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PubMed1988

Vascular vasopressin receptors.

1. Vascular vasopressin receptors are understood because of the specific application of each major technical advance in pharmacology; this review shows that isolated organs, whole animal preparations, hormone synthesis, radioligand binding, and human studies have all played their part. 2. Even so, neither vascular vasopressin receptor heterogeneity nor occupancy-response relationships are fully understood; by way of comparison far more is known about alpha-adrenoceptors. 3. The biochemical pharmacology of vascular vasopressin receptor activation is still in its infancy. Whilst the second messenger molecules resulting from vascular vasopressin receptor activation appear to be component(s) of the pathways of phosphoinositide metabolism, technical difficulties have led investigators to study similar vasopressin receptors in other tissues. 4. It is not certain, for example, that results from hepatic vasopressin receptor studies can be automatically extrapolated to vascular smooth muscle. 5. Lastly, the directions that vascular vasopressin research might take are speculated on. It is not known whether the vascular vasopressin receptor is itself a polymer, whether receptor heterogeneity could be exploited in the clinical uses of vasopressins, nor whether vasopressins are co-released with other neurotransmitters.

Animals↗
PubMed2004

Multiple effects of arginine vasopressin on prostaglandin E2 synthesis in fibroblasts.

Recent evidence supports the viewpoint that vasopressin, a neurohypophyseal peptide, should be also considered as a neuroendocrine modulator of immune and inflammatory responses. In this work we investigated the role of vasopressin in the regulation of prostaglandin E(2) synthesis by human dermal fibroblasts. Recombinant human interleukin-1 beta increased prostaglandin E(2) synthesis in fibroblasts about sixfold. The prostaglandin E(2) response to interleukin-1 beta was attenuated by lower concentrations of vasopressin (10(-10)-10(-9) M). By contrast, higher concentrations (10(-8)-10(-7) M) of vasopressin effected significant enhancement of the interleukin-1 beta-induced prostaglandin E(2) synthesis. In a similar way, vasopressin (10(-8)-10(-7) M), in the absence of interleukin-1, significantly increased prostaglandin E(2) production. An inhibitory effect of lower concentrations of vasopressin was also observed on basal production of prostaglandin E(2). The effects of vasopressin on basal and interleukin-1 beta-induced prostaglandin E(2) synthesis were antagonized by selective vasopressin receptor antagonists. The findings presented here disclose a novel modulatory role of vasopressin on prostaglandin E(2) synthesis in human dermal fibroblasts and suggest a possible role of vasopressin in the regulation of inflammation.

Arginine Vasopressin↗
PubMed2006

A clinical investigation of nocturnal polyuria in patients with nocturia: a diurnal variation in arginine vasopressin secretion and its relevance to mean blood pressure.

PURPOSE: Nocturia is a common lower urinary condition in the elderly population and nocturnal polyuria is recognized as a major factor responsible for nocturia. A functional change in osmotic or nonosmotic control regarding the water-salt balance with aging may contribute to nocturnal polyuria. This study evaluated plasma arginine vasopressin secretion function in symptomatic patients with nocturnal polyuria and the impact of mean blood pressure on nocturnal polyuria. MATERIALS AND METHODS: A total of 29 patients who had nocturnal polyuria with 3 or more voids nightly and were screened with a 24-hour voiding diary were evaluated for their diurnal rhythm of arginine vasopressin secretion and osmotic response during a 5% hypertonic saline infusion test. Moreover, the relationships between the severity of nocturnal polyuria, ie the nocturnal polyuria index, or mean voided volume and mean blood pressure were assessed. RESULTS: Decreased nocturnal baseline arginine vasopressin according to plasma osmolality was found in 11 patients (38%) and the lack of a diurnal rhythm for arginine vasopressin secretion was observed in high proportion. A positive correlation between plasma arginine vasopressin and plasma osmolality was described with a linear regression line, expressed as arginine vasopressin = 0.27 (plasma osmolality - 285), resulting in a 2 to 3 mmol/l upward shift in the threshold of overall plasma arginine vasopressin secretion, although various osmotic sensitivities in arginine vasopressin secretion were observed in individuals. Mean voided volume increased during the night more than during the day (p <0.0001). A significant positive correlation of mean blood pressure with the mean daytime-to-nighttime single voided volume ratio and the nocturnal polyuria index was found (p = 0.0343 and 0.0109, respectively). CONCLUSIONS: An abnormal diurnal variation in arginine vasopressin secretion is highly prevalent in nocturnal polyuria. Moreover, it is relevant to mean blood pressure or sympathetic tone, such that the effects of nonosmotic control seem clinically implicated. Particular emphasis has been applied to the importance of considering comprehensive assessments not only of arginine vasopressin secretion function, but also of the possible underlying cardiovascular condition or hypertension in the treatment modality of nocturnal polyuria.

Aged↗
PubMed1998

Endogenous vasopressin increases acute endotoxin shock-provoked gastrointestinal mucosal injury in the rat.

Administration of a low dose of endotoxin (from Escherichia coli, 3 mg kg(-1), i.v.), which does not affect vascular permeability or blood pressure over 1 h, leads to the release of endogenous vasopressin and damage to the mucosal microvasculature. Thus, endogenous vasopressin could be involved in septic shock. In the present study, we investigated the role of endogenous vasopressin in gastrointestinal mucosal injury induced by acute endotoxin shock, which was generated in rats by administering a high dose of E. coli endotoxin (50 mg kg(-1), i.v.). Tissues were removed 15 min after endotoxin. The vasopressin V1 receptor antagonist, d[CH2]5Tyr[Me]arginine-vasopressin (0.2-1 microg kg(-1), i.v.), was injected 10 min before endotoxin. Monastral blue (30 mg kg(-1), i.v.), which stains damaged vasculature, was injected 10 min before autopsy. Endotoxin reduced systemic arterial blood pressure (from 115+/-5 to 42+/-4 mmHg), generated macroscopic and microvascular injury, and elevated plasma vasopressin levels (from 3.4+/-0.2 to 178+/-16 pg ml(-1)). The vasopressin V1 receptor antagonist reduced this macroscopic injury, and in the vasopressin-deficient Brattleboro rat a similar reduction of gastrointestinal mucosal damage was found. Substantial decreases in endotoxin-induced microvascular damage were observed in each tissue, e.g., the gastric Monastral blue staining was reduced by 47+/-3% and 96+/-3% (P < 0.01) after vasopressin V1 receptor antagonist treatment and in Brattleboro rats, respectively. Vasopressin, acting through its V1 receptors, thus appears to be involved in acute endotoxin shock-provoked gastrointestinal injury.

Animals↗
PubMed1998

Vasopressin opposes locomotor stimulation by ethanol, cocaine and amphetamine in mice.

The effects of arginine8-vasopressin on the stimulation of locomotor activity induced by ethanol, cocaine and amphetamine were examined in DBA/2N mice. Locomotor activity was measured by photocell beam interruption for a period of 45 min following ethanol, cocaine or amphetamine administration. Pretreatment with vasopressin alone in a dose of 2 (but not 1) microg/mouse s.c. reduced locomotor activity. The low dose of vasopressin did not modify the stimulation of locomotor activity induced by i.p. administration of ethanol in doses of either 1.5 or 2 g/kg. The high dose of vasopressin reduced locomotor activity induced by both doses of ethanol, in an apparently additive manner. Cocaine in doses of 15 and 20 mg/kg strongly stimulated locomotor activity, but this stimulation was completely antagonized by pretreatment with 1 microg of vasopressin. Similarly, the stimulation of locomotor activity induced by amphetamine (5 mg/kg) was also blocked by pretreatment with vasopressin. These findings raise the possibility that the effect of vasopressin varies with the extent and nature of dopaminergic involvement in the drug-induced stimulation of activity. For drugs like cocaine or amphetamine which stimulate locomotor activity primarily through the mesolimbic dopaminergic system, vasopressin can completely antagonize the stimulation. For ethanol, which stimulates locomotor activity through action on a number of other neurotransmitters as well as dopamine, vasopressin treatment only reduces its stimulation of locomotor activity in an additive manner. These results suggest a close interaction between vasopressin and dopamine action.

Amphetamine↗
PubMed2000

Prostanoids regulate proliferation of vascular smooth muscle cells induced by arginine vasopressin.

The aim of the present study was to investigate the effect of arginine [Arg(8)]vasopressin (vasopressin) on proliferation of vascular smooth muscle cells and the mechanisms underlying the action of vasopressin. To clarify these issues, we used two different types of vascular smooth muscle cells, cultured adult rat aortic smooth muscle cells and A10 cells, a cell line derived from fetal rat aorta. Vasopressin (10(-8) to 10(-6) M) significantly stimulated the proliferation of rat aortic smooth muscle cells in a dose-dependent manner. In contrast, vasopressin significantly inhibited the proliferation of A10 cells. This inhibition was abolished when A10 cells were treated with indomethacin. Vasopressin stimulated the production of prostanoids several-fold in A10 cells but not in rat aortic smooth muscle cells. These effects were completely blocked by the vasopressin V(1) receptor antagonist, 1-¿1-[4-(3-acetylamino-propoxy)benzoyl]4-piperidyl¿-3, 4-dihydro-2(1H)-quinolinone (OPC21268), but not by the vasopressin V(2) receptor antagonist, (+/-)-5-dimethylamino-1-[4-(2-methylbenzoylamino)benzol]-2, 3,4,5-tetrahydro-1H-benzazepine hydrochloride (OPC31260). These results indicate that vasopressin has diverse effect on proliferation of vascular smooth muscle cells through the vasopressin V(1) receptor, depending on the production of growth regulatory prostanoids.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Vasopressin disrupts radial-maze performance in rats.

The memory enhancing properties of vasopressin, observed in active and passive avoidance procedures, could derive from its influence on central systems, but may also be mediated by its endocrinological properties. Very little is known about the effects of vasopressin on behavior in procedures other than the active and passive avoidance paradigms. The present experiments were designed to assess the effects of vasopressin on behavior observed in the eight-arm radial maze. In Experiment I, male Wistar rats (N = 7), which had been extensively trained to collect food from all eight arms in a radial maze, were subcutaneously injected with different doses of vasopressin 5 min before the start of the session (0.00, 1.25, 3.75, and 6.25 micrograms/kg). In Experiment II, another group of male Wistar rats (N = 7) received the same doses of vasopressin after having been extensively trained to collect food from four of the eight arms. In both experiments, subjects spent more time in the maze as the dose of vasopressin was increased. Vasopressin also disrupted performance by preventing the subjects from visiting all of the baited arms in the maze. Performance thus decreased, not because of the fact that vasopressin interfered with memory processes, but because of the fact that it produced behavioral inhibition. Thus, if vasopressin affects memory processes, such effects are likely to be mediated through vasopressin's actions on endocrine and behavioral systems, rather than through a direct action on the neural substrate underlying memory functioning.

Animals↗
PubMed1994

Vasopressin release and water metabolism in patients with cirrhosis.

Water retention is a complication in many patients with cirrhosis, usually attributed to excessive release of arginine vasopressin. To investigate the responsiveness of arginine vasopressin to osmotic and non-osmotic stimuli and its relationship to free water excretion, we studied 19 patients with cirrhosis under three different conditions: 45 min with legs raised to 60 degrees, to expand the central blood volume; infusion of 1000 ml of 0.45% saline solution to reduce plasma osmolality; and rapid injection of 50 ml of 2 M NaCl to increase plasma osmolality. Both expansion of central blood volume and decrease of plasma osmolality significantly reduced plasma vasopressin levels (from 2.1 +/- 0.6 to 1.39 +/- 0.3 pg/ml, p < 0.04; and from 1.09 +/- 0.25 to 0.41 +/- 0.13 pg/ml, p < 0.0001). The changes in free water excretion differentiated two subgroups of patients during each test: excretors and non-excretors. In the excretors, increased free water excretion was associated with suppressed vasopressin levels (below 0.5 pg/ml) and normal renal function. In the non-excretors, inability to improve free water excretion was associated with high vasopressin levels or with reduced distal delivery of the glomerular filtrate, except in some cases where vasopressin levels had fallen below 0.5 pg/ml and renal function was normal. For these cases the presence of other vasopressin-independent antidiuretic mechanisms is conceivable. The injection of hypertonic saline solution caused significant rises in plasma osmolality (from 287 +/- 1.9 to 292 +/- 1.6 mmol/kg, p < 0.05) and in plasma vasopressin levels (from 1.13 +/- 0.29 to 2.86 +/- 0.52 pg/ml, p < 0.05). These results suggest that vasopressin release in patients with cirrhosis is normally responsive to osmotic and non-osmotic stimuli, although our results show a lower theoretical osmolar threshold for suppression of vasopressin release in non-excretors than in excretors (276 vs 284 mmol/kg).

Adult↗
PubMed2003

[Indications of vasopressin in the management of septic shock].

OBJECTIVE: Vasopressin (antidiuretic hormone) is emerging as a potentially major advancement in the treatment of septic shock. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has haemostatic, gastrointestinal, and thermoregulatory effects. This article reviews the physiology of vasopressin and all the relevant clinical literature on its use in the treatment of septic shock. DATA SOURCES AND EXTRACTION: Extraction from Pubmed database of French and English articles on the physiology and clinical use of vasopressin. The following key words were selected: vasodilatory shock, vasopressin, septic shock, catecholamines, norepinephrine, renal function, diuresis, mesenteric haemodynamic. The collected articles were reviewed and selected according to their quality and originality. DATA SYNTHESIS: Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle. Septic shock causes first a transient early increase in blood vasopressin concentrations that decreases later to very low concentrations compared to other causes of hypotension. Vasopressin infusion of 0.01-0.04 U min(-1) in septic shock patients increases plasma vasopressin concentrations. This increase is associated with a lesser need for other vasopressors. Vasopressin has been shown to produce greater blood flow diversion from non-vital to vital organ beds than does adrenaline. A large randomized clinical trial should be performed to assess its place as a therapeutic agent of septic shock patient.

Clinical Trials as Topic↗
PubMed2002

Possible role of vasopressin in the thermoregulatory response to chlorpyrifos in the rat.

Arginine vasopressin is a naturally occurring antipyretic which is released into the CNS to prevent excessive elevations in body temperature during fever. Circulating levels of arginine vasopressin may also have a role in the tonic control of body temperature. We have found that the organophosphate insecticide chlorpyrifos will raise blood pressure and lower body temperature in the rat. Because arginine vasopressin is a potent hypertensive agent and is capable of lowering core temperature, we suspected that arginine vasopressin may be involved in the thermoregulatory response to chlorpyrifos. To this end, core temperature and motor activity of male and female Sprague-Dawely rats were monitored before and after treatment with the corn oil vehicle or chlorpyrifos (15 mg/kg in females; 30 mg/kg in males; oral) concomitant with injection of a saline vehicle or a type 1 arginine vasopressin antagonist (20 microg/kg in females; 30 microg/kg in males; intraperitoneally). Rats dosed with chlorpyrifos and saline underwent a 2-3 degrees reduction in core temperature >50% decrease in motor activity. The V1 antagonist attenuated the hypothermic effect of chlorpyrifos in both sexes. Chlorpyrifos-induced inhibition in motor activity was unaffected by the V1 antagonist. In another experiment, the V1 antagonist (30 microg/kg) was co-administered with saline or 0.2 mg/kg oxotremorine, a muscarinic agonist that stimulates a heat loss response and partially mimics the effects of chlorpyrifos. The V1 antagonist attenuated the hypothermic effect of oxotremorine in both sexes. Plasma arginine vasopressin levels were determined in male rats 3 hr after corn oil or 30 mg/kg chlorpyrifos. There was no significant effect of chlorpyrifos on plasma levels of arginine vasopressin. That the V1 antagonist blocked the hypothermic effect of chlorpyrifos suggests that the thermoregulatory response to chlorpyrifos is mediated by central and/or systemic vasopressin release. The lack of a significant increase in plasma vasopressin after chlorpyrifos suggests that localized release of vasopressin may be involved in the thermoregulatory response to chlorpyrifos.

Animals↗
PubMedDate not supplied

Magnocellular axons in passage through the median eminence release vasopressin.

Vasopressin (arginine vasopressin, AVP) is present in two types of nerve fibres in the median eminence (ME). First, it is found in nerve terminals that originate in the parvicellular neurones of the hypothalamic paraventricular nucleus (PVN) and abut on the pericapillary space surrounding the fenestrated capillaries of the primary pituitary portal plexus in the external zone (EZ) of the ME. These neurones also synthesize corticotropin-releasing factor (CRF), which acts synergetically with vasopressin to stimulate release of adrenocorticotropin (ACTH) from the pituitary gland (see ref. 7). Second, vasopressinergic axons of the magnocellular neurosecretory system pass through the internal zone (IZ) of the ME to terminate in the neurohaemal contact zone of the neurohypophysis. The involvement of vasopressinergic magnocellular neurones in the control of ACTH secretion is much debated. Of particular interest in this context is the origin of the vasopressin found in pituitary portal blood. Although it has been demonstrated that vasopressin and CRF are present in the same neurosecretory granules of EZ fibres, parallel determinations of vasopressin and CRF in pituitary portal blood have shown alterations of the concentration of vasopressin without a concomitant change in that of CRF. Such a dissociation suggests that either differential release of vasopressin and CRF can occur from a single population of nerve endings, or there are fibres in the pituitary-stalk ME which release vasopressin but not CRF. Here we present evidence for the latter. Our results indicate that stimuli causing depolarization of the axonal membrane in vitro elicit release of vasopressin from nerve fibres in the external and internal zones of the ME.

Adrenocorticotropic Hormone↗
PubMed1994

Products of vasopressin gene expression in small-cell carcinoma of the lung.

Small-cell neuroendocrine carcinoma of the lung is known to express products related to the vasopressin gene, although these products have been reported to sometimes differ from those generated by neurones of the hypothalamo-neurohypophyseal system. To further investigate vasopressin gene expression in neuroendocrine carcinomas, we performed immunohistochemistry on 24 histologically classified small-cell carcinomas using antibodies directed against different regions of the vasopressin precursor. All of the tumours examined contained at least two parts of the vasopressin precursor, suggesting that vasopressin might have a biological role in these tumours and indicating a role for these products in tumour diagnosis and treatment. Sixty-seven per cent of the tumours contained immunoreactivity for all major regions of the precursor: vasopressin, vasopressin-associated human neurophysin, the bridging region between the hormone and the neurophysin, and vasopressin-associated human glycopeptide. However, 33% of the tumours examined appeared to express only part of the vasopressin precursor, as evidenced by the absence of immunoreactivity for the neurophysin and/or the glycopeptide. These results support the proposition that both normal and abnormal vasopressin gene expression occurs in small-cell carcinoma of the lung.

Carcinoma, Small Cell↗
PubMed2006

Vasopressin administration facilitates fluid removal during hemodialysis.

Inadequate secretion of vasopressin during fluid removal by hemodialysis may contribute to the cardiovascular instability that complicates this therapy and administration of exogenous hormone, by supporting arterial pressure, may facilitate volume removal. To test this, we measured plasma vasopressin in patients with end-stage renal disease (ESRD) during hemodialysis and found that despite significant fluid removal, plasma vasopressin concentration did not increase. We further found that ESRD did not alter the endogenous removal rate of plasma vasopressin and that plasma hormone is not dialyzed. Finally, in a randomized, double-blinded, placebo-controlled trial in 22 hypertensive patients, we examined the effect of a constant infusion of a non-pressor dose of vasopressin on the arterial pressure response during a hemodialysis in which the target fluid loss was increased by 0.5 kg over the baseline prescription. We found that arterial pressure was more stable in the patients receiving vasopressin and that while only one patient (9%) in the vasopressin group had a symptomatic hypotensive episode, 64% of the patients receiving placebo had such an episode (P=0.024). Moreover, increased fluid removal was achieved only in the vasopressin group (520+/-90 ml vs 64+/-130 ml, P=0.01). Thus, administration of non-pressor doses of vasopressin to hypertensive subjects improves cardiovascular stability during hemodialysis and allows increased removal of excess extracellular fluid. Inadequate vasopressin secretion during hemodialysis-induced fluid removal is a likely contributor to the intradialytic hypotension that limits fluid removal.

Antidiuretic Agents↗
PubMed1973

Subcellular organization of neurophysins, oxytocin, (8-lysine)-vasopressin and adenosine triphosphatase in porcine posterior pituitary lobes.

Posterior pituitary lobes from young pigs were fractionated by differential and sucrose-density-gradient centrifugation. The distributions of oxytocin and [8-lysine]-vasopressin were measured by bioassay and the distributions of neurophysin-I and -II by radioimmunoassays specific for each of these two proteins. Most of the hormone and neurophysin applied to the density gradient was localized in particles with the density expected of neurosecretory granules. However, the neurosecretory granules were separated into two bands (D and E). A close statistical correlation between the distributions of [8-lysine]-vasopressin and neurophysin-I, and of oxytocin and neurophysin-II on the gradients, suggested that in vivo porcine neurophysin-I binds [8-lysine]-vasopressin within one population of granules and porcine neurophysin-II binds oxytocin within another type of granule. However, there was no significant separation of oxytocin and vasopressin in fractions D and E. The molar ratios of hormones and neurophysins indicated that there was insufficient of either neurophysin to bind the [8-lysine]-vasopressin in the granule fractions or in the whole gland. Polyacrylamide-gel electrophoresis showed that only bands corresponding in mobility to porcine neurophysins-I, -II and -III were present in large amounts in the whole gland and in the granule fractions. The component with the mobility of neurophysin-III was, however, relatively enriched in whole young glands and granule fractions compared with adult gland extracts. It is suggested that the vasopressin that cannot be assigned to neurophysin-I may occur in (a) vesicles containing vasopressin but no neurophysin, (b) vesicles containing vasopressin and a protein that cannot be quantified by the radioimmunoassays used, such as porcine neurophysin-III, or (c) normal vasopressin-neurophysin granules which have accumulated extra vasopressin. Band E of the gradient was rich in adenosine triphosphatase activity, whereas band D possessed very little of this enzyme.

Adenosine Triphosphatases↗
PubMed1994

Vascular responses to vasopressin antagonists in man and rat.

1. The effects of the non-peptide arginine vasopressin V1 receptor antagonist (OPC-21268) and the non-peptide V2 receptor antagonist (OPC-31260) on vasopressin-induced contraction of human internal mammary arteries and rat mesenteric resistance arteries were investigated. 2. In human internal mammary arteries, the non-peptide V1 receptor antagonist, OPC-21268, failed to antagonize vasopressin-induced contraction at low concentrations and potentiated the contraction at higher concentrations (300 nmol/l, P < 0.05). A peptide selective V1 receptor antagonist ([d(CH2)5, sarcosine7]arginine vasopressin) potently inhibited the vasopressin-induced contraction, indicating the presence of functionally constrictor V1 receptors in human internal mammary arteries. Both peptide (desGly-NH29[d(CH2)5, D-Ile2, Ile4]arginine vasopressin) and non-peptide 'selective' V2 receptor antagonists (OPC-31260, 3 mumol/l) significantly antagonized vasopressin-induced contraction (P < 0.01), indicating partial V1 receptor antagonist activity. 3. The vasopressin-induced contraction in human internal mammary arteries was reversed by high concentrations of the non-peptide V2 receptor antagonist, OPC-31260, but not by the non-peptide V1 receptor antagonist, OPC-21268. 4. The effects of OPC-21268 and OPC-31260 were specific to vascular vasopressin receptors as neither compound influenced endothelin- or noradrenaline-induced contraction in human internal mammary arteries. 5. In rat mesenteric resistance arteries, both OPC-21268 (10 nmol/l) and OPC-31260 (1 mumol/l) antagonized vasopressin-induced contraction (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Effects of vasopressin on human renal arteries.

The effects of vasopressin were studied in isolated rings from branches (2-3 mm in external diameter) of human renal arteries obtained from 18 patients undergoing nephrectomy for non-obstructive neoplasia. In arterial rings under resting tension, vasopressin produced concentration-dependent and endothelium-independent contractions with an EC50 of 9.1 X 10(-10) molL-1. The vasopressin V1 receptor antagonist d(CH2)Tyr(Me)AVP (10(-6) molL-1) displaced the control curve to vasopressin 564-fold to the right in a parallel manner. In precontracted arterial rings and previously treated with the V1 antagonist (10(-6) molL-1) vasopressin caused endothelium-independent relaxation. The relaxation to vasopressin was reduced significantly by indomethacin (10(-6) molL-1) and unaffected by the V1/V2 receptor antagonist desGly d(CH2)5-D-Tyr(Et)ValAVP(10(-6) molL-1) or by NG-nitro-L-arginine methyl ester (10(-4) molL-1). These observations indicate that vasopressin is primarily a constrictor of human renal arteries by V1-receptor stimulation. Vasopressin causes prostaglandin-mediated dilation of human renal arteries only if V1-receptor blockade is present. The effects of vasopressin on human renal arteries may be relevant in those clinical situations characterized by increased plasma vasopressin levels.

Adult↗
PubMed2000

The effects of ionotropic agonists of excitatory amino acids on the release of arginine vasopressin in rat hypothalamic slices.

The effects of ionotropic excitatory amino acids agonists on the release of vasopressin from rat hypothalamic slices were studied. Incubation with increasing doses of NMDA, kainate or AMPA decreased the release of vasopressin in a dose-dependent manner. The values of the IC50 were 1.0, 9.6, or 3.7 x 10-8 M, respectively. The inhibitory effect of the various excitatory amino acids tested was blocked by coincubation with their respective antagonists. Vasopressin secretion was stimulated to 140.3 +/- 7.6% of controls when the slices were obtained from chronically (7 days) salt-loaded rats. Addition of 1 x 10-7 M NMDA or 1 x 10-6 M kainate to the incubation medium antagonized the salt loading-induced increase in vasopressin release. Incubation with 1 x 10-4 M tetrodotoxin did not change basal vasopressin release, but it blocked the decrease in vasopressin secretion induced by 1 x 10-7 M NMDA or 1 x 10-6 M kainate or 1 x 10-6 M AMPA. Incubation with 1 x 10-5 M phaclophen (a GABAB antagonist) and 1 x 10-5 M bicuculline (a GABAA antagonist) was without effect on basal vasopressin secretion while it reversed the inhibition of vasopressin release induced by 1 x 10-7 M NMDA. Incubation with 1 x 10-6 M GABA alone decreased vasopressin secretion to 64.6 +/- 6.9% of control values. The inhibitory effect of GABA did not change when 1 x 10-7 M NMDA was added to the incubation medium. These findings demonstrate that ionotropic excitatory amino acids agonists inhibit vasopressin secretion from hypothalamic slices. They strongly suggest that this inhibitory effect is mediated through local GABAergic interneurones.

Animals↗
PubMed2003

Long-term effects of ciliary neurotrophic factor on the survival of vasopressin magnocellular neurones in the rat supraoptic nucleus in vitro.

The use of hypothalamic organotypic cultures for the long-term study of mechanisms in magnocellular neurones (MCNs) of the hypothalamic-neurohypophysial system has been limited by the relatively poor maintenance of the vasopressin MCNs in vitro. Recent studies have shown that addition of ciliary neurotrophic factor (CNTF) to the media significantly reduced the apoptosis of both oxytocin and vasopressin MCNs. Here, we studied various temporal factors in the CNTF treatment that can influence the efficacy of MCN survival. Immunohistochemistry was used to identify and count surviving vasopressin and oxytocin MCNs in the supraoptic nucleus (SON) in hypothalamic slices cultured in the presence of CNTF (10 ng/ml media) for various time intervals, and in situ hybridization for vasopressin mRNA was used to evaluate the vasopressin mRNA gene expression in the SON under the same conditions. The presence of CNTF in the medium for 10 days produced a maximal increase in the survival of vasopressin MCNs (by 11-fold) and in the survival of oxytocin-MCNs (by approximately four-fold) over controls. These effects persisted for an additional 7-10 days even in the absence of CNTF. The ability of CNTF to increase survival of the MCNs or increase vasopressin mRNA levels in the SON required that the CNTF be present during the initial 7-10 days of culture. CNTF failed to rescue vasopressin or oxytocin MCNs when added to the media only for the last 7 days of a total of 14 days in vitro. Similar results were observed when SON vasopressin mRNA levels were measured. These results indicate that the presence of CNTF is required at the outset to rescue the vasopressin and oxytocin MCN from axotomy induced apoptosis, and that, after 10 days in CNTF, the MCNs no longer require the CNTF for survival.

Animals↗