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PubMed1997

Age-dependent accumulation of hybrid vasopressin-oxytocin gene products but not hybrid oxytocin-vasopressin products in the endoplasmic reticulum of Brattleboro rats.

The age-dependence of the incidence of magnocellular neurosecretory neurons containing abnormal accumulations of peptide in the rough endoplasmic reticulum was examined in homozygous Brattleboro rats and in their wild-type Long Evans counterparts. Neurons in which the immunophenotype of the peptide aggregates indicate that somatic cross-over mutations involving the 5' end of the vasopressin gene and the 3' end of the oxytocin gene have occurred, increased with age in homozygous Brattleboro rats, reaching a maximum of 24 cells per hypothalamus (approximately 0.6% of the vasopressin neurons). The increase occurred in both male and female animals but was significantly greater in females. The average incidence of such cells was 6 times greater in the supraoptic than in the paraventricular nucleus. No such cells could be detected in either nucleus of Long Evans rats despite the evidence for hybrid mRNA in these animals. Moreover, no accumulation of peptide translated from the hybrid mRNAs derived from the 5' end of the oxytocin gene and the 3' end of the vasopressin gene could be detected in either Brattleboro or Long Evans animals. These results strongly suggest that the accumulation of peptide in the rough endoplasmic reticulum of vasopressin neurons in homozygous Brattleboro rats is due to an abnormality other than the somatic crossing-over mutation. A second type of abnormal magnocellular neuron with accumulations of peptide in the rough endoplasmic reticulum, in which the immunophenotype of the peptide reveals products derived only from the oxytocin precursor, was present in both Long Evans and Brattleboro rats, but did not increase with age in Brattleboro rats. The incidence of these cells was similar in the supraoptic and paraventricular nuclei.

Aging↗
PubMed1977

[1-deaminopenicillamine,4-valine]-8-D-arginine-vasopressin, a highly potent inhibitor of the vasopressor response to arginine-vasopressin.

In attempting to design an antagonist of the antidiuretic response to arginine-vasopressin (AVP) [1-deaminopenicillamine,4-valine,8-D-arginine]vasopressin (dPVDAVP) was synthesized by the solid-phase method and assayed for antidiuretic, vasopressor, and oxytocic activities. dPVDAVP has an antidiuretic potency of 123 +/- 22 units/mg, one-tenth that of its parent [deamino,4-valine,8-D-arginine]vasopressin (dVDAVP). Like dVDAVP its antidiuretic effect in conscious diabetes insipidus rats is greatly prolonged when compared to AVP. dPVDAVP causes a prolonged inhibition of vasopressor responses to AVP but not to norepinephrine or angiotensin II. It has an antivasopressor pA2 value of 7.82 +/- 0.05 when tested against AVP. Thus the penicillamine substitution at position 1 in dVDAVP increased its antivasopressor activity sixfold (dVDAVP has a pA2 value of 7.03 +/- 0.11). dPVDAVP is thus the most potent vasopressor antagonist yet reported. dPVDAVP was also found to be a potent inhibitor of the in vitro oxytocic response to oxytocin (pA2 value = 7.23 +/- 0.04). dPVDAVP with its potent and specific ability to antagonize the vasopressor effects of AVP should be a useful pharmacological tool with which to explore the possible participation of AVP's potent vasoconstrictor properties in cardiovascular regulation in physiological and pathological states.

Animals↗
PubMed1980

Uterine effects of N-alpha-triglycyl-(8-lysine)-vasopressin and 8-lysine-vasopressin in the first trimester of pregnancy.

Myometrial effects of a vasopressin hormonogen (N-alpha-triglycyl-(8-lysine)-vasopressin, TGLVP) and of 8-lysine-vasopressin (LVP) were studied in early pregnancy. Intrauterine pressure was recorded in 28 women, who were to have a therapeutic abortion at 8-12 weeks of gestation, and intravenous injection of TGLVP (0.5 and 1 mg) or LVP (0.1, 0.2 and 0.4 IU) were given, or control recordings without drug injection were obtained. TGLVP generally caused a biphasic increase in uterine activity with a rise in uterine tone as the most conspicuous initial effect followed by an increase in amplitude and duration of contractions. In the higher dose group the uterine activity remained significantly higher than in the controls during the rest of the recording period of 4-7 h. The magnitude of effect with the two doses of TGLVP did not differ significantly. The initial myometrial response to LVP resembled that to TGLVP but the effects disappeared within 10-45 min. In the controls the uterine activity did not change. It is suggested that vasopressin analogues could have a therapeutic value in the induction of abortion, but further basic studies are required to define this.

Adult↗
PubMed1995

Radioprotective effect of local administration of lysine-vasopressin and triglycyl-lysine-vasopressin on the rectal mucosa in rats.

Reactions from the rectal mucosa often give rise to troublesome side-effects during and after radiotherapy in the pelvic region. Local vasoconstriction in the rectal mucosa will cause an ischemia which will decrease the sensitivity of the mucosal cells to radiation and thereby these side-effects can be reduced. Triglycyl-lysine-vasopressin applied rectally in 1% Blanose solution gave in the present study significant radioprotection of the rectal mucosa in the doses of 0.8, 1.6, and 3.2 mg. These doses are, however, very high. Triglycyl-lysine-vasopressin in 1.2% Natrosol solution in a dose of 128 micrograms did not show any certain protective effects. However lysine-vasopressin in 1.2% Natrosol solution in a dose of 16 micrograms gave significant radioprotection of the rectal mucosa. This dose level has in a previous study not given any significant effects on the systemic circulation. Lysine-vasopressin in Natrosol solution seems to be a suitable combination for further studies.

Animals↗
PubMed1984

Synthesis and characterization of iodinated vasopressin antagonists which retain high affinity for the vasopressin receptor.

The mono- and di-iodinated analogs of lysine and arginine vasopressin have been prepared previously but not well characterized chemically. Their biological activities are greatly reduced with respect to LVP or AVP. In this paper we report a convenient synthesis of iodinated AVP agonists and antagonists, their purification by high performance liquid chromatography, and their characterization by fast atom bombardment mass spectrometry. In contrast to the results obtained with agonists, the mono-iodinated vasopressin antagonist retains virtually the full receptor activity of its non-iodinated parent. This should allow the preparation of labeled vasopressin antagonists of high specific activity for receptor characterization and isolation.

Arginine Vasopressin↗
PubMed1983

Blood pressure and heart rate effect of a vasopressin antagonist in conscious normotensive rats pretreated with exogenous vasopressin.

The blood pressure and heart rate effects of the specific pressor antagonist of vasopressin d(CH2)5Tyr(Me)AVP, 5 micrograms i.v. was evaluated in conscious normotensive rats. Our results suggest that a baroreceptor reflex mediated decrease in sympathetic nerve activity, as reflected by a slowing in heart rate, returns blood pressure to baseline levels shortly after injections of exogenous vasopressin. This has to be taken into account when interpreting the hemodynamic response to vasopressin antagonists in rats pretreated with this vasopressive hormone.

Animals↗
PubMed1978

[1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),4-valine,-8-D-arginine]vasopressin, a potent and selective inhibitor of the vasopressor response to arginine-vasopressin.

As part of a program in which we are attempting the design and synthesis of an antagonist of the antidiuretic response to arginine-vasopressin (AVP) [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),4-valine,8-D-arginine]vasopressin [d(CH2)5VDAVP] was synthesized and assayed for antidiuretic, vasopressor, and oxytocic activities. The required protected intermediate was synthesized by a combination of solid-phase synthesis and an [8 + 1] coupling in solution. d(CH2)5VDAVP has an antidiuretic potency of 0.10 +/- 0.02 unit/mg, less than 1/10000 that of its parent [deamino,4-valine,8-D-arginine]vasopressin (dVDAVP). d(CH2)5VDAVP is a specific antagonist of the vasopressor responses to AVP. It has an antivasopressor pA2 value of 7.68 +/- 0.05 when tested against AVP. It is also an antagonist of the in vitro oxytocic response to oxytocin (pA2 value = 6.62 +/- 0.07). With its negligible antidiuretic activity, absence of oxytocic activity, and its potent and specific ability to antagonize the vasopressor effects of AVP, d(CH2)5VDAVP is one of the most potent and selective vasopressor antagonists reported to date. It should thus be a useful tool with which to probe the possible role(s) that AVP may play in cardiovascular regulation under normal and pathological conditions.

Animals↗
PubMed1993

Influence of sodium and potassium diets on adrenal vasopressin content and direct effects of vasopressin on aldosterone synthesis in adrenocortical cells.

Two questions were investigated to elucidate the adrenal function of arginine vasopressin (AVP) in controlling aldosterone secretion: Are vasopressin tissue concentrations in the adrenal modulated by diets that influence aldosterone secretion? Does its direct stimulation of aldosterone secretion from adrenal cells in vitro suggest that vasopressin plays an important role in controlling aldosterone? Diets that modulate aldosterone secretion from rat adrenals did not modulate concentrations of AVP in this tissue: Adrenal AVP concentrations did not differ significantly between rats on low- and high-sodium (22.9 +/- 3.8 and 32.4 +/- 6.4 pg/g) or between low- and high-potassium (25.6 +/- 2.5 and 12.5 +/- 7.3 pg/g) diets. Although the existence of AVP receptors on adrenocortical cells incubated in vitro and the stability of AVP during cell incubation was confirmed, AVP had only a minor direct effect on steroid secretion in short-term incubations alone and in combination with angiotensin II (A II), potassium and atrial natriuretic factor (ANF). The importance of AVP for an indirect control of aldosterone secretion in vivo is discussed.

Adrenal Cortex↗
PubMed1982

Biological half-lives and organ distribution of tritiated 8-lysine-vasopressin and 1-deamino-8-D-arginine-vasopressin in Brattleboro rats.

The biological half-lives and organ distribution of tritiated 8-lysine-vasopressin and 1-deamino-8-D-arginine-vasopressin were determined in R-Amsterdam rats and in homozygous and heterozygous Brattleboro rats with hereditary central diabetes insipidus. It was found that the biological half-lives of [3H]LVP and [3H]dDAVP in the Brattleboro rats did not differ significantly from that found in the control R-Amsterdam rats. The half-life of [3H]dDAVP proved longer than that of [3H]LVP in all three groups of animals. In the case of [3H]LVP the highest radioactivities were observed in the neurohypophyses, adenohypophyses, and kidneys of both the R-Amsterdam and Brattleboro rats. The accumulation of tritiated material was higher in the small intestine of the Brattleboro rats than in that of the R-Amsterdam animals. In all three groups of rats, [3H]dDAVP was accumulated to the greatest extent in the kidney and the small intestine. The kidney and small intestine contained less radioactivity in homozygous Brattleboro rats than in the controls. There was only a slight radioactivity accumulation in the adenohypophysis and neurohypophysis. From the results it was concluded that the decrease in the rate of enzymatic decomposition may play a role in the increased duration of antidiuretic action of dDAVP. The results have led to the conclusion that the accelerated elimination of vasopressin and its pathologic organ accumulation are probably not involved in the water metabolism disturbance of Brattleboro rats with hereditary diabetes insipidus.

Animals↗
PubMed1998

Arginine vasopressin enhances sympathetic constriction through the V1 vasopressin receptor in human saphenous vein.

BACKGROUND: Arginine vasopressin (AVP) not only acts directly on blood vessels through V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins. METHODS AND RESULTS: Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (3x10[-9] mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.87x10[-7] to 1.04x10[-7] mol/L; P<.05). The V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10[-6] mol/L) prevented the potentiation evoked by AVP. The selective V1 receptor agonist [Phe,2 Orn8]-vasotocin (3x[-10]-9 mol/L) induced potentiation of electrical stimulation-evoked responses, which was also inhibited in the presence of the V1 receptor antagonist (10[-6] mol/L). In contrast, the V2 receptor agonist desmopressin (10[-9] to 10[-7] mol/L) did not modify neurogenic responses, and the V2 receptor antagonist [d(CH2)5, D-Ile,2 Ile,4 Arg8]-vasopressin (10[-8] to 10[-6] mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (10[-6] mol/L) did not affect the potentiating effect of AVP. CONCLUSIONS: The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated.

Aged↗
PubMed2002

[1-deamino-4-cyclohexylalanine] arginine vasopressin: a potent and specific agonist for vasopressin V1b receptors.

To date, there are no vasopressin (VP) agonists that exhibit a high affinity and selectivity for the VP V1b receptor with respect to the V1a, V2, and oxytocin receptors. In this study, we describe the synthesis and pharmacological properties of [1-deamino-4-cyclohexylalanine] arginine vasopressin (d[Cha4]AVP). Binding experiments performed on various membrane preparations revealed that d[Cha(4)]AVP exhibits a nanomolar affinity for V1b receptors from various mammalian species (rat, bovine, human). It exhibits high V1b/V1a and V1b/oxytocin selectivity for rat, human, and bovine receptors. Furthermore, it exhibits high V1b/V2 specificity for both bovine and human vasopressin receptors. Functional studies performed on biological models that naturally express V1b receptors indicate that d[Cha4]AVP is an agonist. Like VP, it stimulated basal and corticotropin-releasing factor-stimulated ACTH secretion and basal catecholamine release from rat anterior pituitary and bovine chromaffin cells, respectively. In vivo experiments performed in rat revealed that d[Cha4]AVP was able to stimulate both ACTH and corticosterone secretion and exhibits negligible vasopressor activity. It retains about 30% of the antidiuretic activity of VP. This long-sought selective VP V1b receptor ligand with nanomolar affinity will allow a better understanding of V1b-mediated VP physiological effects and is a promising new tool for V1b receptor structure-function studies.

Adrenocorticotropic Hormone↗
PubMed2003

A case of a novel mutant vasopressin receptor-dependent nephrogenic diabetes insipidus with bilateral non-obstructive hydronephrosis in a middle aged man: differentiation from aquaporin-dependent nephrogenic diabetes insipidus by response of factor VII and von Willebrand factor to 1-diamino-8-arginine vasopressin administration.

We describe a case of a novel mutant vasopressin 2 receptor (V2R)-dependent nephrogenic diabetes insipidus (NDI) with bilateral non-obstructive hydronephrosis in a middle aged man. This could be distinguished from aquaporin 2 (AQP2)-dependent NDI by the response of factor VIII and von Willebrand factor (vWF) to 1-deamino-8-D-arginine vasopressin (DDAVP) administration. A 47-year-old man was admitted to hospital because of polyuria, which had been present from infancy and was suspected of causing non-obstructive hydronephrosis. His mother's father, the older brother of his mother and his second daughter also all had polyuria. Sodium concentration, osmolality and vasopressin in blood were high, while sodium concentration and osmolality in urine were low. There were no changes in urine osmolality, factor VIII and vWF in response to DDAVP infusion. Neither was heart rate, diastolic blood pressure nor facial flushing affected. These findings suggested this case was V2R-dependent NDI rather than AQP2-dependent NDI. Molecular genetic analysis demonstrated that the patient had a V2R missense mutation involving a substitution of cysteine for arginine at position 104 (R104C) located in the first extracellular loop of the V2R. It was also found that the patient's mother and his second daughter were heterozygous for this R104C mutation.

Aquaporin 2↗
PubMed1989

Interaction of putative vasopressin receptor proteins of rat brain and bovine pituitary gland with an antibody against a nanopeptide encoded by the reverse message of the complementary mRNA to vasopressin.

An antibody directed against the reverse message of the complementary mRNA for arginine vasopressin was demonstrated to be immunoreactive with 62 and 55 kdalton proteins, obtained by affinity chromatography of rat brain and bovine posterior pituitary extracts and believed to be associated with the vasopressin binding site. A similar pattern of immunoreactivity was seen with an anti-idiotypic antibody for arginine vasopressin.

Animals↗
PubMed1991

Effect of vasopressin antagonist d(CH2)5Tyr(Et)VAVP on plasma arginine vasopressin level after osmotic stimulus.

The effect of the vasopressin antagonist d(CH2)5Tyr(Et)VAVP on the immunoreactive arginine vasopressin (AVP) level in plasma was studied in rats after osmotic stimulus. The blood samples were obtained from the eye plexus. An increased AVP level (193.2 +/- 70.0; control: 30.5 +/- 4.3 pmol/l) was detected after the administration of hypertonic NaCl solution. A much higher elevation of AVP level (1180.9 +/- 181.0 pmol/l) was observed when treatment with the antagonist was applied before the osmotic stimulus. The results indicate that this compound exerts a biological effect as a vasopressin receptor blocking agent through a mechanism of competitive antagonism.

Animals↗
PubMed1986

Human vascular vasopressin receptors: analysis with selective vasopressin receptor antagonists.

The vascular activity of arginine vasopressin (AVP) and selective AVP receptor antagonists was investigated in isolated arterial ring segments from human superior mesenteric arteries. AVP elicited a potent and concentration-dependent contraction in human mesenteric arterial rings with an EC50 value of 2.01 X 10(-9) M. The presence or absence of the vascular endothelium did not affect significantly AVP-induced contraction. AVP induced slight, although significant, tachyphylaxis in human mesenteric arteries. The selective vascular (V1) receptor antagonist [d(CH2)5 1Tyr(Me)2]AVP (SK&F 100273) shifted the concentration-response curves for AVP-induced vascular contraction to the right in a parallel manner (KB = 2.23 X 10(-9) M). A mixed V1/V2 receptor antagonist, [d(CH2)5 1D-Tyr(Et)2Val4desGly9]AVP (SK&F 101926), was also a potent antagonist of AVP-mediated vascular contraction; however, inhibition was marked by a nonparallel shift of the concentration-response curves with depression of maximum contraction. Furthermore, a relatively renal (V2) selective receptor antagonist [d(CH2)5 1D-Ile2Val4]AVP (SK&F 101485) was approximately 100-fold less potent at inhibiting AVP-induced vascular contraction (KB = 1.37 X 10(-7) M). These studies illustrate for the first time the in vitro effects of selective vasopressin receptor antagonists in isolated human blood vessels. Studies of other blood vessels and the design of therapeutically useful antagonists should proceed with the hypothesis that the vasopressin receptors mediating vascular contraction in human mesenteric arteries are of the V1 subtype.

Arginine Vasopressin↗
PubMed1985

On the blood-brain barrier to peptides: accumulation of labelled vasopressin, DesGlyNH2-vasopressin and oxytocin by brain regions.

After intracarotid injection of 125I-arginine vasopressin (AVP), 125I- or 3H-lysine vasopressin (LVP), 3H-DesGlyNH2-arginine vasopressin (DGAVP), and 125I- or 3H-oxytocin (OXT), the accumulation of radioactivity was determined in 13 to 18 brain regions and anterior pituitary in rats. Calculated extraction by tight capillary regions amounts to about 1-2% independently of the peptide doses injected (4 X 10(-4) to 5 X 10(-9) mol-1). This indicates a low but measurable extraction of labelled peptides which furthermore is nonsaturable. Among brain regions with tight capillaries, the extraction does not vary obviously. Blood-brain barrier (BBB)-free regions extract up to 30 fold more peptide than BBB-protected regions and the extraction varies considerably between individual regions. Within BBB-free regions, the peptides passed the leaky capillary endothelium, but there is no evidence for a penetration to deeper layers of the brain. It is concluded that endogenous blood-borne peptides cannot pass brain barriers in physiologically significant amounts. This does not exclude a possibility that passive transport of minute but effective amounts might occur if high pharmacological amounts of peptides are injected peripherally. But, as shown, none of the peptides studied possesses properties that favour its passage across the BBB.

Animals↗
PubMed1984

Effect of the vasopressin antagonist d/CH2/5Tyr/Et/VAVP on the antidiuretic action of exogenous and endogenous vasopressin.

The effect of [1-(beta-mercapto-beta, beta- cyclopentamethylene -propionic acid),2-0- ethyltyrosine ,4-valine]-arginine vasopressin on the water metabolism was studied in rats. The compound decreases the antidiuretic action of exogenous vasopressin in Brattleboro rats; in rats without diabetes insipidus it causes temporary polyuria and eliminates the response of antidiuresis to an osmotic stimulus. The results indicate that this compound can block the antidiuretic action of both exogenous and endogenous vasopressin.

Animals↗
PubMed1978

Light- and electron microscopic localization of vasopressin or a vasopressin-like substance in the neurons of the rat suprachiasmatic nucleus.

In the suprachiasmatic nucleus of the rat light microscopic immunostaining for vasopressin reveals a distribution pattern of the immunoreactive material different from that known for the supraoptic nucleus. Among non-stained neurons positive-reacting perikarya display a cap- or tip-like labeling. The area of the suprachiasmatic nucleus is marked by delicate vasopressin-positive fibers. At the ultrastructural level the reaction product, after incubation with anti-vasopressin, is localized in small elementary granules unevenly distributed over the cytoplasm. Groups of axons containing specifically labeled granules contact non-reacting fibers.

Animals↗