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 901 records · Page 50Linked to original sources
PubMed1977

Antidiuretic and urinary cyclic AMP response of vasopressin in normal rats and in rats with lithium-polyuria.

The antidiuretic and urinary cyclic AMP response to supramaximal vasopressin infusion was studied in normal rats and in rats with lithium-polyuria. The animals were anaesthetized and then infused with a solution designed to produce excessive water diuresis and to lower basal cyclic AMP excretion. In 6 control animals not infused with vasopressin (1) urinary cyclic AMP excretion decreased during the infusion period. Vasopressin infusion (300 muU/min.) consistantly induced antidiuresis in all of 13 control rats (II); but the urinary cyclic AMP response varied individually from a significant increase in 6 animals to either no change or to a decrease in the remaining animals. The antidiuretic response to vasopressin was inhibited by 85% in 10 animals with marked polyuria induced by lithium administration (III). None of the animals in this group showed a significant increase of cyclic AMP excretion in response to vasopressin. The average rate of cyclic AMP excretion, which was equal in the two groups before vasopressin, was signifimantly lower in group III than in group II during vasopressin infusion. It is suggested that the increase in cyclic AMP excretion during vasopressin antidiuresis, although not consistant, most likely reflects hormone-induced changes of intracellular cyclic AMP levels in the renal medulla. Thus, the data suggest that the nephrogenic diabetes insipidus syndrome produced by lithium is associated with a defect in the renal formation of cyclic AMP in response to vasopressin.

Animals↗
PubMed1990

The synthesis and biological activity of four novel fluorescent vasopressin analogs.

We synthesized and tested the biological properties of four fluorescent vasopressin analogs: [1-(2-mercapto)propionic acid]-8-lysine-N6-5-dimethylamino-naphthalene-1-sulfonyl vasopressin (D-MLVP), [1-(2-mercapto)propionic acid]-8-lysine-N6-carboxyfluorescein vasopressin (F-MLVP), [1-(2-mercapto)propionic acid]-8-lysine-N6-2-N-methylanthranilamide vasopressin (MA-MLVP), and [1-(2-mercapto)propionic acid]-8-lysine-N6-carboxytetramethylrhodamine vasopressin (R-MLVP). All fluorescent analogs were prepared by coupling the appropriate fluorochrome to the 6-amino group of the lysine residue in [1-(2-mercapto)propionic acid]-8-lysine vasopressin (MLVP) which was synthesized by the Merrifield solid-phase method. The structures of high performance liquid chromatography-purified MLVP and the fluorescent analogs were confirmed by fast atom bombardment mass spectrometry. F-MLVP, MA-MLVP, and R-MLVP effectively competed for 8-arginine vasopressin (AVP)-binding sites in canine renal plasma membranes and on the surface of porcine kidney cells (LLC-PK1, ATCC CL101). Dissociation constants for F-MLVP, MA-MLVP, and R-MLVP of 32, 8.8, and 26 nM, respectively, were calculated from the results of competition binding assays conducted with membranes. D-MLVP did not bind to plasma membranes. Dissociation constants for F-MLVP, MA-MLVP, and R-MLVP of 390, 38, and 160 nM, respectively, were calculated from the results of competition binding assays conducted with cells. F-MLVP, MA-MLVP, and R-MLVP at a concentration of 10(-6) M increased adenylate cyclase activity in canine renal plasma membranes to values 2.4, 2.9, and 2.6 times that of basal activity, respectively. A maximally active concentration of AVP (1 microM) increased adenylate cyclase activity in canine renal plasma membranes to a value 2.7 times that of basal activity. D-MLVP did not stimulate adenylate cyclase activity. F-MLVP, MA-MLVP, and R-MLVP at a concentration of 10(-6) M increased the cAMP content of porcine kidney cells from a basal level of 43 to 267, 160, and 469 pmol/mg of cell protein, respectively. Specific binding of these fluorescent analogs to receptors on the surface of LLC-PK1 cells was observed by fluorescence microscopy. These observations indicate that F-MLVP, MA-MLVP, and R-MLVP are biologically active fluorescent vasopressin analogs which are well-suited to the study of renal vasopressin receptors by fluorescence microscopy.

Adenylyl Cyclases↗
PubMed1989

Vasopressin inhibits type-I collagen and albumin gene expression in primary cultures of adult rat hepatocytes.

The mechanisms that regulate collagen gene expression in hepatic cells are poorly understood. Accelerated Ca2+ fluxes are associated with inhibiting collagen synthesis selectively in human fibroblasts (Flaherty, M., and Chojkier, M. (1986) J. Biol. Chem. 261, 12060-12065). In suspension cultures of isolated hepatocytes, the Ca2+ agonist vasopressin increases cytosolic levels of free Ca2+ (Thomas, A.P., Marks, J.S., Coll, K.E., and Williamson, J. R. (1983) J. Biol. Chem. 258, 5716-5725). However, whether vasopressin's interactions with plasma membrane V1 receptors attenuate hepatic collagen production is unknown. We investigated this problem by studying vasopressin's effects on collagen synthesis and Ca2+ efflux in long-term primary cultures of differentiated and proliferation-competent adult rat hepatocytes. Twelve-day-old quiescent cultures were exposed to test substances and labeled with [5-3H]proline. Determinations of radioactivity in collagenase-sensitive and collagenase-resistant proteins were used to calculate the relative levels of collagen production. Synthetic [8-arg]vasopressin stimulated 45Ca2+ efflux within 1 min and inhibited hepatocyte collagen production within 3 h by 50%; overall rates of protein synthesis were not affected significantly. In cultures labeled with [35S]methionine, vasopressin also decreased the levels of newly synthesized and secreted albumin, but not fibrinogen, detected in specific immunoprecipitates analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Northern blot analyses using specific [32P]cDNA probes revealed 70% decreases in hybridizable levels of collagen alpha 1(I) mRNA in hepatocyte cultures treated with either vasopressin or Ca2+ ionophore A23187; hybridizable levels of albumin mRNA also fell approximately 50% following vasopressin treatment. Vasopressin did not affect collagen production in quiescent cultures of mouse Swiss 3T3, human myofibroblast or rat smooth muscle cells; and hepatocyte collagen production was unaffected by treatment with glucagon or dibutyryl cAMP. Thus, accelerated Ca2+ fluxes induced by vasopressin are associated with decreased production of hepatocyte collagen and albumin in primary cultures that simulate quiescent adult rat liver.

Aging↗
PubMed1985

Stimulation of vasopressin release by gamma-aminobutyric acid antagonists in spinal cord transected rats.

Picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, administered to spinal rats elicited dose-related increases in mean blood pressure and circulating plasma vasopressin concentration which were found to be highly correlated (r = 0.952; P less than .001) 6 min after infusion of picrotoxin. Pretreatment with the vasopressin antagonist d(CH2)5Tyr(Me)arginine vasopressin (10 microgram/kg i.v.) blocked the picrotoxin-induced pressor response. Administration of bicuculline (1.0 mg/kg i.v.), a second GABA antagonist, caused an increase in mean blood pressure and plasma vasopressin, whereas strychnine, another central nervous system stimulant thought not to act via a GABAergic mechanism, failed to evoke a significant change in either mean blood pressure or plasma vasopressin. Midcollicular decerebration decreased base-line plasma vasopressin concentrations and also prevented the picrotoxin-induced increase in pressure and vasopressin. The data from this study suggest that blockade of tonic GABAergic inhibition by GABA antagonists causes the release of vasopressin into the systemic circulation which results in a pressor response in spinal rats. The level at which this GABAergic inhibition occurs is not known; however, the GABA antagonists appear to require an intact supraspinal neuraxis to cause the release of vasopressin from the neurohypophysis.

Animals↗
PubMed1985

Dietary sodium intake increases vasopressin secretion in man.

Plasma vasopressin concentration and urinary vasopressin excretion were measured in a control situation, during sodium depletion and on days 1, 2, and 7 during high sodium intake in twelve 23-26-year-old men on a free-water intake. Urinary vasopressin excretion decreased from 6.7 +/- 1.0 ng/hr (control) to 3.9 +/- 0.3 ng/hr (p less than 0.01) when sodium excretion decreased from 188 +/ 18 to 16 +/- 2 mmol/24 hr. During the first day of high sodium intake, the urinary vasopressin excretion increased to 10.0 +/- 1.2 ng/hr (p less than 0.01) compared with control and remained high throughout the sodium repletion. Through all collection periods at low, normal, and high sodium intake, vasopressin excretion increased concomitantly with serum sodium concentration and osmolality. After low sodium intake for 7 days, the serum vasopressin concentration averaged 2.7 +/- 0.6 ng/l, and this level was maintained throughout the sodium repletion period. These results are compatible with a stimulatory effect of dietary sodium intake on pituitary vasopressin secretion in man. Dietary sodium may stimulate vasopressin secretion through extracellular osmolality or even by a direct effect of extracellular sodium on periventricular receptors. Plasma renin concentrations or sympathetic nervous activity offered no further explanations. Urinary vasopressin excretion provides more useful information than do plasma concentrations, as the latter can fluctuate rapidly.

Adult↗
PubMed1981

Opiate regulation of angiotensin-induced drinking and vasopressin release.

In rats, intracerebroventricular (i.v.t.) administration of endogenous opioid peptides inhibited angiotensin II-stimulated increase in plasma vasopressin concentration and drinking behavior. Naloxone and naltrexone were used to evaluate the effect of opiate receptor blockade on angiotensin drinking behavior. Both antagonists reduced the amount of water consumed and number of animals drinking in response to angiotensin II (i.v.t.). The time to onset of drinking was unaffected. Leucine5-enkephalin inhibition of angiotensin-stimulated release of vasopressin was also studied. Changes in plasma vasopressin concentration with time (5, 45, 90, 150 and 300 sec) were measured after a single i.v.t. injection of angiotensin II (50 ng), with and without pretreatment with leucine5-enkephalin (100 microgram i.v.t.). Vasopressin was measured by radioimmunoassay. The onset of vasopressin release occurred 5 to 45 sec after angiotensin, reaching peak response between 45 to 90 sec. Leucine5-enkephalin did not affect the onset but reduced the peak response to angiotensin (P less than .05). Saralasin, i.v.t., abolished angiotensin-stimulated increase in plasma vasopressin concentration and prevented the residual, but significant, increase in plasma vasopressin concentration in angiotensin-treated rats given enkephalin. It is concluded that angiotensin stimulates release of vasopressin by interaction with specific, saralasin-sensitive, receptors; leucine5-enkephalin inhibits angiotensin release of vasopressin; and an endogenously synthesized opiate ligand(s) may affect angiotensin drinking behavior.

Angiotensin II↗
PubMed1994

The relationship between vasopressin and endolymphatic hydrops in the guinea pig.

Clinical studies have shown that plasma vasopressin level is significantly elevated in patients with Meniere's disease. Other reports indicated that histamine induced a very quick and high elevation of vasopressin level and caused nystagmus in experimentally produced endolymphatic hydrops. We became interested in further investigating the details of this relationship by studying the effect of experimental endolymphatic hydrops and histamine upon plasma vasopressin level in the guinea pig. The results are as follows: 1) Histamine increased the plasma vasopressin level in normal guinea pigs. 2) There was no statistically significant difference in the plasma vasopressin level between the hydrops model and normal guinea pigs. 3) Histamine increased the plasma vasopressin level more in the hydrops model group than in normals. 4) Plasma vasopressin level was elevated in the vertiginous model caused by inner ear anesthesia. Our results support those of clinical investigators who reported that the plasma vasopressin level was elevated more in the Meniere's disease group than any other equilibrium disorder group. It is possible that vasopressin is in someway involved in the development of endolymphatic hydrops.

Animals↗
PubMed1994

V1-like [Arg8]vasopressin binding sites occur in rat hepatocyte nuclei.

Arginine vasopressin binding site characterisation was performed on purified nuclei and plasma membranes from livers of Sprague-Dawley rats. [125I][d(CH2)5,Sarc7,Arg8]vasopressin, a selective V1 vasopressin receptor antagonist radioligand, bound to the nuclei in a protein concentration and time dependent manner. Scatchard analysis of nuclear binding sites revealed a single binding site with maximal binding site density (Bmax) of 115 +/- 13 fmol/mg protein and affinity (KD) of 5.2 +/- 0.7 nM. Plasma membrane binding demonstrated a Bmax of 529 +/- 25 fmol/mg protein and KD of 1.9 +/- 0.1 nM. The displacement profile for nuclear binding sites using vasopressin analogues was similar to that for plasma membrane binding sites and was typical of a V1 vasopressin receptor type. There was no evidence of V2-like vasopressin receptor binding using [3H]des-Gly-NH9(2)[d(CH2)5,D-Ile2,Ile4,Arg8]vasopressi n, a selective V2 vasopressin receptor radioligand, in the nuclear or membrane fractions. These results suggest the existence of nuclear V1-like vasopressin binding sites.

Animals↗
PubMed1999

Up-regulation of vasopressin V(1a) receptor mRNA in rat facial motoneurons following axotomy.

We have reported previously that axotomy induced a marked increase of vasopressin receptor binding in the adult rat facial nucleus, suggesting an increased number of vasopressin receptors. These receptors were pharmacologically undistinguishable from peripheral V(1a) vasopressin receptors. In the present study, we show, using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR), that axotomy regulates the expression of the vasopressin V(1a) receptor mRNA in the facial nucleus. Results were obtained from adult male rats killed 1 week following crush of the right facial nerve. In situ hybridization was performed with a (35)S-labelled riboprobe. A specific hybridization signal was detected in both left and right facial nuclei, with a significantly higher intensity in the nucleus ipsilateral to the lesion. V(1a) receptor transcripts were found associated with large facial motoneuronal cell bodies, not with other cells present in the nucleus, i.e., glial or epithelial cells. RT-PCR analysis of unlesioned facial tissue revealed the presence of mRNAs encoding vasopressin V(1a), vasopressin V(1b) and oxytocin receptors, whereas only the V(1a) receptor mRNA was found to be increased following axotomy in the lesioned facial tissue. These data suggest that the axotomy-induced expression of vasopressin receptors in the rat facial nucleus is due, at least to a large extent, to an increase of the V(1a) vasopressin receptor mRNA in facial motoneurons.

Animals↗
PubMed1987

Electrophysiological and autoradiographical evidence of V1 vasopressin receptors in the lateral septum of the rat brain.

Extracellular recordings were obtained from single neurons located in the lateral septum, an area known to receive a vasopressinergic innervation in the rat brain. Approximately half of the neurons tested responded to 8-L-arginine vasopressin (AVP) by a marked increase in firing rate at concentrations greater than 1 nM. The effect of vasopressin was blocked by synthetic structural analogues possessing antagonistic properties on peripheral vasopressin and oxytocin receptors. Oxytocin was much less potent than vasopressin in firing septal neurons, and a selective oxytocic agonist was totally ineffective. The action of vasopressin on neuronal firing was mimicked by the vasopressor agonist [2-phenylalanine,8-ornithine]vasotocin but not by the selective antidiuretic agonist 1-deamino[8-D-arginine]vasopressin. In a parallel study, sites that bind [3H]AVP at low concentration (1.5 nM) were found by in vitro autoradiography in the lateral septum. Adjacent sections were also incubated with 1.5 mM [3H]AVP and, in addition, with 100 nM [2-phenylalanine,8-ornithine]vasotocin or 1-deamino[8-D-arginine]vasopressin--i.e., the same compounds as those used for the electrophysiological study. Results showed that the vasopressor agonist, but not the antidiuretic agonist, displaced [3H]AVP, thus indicating that the vasopressin binding sites detected by autoradiography in the septum were V1 (vasopressor type) rather than V2 (antidiuretic type) receptors. Based on the electrophysiological evidence, we conclude that these receptors, when occupied, lead to increased firing of lateral septal neurons.

Animals↗
PubMed1994

Relaxation of human isolated mesenteric arteries by vasopressin and desmopressin.

1. The effects of vasopressin and deamino-8-D-arginine vasopressin (DDAVP, desmopressin) were studied in artery rings (0.8-1 mm in external diameter) obtained from portions of human omentum during the course of abdominal operations (27 patients). 2. In arterial rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions with an EC50 of 0.59 +/- 0.12 nM. The V1 antagonist d(CH2)5Tyr(Me)AVP (1 microM) and the mixed V1-V2 antagonist desGly-d(CH2)5D-Tyr(Et)ValAVP (0.01 microM) displaced the control curve to vasopressin to the right in a parallel manner without differences in the maximal responses. In the presence of indomethacin (1 microM) the contractile response to vasopressin was significantly increased (P < 0.01). 3. In precontracted arterial rings, previously treated with the V1 antagonist, d(CH2)5Tyr(Me)AVP (1 microM), vasopressin produced endothelium-dependent relaxation. This relaxation was reduced significantly (P < 0.05) by indomethacin (1 microM) and unaffected by the V1-V2 receptor antagonist desGly-d(CH2)5D-Tyr(Et)ValAVP (1 microM) or by NG-nitro-L-arginine methyl ester (L-NAME, 0.1 mM). 4. The selective V2 receptor agonist, DDAVP, caused endothelium-independent, concentration-dependent relaxations in precontracted arterial rings that were inhibited by the mixed V1-V2 receptor antagonist, but not by the V1 receptor antagonist or by pretreatment with indomethacin or L-NAME. 5. Results from this study suggest that vasopressin is primarily a constrictor of human mesenteric arteries by V1 receptor stimulation; vasopressin causes dilatation only during V1 receptor blockade. The relaxation appears to be mediated by the release of vasodilator prostaglandins from the endothelial cell layer and is independent of V2 receptor stimulation or release of nitric oxide. In contrast, the relaxation induced by DDAVP is largely dependent on stimulation of V2 receptors.

Adult↗
PubMed1983

Contribution of vasopressin to the maintenance of blood pressure during dehydration.

Normal Long-Evans rats, when dehydrated for up to 72 h, have a progressive rise in plasma vasopressin that is associated with a fall in body weight and urine volume, a rise in plasma and urine osmolality, and the maintenance of normal systolic blood pressure. In contrast, Brattleboro diabetes insipidus rats, genetically deficient in vasopressin, when dehydrated to achieve an equivalent body weight loss, have a significant 15 mmHg fall in systolic blood pressure. Even when fluid balance is corrected in the Brattleboro rats by the continuous administration of 1-desamino-8-D-arginine vasopressin, a synthetic vasopressin analogue with potent antidiuretic properties but minimal pressor activity, blood pressure still falls when the animals are dehydrated. In contrast, Brattleboro rats infused with exogenous arginine vasopressin to produce a plasma vasopressin level of 18.9 +/- 3.5 pg X ml-1 are able to maintain normal blood pressure during 48 h of dehydration. This level of vasopressin is comparable to the level found endogenously in dehydrated Long-Evans rats and is nonpressor in normal rats. These results suggest that both the antidiuretic and vasoconstrictor properties of vasopressin are important in the cardiovascular response to dehydration.

Angiotensin II↗
PubMed1986

Characteristics of the receptors which mediate the stimulation of ACTH secretion by vasopressin in conscious dogs.

In order to characterize the receptors which mediate the adrenocorticotropic hormone (ACTH) response to vasopressin in conscious animals, plasma 11-hydroxycorticosteroid concentration was measured in conscious dogs during the infusion of vasopressin or structural analogs of vasopressin which exhibit selective antidiuretic or vasoconstrictor activity. Vasopressin (1.0 ng/kg/min for 60 min) increased mean arterial pressure, decreased heart rate and increased plasma corticosteroid concentration from 1.0 +/- 0.2 to 2.2 +/- 0.2 micrograms/dl (p less than 0.001). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and corticosteroid responses to vasopressin. A selective vasoconstrictor (V1) agonist, PheOrnOT (1.0 ng/kg/min), which produced the same cardiovascular responses as vasopressin, increased plasma corticosteroid concentration from 1.1 +/- 0.1 to 2.9 +/- 0.9 micrograms/dl (p less than 0.005). In marked contrast, a selective antidiuretic (V2) agonist, dDAVP (1.0 ng/kg/min) had no effect on blood pressure, heart rate or plasma corticosteroid concentration. These results indicate that the stimulation of ACTH release by vasopressin in conscious dogs is mediated by receptors which resemble vasoconstrictor-type (V1) receptors rather than antidiuretic-type (V2) receptors.

Adrenal Cortex Hormones↗
PubMed1990

Cardiovascular depression and stabilization by central vasopressin in rats.

The role of endogenous vasopressin in cardiovascular homeostasis was examined using vasopressin-deficient rats (Brattleboro) (n = 194) and their parent strain, Long-Evans rats (n = 181). Mean arterial pressure (blood pressure) and heart rate were measured every 4 seconds with or without infusion of drug solution for 21 hours, and mean values and their standard deviations (lability) were calculated. Blood pressure in Brattleboro rats (116 +/- 1.1 mm Hg, mean +/- SEM) was significantly higher than that in Long-Evans rats (96 +/- 0.7 mm Hg, p less than 0.001), whereas heart rates (381 +/- 3.3 and 375 +/- 2.9 beats/min, respectively) were similar. The lability of blood pressure and heart rate in Brattleboro rats (9.2 +/- 0.1 mm Hg and 42.3 +/- 0.7 beats/min) was also greater than that in Long-Evans rats (6.7 +/- 0.1 mm Hg, p less than 0.001 and 38.4 +/- 0.8 beats/min, p less than 0.01, respectively). In Brattleboro rats, intravenous vasopressin (0.1 ng/kg/min or 0.6 ng/kg/min) did not affect blood pressure, although it did reduce heart rate and decreased lability of blood pressure and heart rate. Intracerebroventricular (central) infusion of vasopressin (2 pg/kg/min) in Brattleboro rats induced initial hypertension and tachycardia followed by long-lasting hypotension and bradycardia, whereas in Long-Evans rats it induced only hypertension and tachycardia. In both strains, central vasopressin dramatically decreased the lability of blood pressure and heart rate. Neither intravenous (0.2 ng/kg/min) nor central desmopressin (2 pg/kg/min or 0.2 ng/kg/min), a V2 renal receptor agonist, changed any of these parameters in Brattleboro rats, although both diminished urinary volume. Neither intravenous (50 ng/kg/min) nor central (3.3 pg/kg/min) d(CH2)5-Tyr(Me)-arginine vasopressin, a vasopressin V1 receptor antagonist, modulated any of these parameters in Long-Evans rats. These results suggest that endogenous as well as exogenous vasopressin acts centrally as a cardiovascular inhibitor and stabilizer through a receptor mechanism other than V1 or V2 receptor mechanisms.

Animals↗
PubMedDate not supplied

Contribution of vasopressin and the sympathetic nervous system in the early phase of high sodium one-kidney renal hypertension.

This study assessed the contributions of the sympathetic nervous system and arginine vasopressin to the onset of one-kidney, one-wrap (1K1W) renal hypertension in rats fed a high sodium diet. Two weeks before renal wrap or sham wrap, rats were given a high sodium diet and water ad libitum. At 3 days postwrap, resting mean arterial pressure (MAP) was significantly greater in renal-wrapped rats. The contributions of the sympathetic nervous system and vasopressin to blood pressure (BP) were assessed by ganglionic blockade and vascular vasopressin receptor antagonism, respectively. Depressor responses to ganglionic blockade were significantly greater in the normotensive rats as compared to the hypertensive rats. Administration of vasopressin antagonist caused a significant fall in pressure only in wrapped rats. In addition, enhanced pressor responses to bolus injections of vasopressin were observed in hypertensive rats. These results indicate that during this phase of the hypertension there is an activation of the vasopressin pressor system without an increase in neurogenic function. Equalization of arterial pressure occurred only when both systems were blocked, regardless of the order of blockade, which indicated that the sympathetic nervous system and vasopressin interact to maintain the hypertension. Comparison of depressor responses to the blocking agents revealed that the interaction is compensatory in nature since the contributions of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure were greater when the other system was blocked.

Angiotensin II↗
PubMed1983

Vasopressin-induced antinociception: an investigation into its physiological and hormonal basis.

Systemically administered lysine-8-vasopressin (LVP; 16-128 micrograms/kg) was found to induce a potent and dose-dependent antinociceptive effect, as measured by the tail-flick test in the rat. This effect could be seen in the absence of any significant change in general activity, indicating that it was not due to sedation or general motor debilitation. The antinociceptive effect of LVP does not appear to be mediated by endogenous opiates or other pituitary hormones, as evidenced by: 1) the lack of antagonism by the opiate receptor blocker naloxone, 2) the lack of cross-tolerance with morphine, and 3) its persistence after hypophysectomy. Des-glycinamide-LVP, a vasopressin analog with no appreciable pressor or antidiuretic action, showed no antinociceptive activity (128 micrograms/kg), and des-amino-arginine-vasopressin, a vasopressin analog with minimal pressor activity but greatly enhanced antidiuretic activity, was also relatively ineffective (128 micrograms/kg). These results suggest that the antinociceptive activity of vasopressin may be related to receptor types similar to those mediating its pressor effects. Nevertheless, the antinociceptive action of vasopressin does not appear to be secondary to its pressor activity, since phenylephrine failed to induce an antinociceptive effect at a dosage that mimicked the pressor response to vasopressin. These results are in concert with a growing body of evidence suggesting that vasopressin may be one of several nonopiate peptides that play a role in the modulation of pain sensitivity.

Animals↗
PubMed1985

Systemic and renal hemodynamic responses to vascular blockade of vasopressin in conscious dogs with ascites.

A role for arginine vasopressin has been implicated in the compensatory control of arterial blood pressure in several animal models with reported increases in plasma levels of arginine vasopressin. A threefold elevation in plasma vasopressin has been reported in conscious dogs following constriction of the inferior vena cava. In the present study, infusion of the arginine vasopressin antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine] Arg8-vasopressin into conscious dogs with chronic caval constriction did not decrease mean arterial blood pressure. However, the dose of infused antagonist completely blocked the pressor response to 2 micrograms of exogenous vasopressin. Also the antagonist produced no effect on heart rate, plasma renin activity, or urinary volume and electrolyte excretions. A slight, transient increase (P less than or equal to 0.05) was observed in creatinine clearance and in PAH clearance following antagonist infusion, suggesting a possible decrease in renal vascular resistance. These data suggest that the direct vasoconstrictor actions of vasopressin contribute minimally, if at all, to blood pressure maintenance following chronic caval constriction. Alternatively, blockade of endogenous vasopressin receptors at the level of peripheral arterioles may have resulted in no depressor response due to a masking of this response by other compensatory hormonal and neural pressor systems.

Animals↗
PubMed1990

Interaction of vasopressin and oxytocin with human breast carcinoma cells.

The arginine vasopressin and oxytocin content of normal and cancerous human breast tissue were measured using radioimmunoassay. Both peptides were present in amounts greater than that found in the circulation, but no difference between normal and malignant tissues was found. Binding of [3H]oxytocin and [3H]vasopressin were characterized in human breast carcinoma cells (MCF7 cells). Binding of both hormones to MCF7 cells was specific and saturable, the vasopressin receptor found to be of the V1 subtype. Scatchard analyses of the data were linear, indicating a single high affinity, low capacity binding site for each hormone (vasopressin: KD = 47.4 +/- 1.6 nmol/liter, Bmax = 27,300 +/- 6,500 sites/cell; oxytocin: KD = 51.3 +/- 0.4 nmol/liter, Bmax = 87,000 +/- 4,000 sites/cell). The effects of vasopressin and oxytocin on the growth of MCF7 cells were assessed using protein accumulation and cell numbers. Vasopressin at 10-1000 pmol/liter was mitogenic for MCF7 cells, but higher doses (10 nmol/liter) were growth inhibitory. Oxytocin was also mitogenic for MCF7 cells but to a lesser extent than vasopressin. In conclusion, we suggest that vasopressin and possibly oxytocin may be important modulators of the growth of some human breast carcinomas.

Arginine Vasopressin↗