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 847 records · Page 47Linked to original sources
PubMed2002

Increased contraction to noradrenaline by vasopressin in human renal arteries.

OBJECTIVE: Arginine vasopressin (AVP) not only acts directly on blood vessels through vasopressin V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments. The aim of the present study was to assess whether subpressor concentrations of AVP could contribute to an abnormal adrenergic contractile response of human renal arteries. METHODS: Renal artery rings were obtained from 27 patients undergoing nephrectomy. The rings were suspended in organ bath chambers for isometric recording of tension. RESULTS: AVP (10(-10) mol/l) and the vasopressin V1 receptor agonist [Phe2, Orn8]-vasotocin (10(-10) mol/l) produced a leftward shift of the concentration-response curve to noradrenaline (half-maximal effective concentration decreased from 1.1 x 10(-6) mol/l to 3.1 x 10(-7) mol/l). The enhancement of noradrenaline-induced contractions was inhibited by the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10-8 mol/l) and unaffected by endothelium removal or pretreatment with the inhibitor of nitric oxide (NO) synthase NG-monomethyl-l-arginine (l-NMMA). The vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) (10(-10)-10(-8) mol/l) did not modify contractile responses to noradrenaline. In the presence of the dihydropyridine calcium antagonist nifedipine (10(-6) mol/l), vasopressin failed to enhance the contractile response to noradrenaline. CONCLUSIONS: The results demonstrate that subpressor concentrations of vasopressin potentiate the contractile effects of noradrenaline without intervention of the NO system. The effects appear to be mediated by vasopressin V1 receptor stimulation, which brings about an increase in calcium entry through dihydropyridine-sensitive calcium channels.

Aged↗
PubMedDate not supplied

Role of the renin-angiotensin system in isoprenaline-induced vasopressin release.

We examined whether the activation of the renin-angiotensin system after intramuscular isoprenaline injection contributes to the simultaneous increase in vasopressin release. Plasma concentrations of vasopressin and angiotensin II were measured in conscious rats using specific radioimmunoassays. Intravenous infusions of angiotensin II caused a dose-dependent increase in vasopressin release. Intravenous infusions of the angiotensin II antagonist saralasin did not diminish the isoprenaline-induced vasopressin release. However, the curve relating the isoprenaline-induced decrease in blood pressure and the concomitant increase in vasopressin levels was shifted to the right and no longer linear in saralasin-treated rats. Nephrectomy diminished the vasopressin release caused by isoprenaline when compared to sham-operation. The correlation between the decrease in blood pressure and the simultaneous vasopressin release was changed in a strikingly similar manner by nephrectomy and by saralasin infusions. It may be concluded that small doses of isoprenaline, which cause only minor decreases in blood pressure, induce vasopressin release via the renin-angiotensin system. However, the contribution of this system to vasopressin release declines as hypotension becomes more severe.

Angiotensin II↗
PubMed1986

Vasopressin and hypertension in man.

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.

Blood Pressure↗
PubMed2004

Effect of vasopressin on postresuscitation ventricular function: unknown consequences of the recent Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.

OBJECTIVE: To compare the effect on postresuscitation left ventricular function of vasopressin vs. epinephrine used during cardiopulmonary resuscitation in a swine model of prolonged prehospital ventricular fibrillation. DESIGN: Prospective, randomized experimental study. SETTING: University large animal resuscitation research laboratory. SUBJECTS: Forty-eight swine (29 +/- 1 kg). INTERVENTIONS: Resuscitation after 12.5 mins of untreated ventricular fibrillation, randomizing animals during cardiopulmonary resuscitation to treatment with epinephrine, vasopressin, or vasopressin followed by a vasopressin antagonist administered in the postresuscitation period. MEASUREMENTS AND MAIN RESULTS: Serial measurements of left ventricular systolic and diastolic function (prearrest, postresuscitation at 30 mins and 6 hrs) and 24-hr survival. Animals receiving vasopressin had more postresuscitation left ventricular dysfunction than those receiving epinephrine (p < .05). The vasopressin antagonist produced vasodilation and improved early postresuscitation left ventricular systolic and diastolic function but did not have a lasting effect on such postresuscitation ventricular function and decreased 24-hr survival compared with the use of vasopressin alone (3/16 vs. 10/16 survivors; p < .05). CONCLUSIONS: Vasopressin use during cardiopulmonary resuscitation results in worse postresuscitation left ventricular function early but did not compromise 24-hr outcome. Reversal of vasopressin's effect with a specific V-1 antagonist in the postresuscitation period did not improve survival.

Animals↗
PubMed1986

Development of a cytochemical assay for plasma vasopressin: application to studies on water loading normal man.

A cytochemical assay has been developed to measure human plasma arginine vasopressin. It is based on the stimulation of Na+-K+, ATPase activity located in the outer medulla of the rat kidney, and is capable of detecting very low plasma arginine vasopressin concentrations, limit of detection 0.01 pmol/l. Specificity for vasopressin stimulation of the enzyme is conferred on the assay by the use of specific vasopressin antiserum. Index of precision of the assay is 0.21. Degradation of arginine vasopressin in plasma in inhibited by phenanthroline. Samples may be stored up to 8 weeks at -70 degrees C. Intra- and inter-assay coefficients of variation were 22% (n = 8) and 104% (n = 12), respectively. A sustained water load in eight healthy male adults caused a fall in plasma osmolality from a basal of 286.5 +/- 2.0 (mean +/- SEM) to 279.2 +/- 2.4 mmol/kg after the load (P less than 0.001), which was associated with a reduction in urine osmolality from 867 +/- 54 to 69 +/- 3 mmol/kg. Plasma immunoreactive arginine vasopressin fell from 1.3 +/- 0.3 pmol/l to become undetectable (less than 0.3 pmol/l), but plasma cytochemical arginine vasopressin decreased from 0.96 +/- 0.14 to 0.07 +/- 0.02 pmol/l. There was a curvilinear relationship between plasma osmolality and plasma cytochemical arginine vasopressin, which militated against the concept of an osmotic threshold for vasopressin release.

Adult↗
PubMed1996

Changing effect of i.c.v. IL-1 beta on vasopressin release in anaesthetized, female rats at different stages of lactation: role of prostaglandins and noradrenaline.

Interleukin-1 beta stimulates oxytocin and vasopressin release in conscious, male rats and causes a rise in blood pressure. These experiments were done to : A) examine the effect of i.c.v. interleukin-1 beta (1 ng/microliter) on circulating levels of vasopressin in female rats at different stages of lactation and B) determine if alpha-adrenergic mechanisms and/or prostaglandins were involved as mediators. Urethane-anaesthetized nonlactating rats and rats at Day 7, 10, 20 and 26 of lactation were set up for arterial blood sampling and i.c.v. injections. One mL blood samples were obtained in one min periods before, and at 1, 2.5, 5, 10, 30, 60 and 120 min after the following treatments: i.c.v. treatment with either interleukin-1 beta (1 ng in 1 microliter PBS-BSA) or PBS-BSA (1 microliter) as a vehicle control; or i.c.v. treatment with interleukin-1 beta following pretreatment with either phentolamine (1.7 micrograms/microliter i.c.v.) or indomethacin (1 microgram/microliter i.c.v.). As blood was sampled, isotonic saline was infused (1 mL per min) and blood pressure was monitored to minimize any hypovolemic effects due to sampling. Extracted plasma was assayed using a specific vasopressin radioimmunoassay. Interleukin-1 beta i.c.v. stimulated the release of vasopressin above that elicited by PBS-BSA alone in non-lactating rats resulting in an approximate 1.2 to 2-fold increase in plasma hormone levels. Throughout the first half of lactation, vasopressin responsiveness to i.c.v. interleukin-1 beta treatment was markedly attenuated. In latter stages of lactation, the response recovered and resembled that of non-lactators around the time of weaning. Prostaglandins consistently mediate a stimulatory action of interleukin-1 beta on vasopressin release whereas alpha-adrenergic mechanisms mediate a depression of interleukin-1 beta-induced vasopressin release during the early to middle stages of lactation. It is possible that the depression in interleukin-1 beta-stimulation of vasopressin release in early to mid-lactation is conducive for nursing to occur and that the increase in vasopressin responsiveness towards the latter stages of lactation represents a component of the weaning process.

Anesthesia↗
PubMed1980

N.M.R. and equilibrium dialysis studies of the interaction of bovine neurophysin-1 with vasopressin and small peptides.

The binding to bovine neurophysin of lysine-vasopressin and of lysine-vasopressin selectively deuterated at the protons ortho to the tyrosine hydroxyl was studied by proton n.m.r. and equilibrium dialysis. The principal object of these studies was to investigate reports that, at standard salt concentrations, neurophysin contained a second site specific for vasopressin. At pH 6, the effects of neurophysin-I on the line-width, longitudinal relaxation rate and nuclear Overhauser properties of the lysine-vasopressin tyrosine ring protons were interpretable in terms of a slow-exchange 1:1 interaction between lysine-vasopressin and neurophysin. Additionally, n.m.r. competition studies between lysine-vasopressin and L-phenylalanyl-L tyrosinamide suggested 1:1 competition for a single binding site on neurophysin. No evidence pointing to a significant second lysine-vasopressin-binding site was obtained from the n.m.r. studies. The lack of a moderately strong second binding site for lysine-vasopressin at neutral pH was also indicated by equilibrium dialysis studies at relatively high free hormone concentrations. These studies demonstrated only a single thermodynamically significant site for either oxytocin or vasopressin and failed to confirm a reported effect of LiCl on the number of sites available to oxytocin. It is suggested that secondary sites for the hormones are probably markedly weaker and less specific than reported elsewhere.

Amino Acids↗
PubMed1976

The effect of high rates of vasopressin administration on renal potassium and sodium excretion during potassium loading in the sheep.

1 The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep. 2 Adrenalectomized sheep were infused with 0.43 M KCl at 2 ml/min for 2-2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute-free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (COsm) and solute-free water reabsorption (TcH2O) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration. 3 After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute-free water reabsorption to values above those anticipated from the pre-vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period. 4 Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returnied to values which approximated the pre-vasopressin relations between plasma potassium and the urinary excretions of these ions. 5 Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant. 6 The large increments in potassium excretion (averaging greater than 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.

Animals↗
PubMed1987

L-vasopressin inhibits oxytocin-induced increases of plasma levels of insulin conscious dogs.

Oxytocin is known to increase plasma levels of insulin, glucagon and glucose in dogs. Plasma levels of vasopressin rise during stressful conditions. Since vasopressin counteracts several oxytocin-induced effects, it was decided to study how vasopressin influences the oxytocin-induced elevation of plasma levels of insulin, glucagon and glucose. Therefore oxytocin at 0.11 (which gives rise to physiological plasma concentrations) was infused i.v. for 10 min into fasted, conscious dogs either alone or in combination with 0.033 or 0.17 nmol kg-1 h-1 of L-vasopressin. Accordingly, 1.1 nmol kg-1 h-1 of oxytocin was infused alone or in combination with 0.67 or 1.7 nmol kg-1 h-1 of L-vasopressin. Repeated blood samples were drawn during and after the infusions and insulin and glucagon levels were determined by radioimmunoassay. Plasma levels of insulin increased three- and six-fold in response to 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, respectively, and the elevations were inhibited by L-vasopressin. Slight (1.5-fold) increases in plasma levels of glucagon were observed following 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, although the effect was significant only after the latter dose. Concomitant infusion with L-vasopressin did not markedly influence the effect caused by oxytocin. Small, insignificant increases in blood glucose levels were induced by both doses of oxytocin. These effects were not affected by concomitant infusions of L-vasopressin. The insulin levels rose before glucose levels suggesting that oxytocin stimulates the release of insulin without a previous rise in glucose levels. In conclusion, it has been shown that vasopressin, in amounts which give rise to physiological plasma concentrations, inhibits oxytocin-induced effects on insulin levels, and that oxytocin stimulates the release of insulin via a mechanism which is independent of elevations in blood glucose levels.

Animals↗
PubMed1995

Vasopressin and oxytocin in stress.

Though oxytocin and vasopressin are similar in structure and are produced in the same brain regions, they show specific responses under stress conditions. In humans, increases in peripheral blood vasopressin appear to be a consistent finding during many acute stress situations, while in rats, vasopressin secretion is unresponsive to several stimuli known to induce ACTH and catecholamine release. Even decreases in vasopressin levels during stress were described. In accordance with others, we observed enhanced vasopressin release in response to stress stimuli with an osmotic component such as hypertonic saline injection but also during exposure of rats to a warm environment. Immobilization stress which fails to induce vasopressin release was reported to increase hypothalamic vasopressin mRNA and plasma vasopressin levels in chronically adreno-demedullated rats. Unlike vasopressin, oxytocin may be considered a typical stress hormone responding to osmotic as well as other stress stimuli. We found that acute exposure of rats to immobilization stress resulted in an increase in oxytocin mRNA level. In addition, we have shown that magnocellular neurons of the paraventricular nucleus, but not the supraoptic nucleus, are essential for oxytocin release during immobilization stress. The release of posterior pituitary hormones represents an important component of the stress response.

Animals↗
PubMed1969

The release of vasopressin in response to haemorrhage and its role in the mechanism of blood pressure regulation.

1. The release of vasopressin in response to haemorrhage and the effects of vasopressin infusions on blood pressure and heart rate have been investigated in anaesthetized dogs. Haemorrhage was produced by the method of Lamson & de Türk (1945), which allows for a precise control of the changes in arterial blood pressure.2. Blood samples were collected from an external jugular vein, from a femoral vein or from a femoral artery and extracted with alcohol; blood extracts were assayed for antidiuretic activity.3. Haemorrhage experiments showed that vasopressin secretion is increased when the fall in diastolic blood pressure (diastolic DeltaP) is 25 mm Hg or more. Mild hypotensions (diastolic DeltaP ranging from 21 to 30 mm Hg) produce an average fourfold increase in the concentration of vasopressin in blood. Such increase is maintained throughout the oligaemic period. Severe hypotensions produce, in most cases, a biphasic secretory response, with an initial high peak followed by a lower, constant, secretory plateau. In all experiments, the retransfusion of blood restored vasopressin to control levels.4. Vasopressin infusion experiments showed that the amounts of hormone secreted in response to haemorrhage are sufficient to cause vasopressor response, provided that the buffering action of blood pressure regulation mechanisms is suppressed. It was also found that the amounts of vasopressin secreted in response to haemorrhage are apparently adequate, if the function of such secretion is to combat the hypotension which follows haemorrhage.5. The effect of hypophysectomy on the blood pressure of animals previously submitted to bilateral division of the vagi and sinus nerves (deafferented animals) was also investigated. It was found that hypophysectomy is followed by a fall in arterial blood pressure which is positively correlated to the previous existing amounts of vasopressin. The time course of this hypotension is similar to that following the stopping of an infusion in a deafferented hypophysectomized animal. In some experiments it was shown that, following hypophysectomy, blood pressure can be restored to its pre-hypophysectomy level by an adequate infusion of vasopressin.6. It is proposed that the release of vasopressin in response to stimuli arising from cardiovascular sensory receptors plays a part in the mechanism of blood pressure regulation.

Animals↗
PubMed1977

Characterization of the responses of oxytocin- and vasopressin-secreting neurones in the supraoptic nucleus to osmotic stimulation.

1. Extracellular action potentials were recorded from forty antidromically identified single units in the supraoptic nucleus of lactating, urethane-anaesthetized female rats. The activity was monitored both during reflex milk ejection and during an increase of 10-15 m-osmole/kg in plasma osmotic pressure induced by intraperitoneal injection of 1 ml. of 1.5 M-NaCl solution.2. About half (eighteen) the cells showed a burst of activity before reflex milk ejection and were dubbed oxytocin cells. Oxytocin cells responded to a hypertonic injection with a smooth sustained threefold increase in firing rate.3. The remainder (twenty-two) showed no burst of activity before reflex milk ejection and were dubbed vasopressin cells. Vasopressin cells doubled their firing rate as plasma osmotic pressure increased. Neither cell type increased its firing rate after injections of isotonic NaCl.4. A phasic firing pattern was rarely seen in slow firing vasopressin cells (< 2 spikes/sec) but was seen in almost all vasopressin cells (twelve out of fourteen) firing between 3 and 8 spikes/sec. Above 8 spikes/sec, some vasopressin cells fired continuously. Phasic firing was only once encountered in an oxytocin cell.5. The firing rate of both oxytocin and vasopressin cells decreased when plasma osmotic pressure was reduced 10-15 m-osmole/kg by an intragastric water load of 10 ml.6. Hypothalamic cells lying just outside the supraoptic nucleus did not show a consistent response to injection of hypertonic NaCl.7. Clearly, both oxytocin and vasopressin cells are osmoresponsive, but phasic firing is characteristic of stimulated vasopressin cells. Thus, osmotic activation allows discrimination between oxytocin- and vasopressin-secreting neurones.

Action Potentials↗
PubMed1979

Phasic firing enhances vasopressin release from the rat neurohypophysis.

1. Isolated rat neural lobes were incubated in vitro and electrically stimulated to release vasopressin. The released vasopressin was assayed using a radioimmunoassay and there was a reasonably good correlation (r = 0.81) between results obtained with this assay and those obtained by bioassay with the rat blood pressure method.2. Regular stimulation at frequencies of 5, 10 and 20 Hz released progressively more vasopressin and the release could be blocked by addition of tetrodotoxin to the incubation medium.3. Stimulation with pulse patterns derived from tape recordings of phasically firing units in the supraoptic nucleus of dehydrated rats released more vasopressin than the same number of pulses regularly spaced in time. In the range 2-8 pulses/sec vasopressin release was related to the pulse frequency within the bursts (r = 0.90) and the number of short (< 100 msec) interpulse intervals (r = 0.92). Vasopressin released per pulse increased over the frequency range 3-6 pulses/sec, but above 6 pulses/sec vasopressin release per pulse tended to diminish.4. We conclude that phasic firing of vasopressin neurosecretory cells may enhance vasopressin release in vivo and that an important factor in determining release is the number of short interspike intervals.

Action Potentials↗
PubMed1987

Contractile effects of perivascularly applied vasopressin on the pial artery of the cat brain.

1. The effects of perivascularly applied vasopressin on the diameter of pial arteries (control 298 +/- 14 S.E. micron) of the brain were examined after chronic implantation of a cranial window in fifteen anaesthetized cats. 2. Application of vasopressin resulted in a dose-dependent contraction. The threshold concentration for contraction was 3 X 10(-10) M, the half-maximal effective concentration (ED50) (1.6 +/- 0.2) X 10(-9) M, and the maximum reduction in artery diameter 37 +/- 2%. 3. The contraction was powerfully inhibited by perivascular application of a 10(-7) M solution of the vasopressin antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin. 4. Perivascular application of noradrenaline induced a dose-dependent contraction of the pial artery. The ED50 was (8.9 +/- 2.5) X 10(-7) M, and the maximum reduction in artery diameter was 33 +/- 2%. 5. Such noradrenaline-induced contraction was not modified at all in the presence of a subthreshold dose (2 X 10(-10) M) of vasopressin (P greater than 0.05, for the over-all difference in size of the contraction, ED50 and maximum contraction). 6. In another experimental setting it was also found that neither the subthreshold nor a suprathreshold (10(-9) M) dose of vasopressin modified the contraction induced by 10(-6) M-noradrenaline (P greater than 0.05, compared to the contraction in the absence of vasopressin). 7. Thus a powerful and sensitive contractile response of the pial arteries to perivascularly applied vasopressin was demonstrated. However, the modifying effect of vasopressin on the contraction induced by perivascularly applied noradrenaline was minimal.

Animals↗
PubMed1997

A new linear V1A vasopressin antagonist and its use in characterizing receptor/G protein interactions.

We characterized a new iodinated, high affinity, linear V1a vasopressin antagonist, phenylacetylD-Tyr(Et)Phe-Gln-Asn-Lys-Pro-Arg-Tyr-NH2. The antagonist bound specifically to the V1a vasopressin receptor in crude rat liver membranes with an apparent Kd value of 0.168 nM. This affinity is approximately 1 order of magnitude greater than that of the natural agonist, vasopressin. The inhibitory activity of the antagonist can be demonstrated by its inability to elicit activation and uncoupling of G proteins from the receptor. Thus, after occupancy of receptor sites in rat liver membranes with labeled antagonist and detergent solubilization, the labeled receptor (approximately 60 kDa) was eluted as a stable 400-kDa complex on size-exclusion chromatography. In contrast, when the receptor sites were occupied by the agonist [3H]vasopressin, the receptor eluted as a 60-kDa peak. Coincubation of membranes with iodinated antagonist and an excess of unlabeled vasopressin caused both reduced antagonist binding and a complete shift from the 400-kDa to the 60-kDa peak. The addition of vasopressin to unliganded 400-kDa fractions resulted in a 75% increase in [35S]guanosine-5'-O-(3-thio)triphosphate binding activity, indicating that the 400-kDa fraction contains complexes between the V1a receptor and G proteins. The vasopressin-elicited increase was inhibited by antagonist. Using specific antibodies and immunoadsorption to protein A/Sepharose columns, we found that G protein isotypes G(alpha q/11), G(alpha i3), and G(alpha s), and effector enzymes PLC-beta1, PLC-gamma2 and PLA-2 were associated with the antagonist-labeled receptor in the 400-kDa fraction. Because the 400-kDa complex was found in the absence of ligand, the V1a receptor and the appropriate G proteins and effector enzymes are likely preassociated with each other and do not aggregate after antagonist addition. The association of V1a receptor with the different specific G proteins and effector enzymes is consistent with the multiple actions of vasopressin on liver cells. Antibodies directed against a portion of the carboxyl-terminal domain of the V1a receptor interacted with 60-kDa antagonist-occupied receptor but not with receptor in the 400-kDa complex. These results suggest that the carboxyl-terminal region of the receptor is sterically hindered when coupled to G proteins. The iodinated linear vasopressin antagonist therefore allows stable receptor/G protein complexes and can be an important tool (along with the antisera) for use in the study of factors that control V1a receptor/G protein coupling.

Animals↗
PubMed1981

Vasopressin function in familial cranial diabetes insipidus.

A family suffering from cranial diabetes insipidus, that extends over 4 generations, is described. Inheritance of polyuria was autosomal dominant. Vasopressin function was studied in members of the last 2 generations, 4 of whom had polyuria. Osmoregulation of vasopressin secretion was assessed by infusion of hypertonic saline. Plasma vasopressin remained undetectable in one patient, while 2 others had very blunted vasopressin responses to osmotic stimulation. Three non-osmotic stimuli were applied. Controlled hypotension produced by trimetaphan infusion and insulin-induced hypoglycaemia did not increase plasma vasopressin but apomorphine-induced nausea caused a minimal rise in plasma vasopressin to 0.7 pg/ml. Polyuria and thirst resolved with antidiuretic therapy in all patients studied. Congenital absence of vasopressin as in Brattleboro rats is unlikely to account for diabetes insipidus in this disorder since small increases in vasopressin have been demonstrated in these patients. In view of previous post-mortem findings, familial cranial diabetes insipidus is most likely to be due to degeneration of vasopressin-synthesizing neurones.

Adult↗
PubMed1983

Role of vasopressin in the control of arterial pressure.

Elevations in the circulating levels of vasopressin within the physiological range (less than 30 fmol X mL-1) in conscious animals cause vasoconstriction of resistance vessels, the most profound effect occurring in the muscle, skin, and intestinal vascular beds. In the organism with normal baroreceptor function, the vasoconstriction is not expressed as an increase in arterial pressure because of a corresponding fall in cardiac output associated with enhanced cardiovascular reflex activity. When compensatory reflex mechanisms are impaired (baroreceptor-denervated dogs, patients with autonomic insufficiency, hypertensive rats), the vasoconstrictor activity of vasopressin is exposed and is reflected as an increase in arterial pressure. Inactivation of the vasopressin system alone by hypophysectomy or by administration of antagonists of the pressor activity of vasopressin is often accompanied by compensatory activation of the renin-angiotensin system. Thus, under certain conditions, the vasopressin system and the renin-angiotensin system operate as reciprocal or redundant mechanisms in the control of resistance vessels and of arterial pressure. In two rat models of hypertension (spontaneously hypertensive rats and DOC-salt hypertensive rats) plasma levels of vasopressin are elevated, inactivation of the vasopressin system lowers arterial pressure, and pressor responsiveness to the peptide is enhanced. The enhanced pressor responsiveness appears related in part to impaired reflex activity. The mechanism of the impaired reflexes is unknown but in spontaneously hypertensive rats it might be related to a vasopressin deficit in the paraventricular nucleus and brain stem. The evidence is consistent with the possibility that vasopressin is one factor among many that may play a role in the maintenance of arterial pressure in the adult spontaneously hypertensive rat and in the development and maintenance of the hypertensive state in DOC-salt hypertensive rats.

Angiotensin II↗
PubMed1985

Regulation of plasma vasopressin in insulin-dependent diabetes mellitus.

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be accounted for totally by recognized osmotic or nonosmotic stimuli. To investigate the possibility that regulation of vasopressin secretion is abnormal in this disease, we characterized the vasopressin response to osmotic and hemodynamic stimuli in five uncomplicated, well-controlled insulin-dependent diabetics, and compared the results with those found in nondiabetic volunteers. During osmotic stimulation with hypertonic saline, plasma vasopressin increased in close linear correlation with plasma osmolality or sodium in both groups. However, in the diabetics, the lines describing the relationships between plasma sodium and vasopressin were shifted significantly to the left of normal, suggesting resetting of the osmostat. This shift was not due to abnormal stimulation by hyperglycemia, because increasing plasma glucose and osmolality by intravenous infusion of hypertonic dextrose produced no increase in plasma vasopressin in diabetics or normals. Tilt tests produced a slightly exaggerated increase in plasma vasopressin in diabetics, but their basal and upright pulse rate, blood pressure, plasma renin activity, norepinephrine, and hematocrit were all normal. The results indicate that in diabetic patients the osmoreceptor for osmotic regulation of vasopressin secretion is reset in such a way that higher plasma vasopressin levels are observed at comparable levels of plasma sodium. The exact cause and consequence of this abnormality remain to be determined.

Blood Pressure↗