects on memory have been described, and would justify complementary clinical investigation. 4. New synthetic vasopressin derivatives which would eliminate metabolic effects while maintaining behavioral effects intact, and the definition of clinical, neuroendocrine, and neurophysiological prognostic criteria, will be the two most important paths for investigation over the next years.

Cognition↗
PubMedDate not supplied

Effects of oxytocin, arginine-vasopressin and lysine-vasopressin on insulin and glucagon secretion in sheep.

The effects of the posterior-pituitary peptides oxytocin (OT), arginine-vasopressin (AVP) and lysine-vasopressin (LVP) on insulin and glucagon secretion were examined in adult sheep. Each peptide was injected intravenously at doses from 1 to 3000 pmol kg-1. All three peptides increased plasma insulin and glucagon concentrations, but their dose-response relationships revealed differences between them. The maximal insulin responses induced by OT and AVP were very similar, but the threshold and maximal doses of AVP for increasing plasma insulin were higher than those of OT. OT and AVP had the same activity for stimulating glucagon secretion in respect of the threshold and maximal doses and the maximal hormone response. LVP also increased plasma insulin and glucagon concentrations, but it had the weakest activity for stimulating both hormones. These results suggest that in sheep posterior-pituitary peptide may play a role in regulating nutrient metabolism by influencing pancreatic hormone secretion.

Animals↗
PubMed1997

Vasopressin and memory. I. The vasopressin analogue AVP4-9 enhances working memory as well as reference memory in the radial arm maze.

The present study examined the effects of vasopressin on memory. Healthy rats were injected with the arginine vasopressin fragment AVP4-9 and the AVP antagonist [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,O-Et-Pyr 2,Val4,Arg8] and were tested in an eight-arm radial maze for 60 sessions. All injections were given s.c. 30 min prior to testing. AVP4-9 enhanced radial arm maze performance. AVP4-9 treated animals showed enhancement in performance as well as increases in the rate of learning, indicating that they learned the task faster. Furthermore, the overall memory enhancement was due to improved working memory as well as to improved reference memory. These results cannot be explained in terms of changes in locomotor activity because an open field test revealed no differences between groups for both of these compounds. The AVP antagonist did not impair performance in the radial maze. It is concluded that AVP4-9 has a more general effect on memory, one that is not limited to a specific type of memory.

Animals↗