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PubMed1991

Role of afferent renal nerves in the control of vasopressin secretion.

Several lines of evidence indicate that the kidneys can influence the secretion of vasopressin. We have reported that electrical stimulation of the renal nerves increases plasma vasopressin concentration in dogs and rabbits, and other investigators have reported that selective stimulation of afferent renal nerves in cats and rats increases plasma vasopressin concentration or the activity of neurosecretory neurons in the supraoptic nucleus. Intrarenal infusion of bradykinin, which is known to excite afferent renal nerves, has also been reported to increase the activity of putative vasopressin neurons in the supraoptic nucleus of rats. Recently, we observed that intrarenal infusion of bradykinin in rabbits increases plasma vasopressin concentration, and that this response is markedly reduced by renal denervation. We have also reported that activation of renal mechanoreceptors by elevating intrarenal pressure increases plasma vasopressin concentration in rabbits, and that this response is blocked by renal denervation. In order to determine if the kidneys participate in the physiological regulation of vasopressin release, we investigated the effect of renal denervation on the osmotic and non-osmotic control of vasopressin secretion in conscious, chronically-prepared rabbits. We found that renal denervation did not significantly reduce the vasopressin responses to hypertonic saline infusion, 24-hour water deprivation, hemorrhage or nitroprusside infusion. In summary, these observations indicate that the kidneys can influence the secretion of vasopressin via the afferent renal nerves. However, the physiological significance of the observations remains to be determined.

Animals↗
PubMed1989

Noncyclic vasopressin analogs are effective diuretics in conscious rats.

Linear vasopressin analogs lacking a cyclic hexapeptide ring have recently been reported to possess vasopressin antagonist activity. In conscious, chronically catheterized, euhydrated Sprague-Dawley rats, we have compared the effects of two noncyclic vasopressin analogs, peptide 1 ([1-admantaneacetic acid,2-(O-ethyl)-D-tyr,4-val,6-(2-aminobutyric acid),9-arg]arginine vasopressin) and peptide 2 ([1-propionic acid, 2-(O-ethyl)-D-tyr,4-val,6-(2-aminobutyric acid),9- arg]arginine vasopressin), with a cyclic arginine vasopressin antagonist (SK&F 105494; [1-des cysteine, cyclo(2-O-ethyl-D-tyrosine,6-L-(2-amino-6,6-cyclopentamethylene suberic acid], 4-valine,7-arginine,8-D-arginine, 9-des glycine]-vasopressin). All three analogs caused a dose-dependent increase in urine flow by increasing free-water clearance without significantly changing osmotic clearance or sodium excretion, indicating true functional vasopressin antagonism. Peptides 1 and 2 were as efficacious in inducing a diuresis as SK&F 105494. The order of diuretic potency among the three analogs in vivo was the same as the order of potency determined by in vitro binding to rat renal membrane homogenates, suggesting that the analogs exerted their diuretic effect by acting at renal vasopressin receptors. Thus, noncyclic vasopressin analogs, which are easier to synthesize then cyclic structures, could provide new strategies in the design of drugs for the treatment of water balance disorders.

Animals↗
PubMed1988

Pathway of phospholipase C activation initiated with platelet-derived growth factor is different from that initiated with vasopressin and bombesin.

The mode of phospholipase C activation initiated with platelet-derived growth factor (PDGF) has been studied in comparison with that initiated with vasopressin and bombesin in a rat fibroblast line, WFB. Stimulation of WFB cells by PDGF, vasopressin, and bombesin elicites rapid hydrolysis of polyphosphoinositides and an increase in cytoplasmic free Ca2+ concentration ([Ca2+]i). On stimulation by PDGF, there was a lag period of about 10 s before an increase in [Ca2+]i. No measurable lag period was observed in the [Ca2+]i response induced by vasopressin or bombesin. Pretreatment of WFB cells with phorbol 12-myristate 13-acetate profoundly inhibited inositol phosphate formation evoked by vasopressin and bombesin, but enhanced to some extent inositol phosphate formation stimulated by PDGF. In membranes prepared from WFB cells, GTP markedly augmented inositol polyphosphate formation induced by vasopressin and bombesin. It was not successful in showing the PDGF-stimulated formation of inositol phosphates in the membrane preparation. The effects of GTP, guanosine 5'-O-(2-thiodiphosphate) (GDP beta S), and guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) on polyphosphoinositide hydrolysis stimulated by growth factors were studied in WFB cells made permeable to nucleotides by treatment with either saponin or Pseudomonas aeruginosa cytotoxin. PDGF, vasopressin, and bombesin elicited inositol phosphate production in the permeabilized WFB cells in the absence of added GTP. GDP beta S, a competitive inhibitor of GTP-binding proteins (G-proteins), markedly reduced the bombesin- and vasopressin-stimulated production of inositol phosphates. However, the PDGF-stimulated production of inositol phosphates was not affected by the addition of GDP beta S. GTP gamma S, an agonist of G-proteins, largely enhanced the vasopressin- and bombesin-stimulated hydrolysis of inositol lipids when added at 10-100 microM. In the presence of GTP gamma S, the PDGF-stimulated hydrolysis of inositol lipids was not enhanced, but was reduced: 100 microM GTP gamma S reduced the stimulated hydrolysis to about a half of the control level. Only GTP gamma S, and no other nucleoside triphosphates, was found to have these effects. Activation of G-proteins in WFB cells by fluoroaluminate resulted in the inhibition of inositol phosphate production elicited with not only PDGF, but also with vasopressin and bombesin. These results indicate that a G-protein couples vasopressin and bombesin receptors to the activation of phospholipase C. Moreover, these results suggest that coupling of the PDGF receptor to phospholipase C is not mediated through a G-protein.(ABSTRACT TRUNCATED AT 400 WORDS)

Aluminum↗
PubMed1979

Interrelations between vasopressin and the renin-angiotensin system.

The interrelationships between vasopressin and the renin-angiotensin system are reviewed. Vasopressin can inhibit the release of renin by the kidney. This effect can occur at physiological plasma concentrations of vasopressin. Centrally administered angiotensin II can stimulate the release of vasopressin, a response that may be partially mediated by brain prostaglandins. The significance of this action of angiotensin II depends on whether there is an effective brain renin-angiotensin system and on whether peripherally generated or administered angiotensin can reach sites in the brain where it can act on vasopressin release. Peripherally administered angiotensin II can under certain, but not all, conditions stimulate vasopressin release. Peripheral angiotensin II can also potentiate the vasopressin response to an osmotic stimulus and to dehydration, but has little effect the release of vasopressin and renin, there is a failure to demonstrate any correlation between the two. Blockade of the renin-angiotensin system fails to modify the vasopressin response to a reduction in blood volume. In conclusion, the physiological significance of the interactions between the vasopressin and the renin-angiotensin system is not as yet clearly established.

Angiotensin II↗
PubMed1995

Central vasopressin in experimental aortic stenosis in the rat.

OBJECTIVE: In several forms of heart disease characterised by low cardiac output, activated neurohumoral systems including increased vasopressin plasma levels play a key role in the changes in cardiovascular function. The aim of this study was to test the hypothesis that under such conditions the central vasopressin system might also be altered, which could contribute to deranged cardiovascular control. METHODS: Aortic stenosis was produced in 22 rats by placing a Silver clip (inner diameter 0.6 mm) on the ascending aorta. After 12 weeks, haemodynamic and hormonal measurements were performed, and vasopressin content was determined in 20 microdissected brain areas (micropunch technique). Twenty two sham operated rats served as controls. RESULTS: Twelve weeks after placing the supravalvular clip, significant aortic stenosis was documented by left ventricular myocardial hypertrophy. Cardiac index was significantly reduced and the peripheral vascular resistance index was increased, while poststenotic aortic pressure was non-significantly decreased. Plasma renin concentration [6.8(SEM 0.9) v 2.1(0.2) ngAI.ml-1.h-1 in controls] and plasma vasopressin [32.9(12.5) v 18.4(6.0) pg.ml-1] were significantly increased, while plasma and urinary noradrenaline remained unaltered. The vasopressin content was significantly altered in eight out of 20 brain areas investigated. Concerning the vasopressin producing hypothalamic nuclei, concentrations were increased in the paraventricular [7494(360) v 4744(237) pg.mg-1 protein, P < 0.05] and suprachiasmatic [3613(170) v 1784(197) pg.mg-1 protein, P < 0.01], but not in the supraoptic nuclei. Rats with aortic stenosis showed significantly raised vasopressin concentrations in the median eminence [25 186(1682) v 37 367(1345) pg.mg-1 protein, P < 0.01], where the hormone is mainly concentrated in the hypothalamo-hypophysial tract. Vasopressin content was significantly decreased in locus coeruleus [49(5) v 89(6) pg.mg-1 protein], which is known to be involved in modulation of sympathetic activity. CONCLUSIONS: As well as showing increased secretion of vasopressin into the blood with consecutive peripheral antidiuretic and vasoconstrictive effects, these data suggest an alteration in the central vasopressin system in aortic stenosis which might transmit cardiovascular effects by neuromodulation and neuroregulation.

Animals↗
PubMed1993

[Effect of arginine-vasopressin infusion on the secretion of tracheal fluid in sheep fetuses].

Timely evacuation of alveolar fluid, release of surfactant and the beginning of continuous breathing, are key processes for an adequate adaptation of the fetus to the extrauterine life. Fetal vasopressin increases during labor and inhibit the secretion of tracheal fluid through a mechanism still unknown. The aim of this study was to elucidate the mechanism whereby vasopressin inhibit the secretion of lung fluid. We used fetal sheep chronically catheterized and infused either with vasopressin, vasopressin agonist (V2; dDAVP) or vasopressin antagonist (V1). Tracheal flow was measured during basal and infusions periods of 2 hours, monitoring fetal blood pressure, heart rate and blood pH and gases. Vasopressin and the V1 vasopressin antagonist caused a significant reduction in tracheal fluid flow, effect that was potentiated when both peptides were infused together. The V2 vasopressin agonist had no effect on the secretion of lung fluid. We concluded that vasopressin causes a significant inhibition of lung liquid secretion through a mechanism different to the activation of V1 and V2 receptors, and we propose the existence of other (s) kind of receptors (or receptors) for vasopressin that is (are) active during fetal life.

Animals↗
PubMed2001

Endogenous endothelin and vasopressin support blood pressure during epidural anesthesia in conscious dogs.

UNLABELLED: We studied whether endogenous endothelin, like endogenous vasopressin, helps to maintain blood pressure during high epidural anesthesia when efferent sympathetic drive is diminished. On different days, six awake dogs underwent each of the following five interventions: blockade of vasopressin V(1a) receptors using [d(CH(2))(5)Tyr(Me(2))]AVP, (40 microg/kg) or endothelin receptors using tezosentan (3 mg/kg followed by 3 mg. kg(-1). h(-1)) with or without epidural anesthesia (1% lidocaine, intraindividual dose did not differ between experiments), and epidural saline (n = 5). The effects of endothelin- or vasopressin-receptor blockade were analyzed (means +/- SEM) and compared by an analysis of variance for repeated measures (paired Student's t-test, alpha-adjusted, P < 0.05). Vasopressin-receptor blockade decreased blood pressure (10 +/- 2 mm Hg) only in the presence of epidural anesthesia, whereas endothelin-receptor blockade reduced blood pressure both in the presence and absence of epidural anesthesia (12 +/- 3 versus 10 +/- 1 mm Hg). During baseline and each intervention, plasma concentrations of vasopressin and big-endothelin were measured and compared by a Wilcoxon's rank sum test; P < 0.05. Vasopressin concentrations increased during epidural anesthesia and after additional endothelin receptor blockade, but big-endothelin concentrations remained unchanged during each intervention. We conclude that vasopressin acts as a reserve system, as it stabilizes blood pressure specifically during epidural anesthesia, whereas the unchanged concentrations of big-endothelin indicate that the endothelin system is not specifically activated to support blood pressure during epidural anesthesia. IMPLICATIONS: We studied in awake dogs whether endogenous endothelin, like endogenous vasopressin, helps to maintain blood pressure during resting conditions and epidural anesthesia. Only vasopressin was specifically activated to support blood pressure during epidural anesthesia, whereas endothelin supported blood pressure to the same extent during epidural anesthesia and during resting conditions.

Anesthesia, Epidural↗
PubMed1991

An investigation into the influence of vasopressin on perfusion of the cortex and papilla of the rat kidney.

An investigation was undertaken to examine the effects of vasopressin on blood pressure and perfusion of the cortical and papillary regions of the kidney, and to determine the receptor subtype involved. Pentobarbitone-anaesthetized rats were used and laser-Doppler flowmetry applied to measure regional renal haemodynamics. Infusion of vasopressin at 10, 20 and 40 mU kg-1 min-1 caused dose-related increases in blood pressure and reductions in cortical and papillary perfusion of approximately 21, 35 and 41%, respectively at the highest dose. Administration of the V1-receptor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(o-methyl)tyrosine]-Arg8-vasopressin, at 1 microgram kg-1 plus 5 micrograms kg-1 h-1 or four times this dose had no effect on the basal levels of any variable. Vasopressin administration during the low dose of antagonist increased blood pressure and reduced papillary perfusion, the magnitudes of which were only slightly less than those obtained in the absence of the drug, whereas there was a significant attenuation of the response in cortical perfusion. During infusion of the V1 antagonist at 4 micrograms kg-1 plus 20 micrograms kg-1 h-1, vasopressin had no effect on either blood pressure or renal haemodynamics. Infusion of the V2 antagonist, [d(CH2)5, D-Phe2, Ile4, Arg8, Ala9-NH2]-vasopressin at 1 microgram kg-1 plus 5 micrograms kg-1 h-1, and twice this dose had no effect on the basal value of any variable and had no effect on the ability of vasopressin to induce an increase in blood pressure or cause reductions in renal cortical and papillary perfusions. However, the administration of the V2 antagonist at 4 micrograms kg-1 plus 20 micrograms kg-1 h-1 significantly attenuated blood pressure, cortical and papillary perfusion responses to the vasopressin. These studies have shown that vasopressin, given at doses which increased blood pressure, caused dose-related decreases in perfusion of renal cortex as well as the papilla. The data further show that these systemic and renal actions were mediated primarily by V1-receptors and that the contribution of V2-receptors at these vascular beds was very small.

Angiotensin Receptor Antagonists↗
PubMed1991

Modulation of vasopressin antidiuretic action by alpha 2-adrenoceptors is species specific.

There is evidence in the rat that stimulation of renal alpha 2-adrenoceptors modulates vasopressin antidiuretic action and vasopressin-stimulated adenylate cyclase activity. In the present study, we tested the ability of various alpha 2-adrenoceptor agonists to antagonize vasopressin-induced antidiuresis in the conscious hydrated dog and to inhibit vasopressin-induced adenosine 3',5'-cyclic monophosphate (cAMP) generation in rat and dog cortical collecting tubules. Vasopressin infusion (0.01 ng.kg-1.min-1) in five dogs resulted in a decrease in free water clearance from 2.90 +/- 0.42 to -0.34 +/- 0.08 ml/min. The vasopressin receptor antagonist SKF 105494 inhibited this response. Administration of norepinephrine (0.5 microgram.kg-1.min-1) or clonidine (20 micrograms/kg), however, failed to alter the vasopressin-induced antidiuresis. In vitro studies demonstrated that epinephrine caused a dose-dependent reduction in vasopressin-stimulated cAMP levels in cortical collecting tubules from the rat (50% effective concentration 32 nM) but not from the dog. The data indicate that there is a species difference in alpha 2-adrenoceptor modulation of vasopressin action.

Adenylyl Cyclases↗
PubMed1993

Sex difference in the antidiuretic activity of vasopressin in the rat.

A possible gender difference in the antidiuretic activity of vasopressin was studied in male and female Sprague-Dawley rats. Infusion of vasopressin (3-100 pg.kg-1.min) into conscious, chronically instrumented water-loaded rats resulted in a dose-dependent antidiuresis in both male and female rats. Male rats, however, were more than three times more sensitive to vasopressin than female rats. Thus the effective doses of vasopressin (pg.kg-1.min-1) to decrease urine flow to 30 microliters.min-1.100 g-1 (18 +/- 5 in males; 58 +/- 12 in females), to increase urine osmolality to 600 mosmol/kgH2O (35 +/- 5 in males; 119 +/- 15 in females), and to decrease free water clearance to 30 microliters.min-1.100 g-1 (8 +/- 3 in males; 28 +/- 7 in females) were significantly (P < 0.05) lower in males. Furthermore, in vitro studies in papillary collecting duct cells demonstrated a significantly higher density of vasopressin V2 receptors and a greater ability of vasopressin to stimulate adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in males than in females. Vasopressin V2-receptor density (maximum binding) was 359 +/- 47 and 238 +/- 22 fmol/mg in male and female rats, respectively (P < 0.05). There was no difference in apparent dissociation constants (Kd). Vasopressin resulted in a dose-dependent increase in cAMP accumulation in papillary collecting duct cells, and at the highest concentration of vasopressin used (10(-8) M) cAMP increased from 44 +/- 10 to 182 +/- 51 fmol/micrograms protein in males and from 30 +/- 4 to 91 +/- 18 fmol/micrograms protein in females (P < 0.05). (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Animal and clinical studies of vasopressin effects on learning and memory.

Cognitive deficits of attention deficit disorder in childhood are poorly responsive to presently available medication. Vasopressin derivatives have been reported to enhance learning and memory in animals and in normal humans in controlled studies. This study reports on the effects of vasopressin on learning in rats and in children with learning disorders. Vasopressin treatment three times weekly for 6 weeks in rats appeared to be more effective in enhancing learning and retarding extinction than did vasopressin treatment given only at the beginning of learning and again at the start of extinction. These effects were also shown to be affected by pharmacogenetic factors, since in six inbred mouse strains some showed retarded extinction with vasopressin and others did not. In 17 children with attention and learning disorders, vasopressin derivative was given daily for 10 days and compared with 10 days of placebo treatment in a randomized, crossover, double-blind design. Story memory plus position learning were significantly improved by vasopressin derivative compared with placebo. The same trend of improvement was observed in nine Down's syndrome patients. In 15 other children with attention and learning disorders, a single dose of vasopressin derivative was compared with placebo in a randomized, crossover, double-blind design, and no benefit was found. These parallel animal and human studies suggest that repeated, but not single-dose, vasopressin treatment may benefit childhood learning disorders.

Animals↗
PubMed1987

Vasopressin antagonism in the squirrel monkey (Saimiri sciureus).

Vasopressin antagonism and water diuresis (aquaresis) is demonstrated after i.p. or i.v. administration of vasopressin antagonists in a primate species, the squirrel monkey (Saimiri sciureus). Antagonism of vasopressin-stimulated renal medullary adenylate cyclase activity was evaluated in vitro; the most potent antagonists were those with D-tyrosine (alkyl) substitutions at position 2. Aquaresis was evaluated in vivo; the most potent aquaretic agents were again those with D-tyrosine (alkyl) substitutions at position 2. Correlation of in vitro vasopressin antagonist and in vivo aquaretic potencies for a series of antagonists was r = 0.7880 (P less than .05). Renal excretion of electrolytes, creatinine and urea tended to increase slightly as a function of vasopressin antagonist dose; the rates of solute excretion approached but seldom exceeded those rates associated with water diuresis in squirrel monkeys. The vasopressin antagonists antagonized the antidiuretic activity of exogenous vasopressin in vivo. Onset of the aquaretic response to i.v. administration of desGlyd(CH2)5D-Tyr(Et)VAVP was within 30 min; duration was greater than 120 min. These studies establish vasopressin antagonism and aquaresis associated with administration of vasopressin antagonists in a primate species.

Adenylyl Cyclases↗
PubMed1994

Aggressive role of vasopressin in development of different gastric lesions in rats.

The effects of endogenous or exogenous vasopressin in models of gastric mucosal injury with a different pathophysiology (ethanol, indomethacin, reserpine, cold-restraint stress and haemorrhagic shock-induced lesions) were investigated in rats. [Mca1,TyrMe2,Arg8]vasopressin, a vasopressin pressor (V1) receptor antagonist, was found to reduce dose dependently the extent of the lesions in all models, and to protect the deeper layer of the mucosa (assessed by histology). Endogenous vasopressin deficiency, as in Brattleboro homozygous rats, had a similar effect. [Lys8]Vasopressin injected exogenously aggravated all types of lesions in normal rats. Circulating vasopressin levels were increased by ethanol, reserpine, cold-restraint stress and haemorrhagic shock, but not by indomethacin, whereas the intramucosal vasopressin content was found to be elevated in all models. Additionally, specific binding sites for vasopressin were shown on the blood vessels of the gastric mucosa (assessed by autoradiography). It is concluded that vasopressin plays a significant aggressive role in the generation of these types of lesions.

Animals↗
PubMed1984

Plasma antidiuretic hormone levels and kidney responsiveness to vasopressin in the jerboa, Jaculus orientalis.

The plasma antidiuretic hormone (ADH) concentration and the kidney medulla responsiveness to vasopressin were measured in adult jerboas ( Jaculus orientalis) in different states of hydration. In 15 jerboas adapted to 30 degrees and fed a dry diet, the average ADH concentration in blood plasma was 479 +/- 59 pg/ml, as measured by a radioimmunoassay. About 6 hr after receiving a 5% body wt water load by gavage, the plasma ADH concentration fell to 130 +/- 30 pg/ml in the 5 jerboas still producing hypertonic urine (1022 +/- 267 mosmol/liter) and to 41.5 +/- 8.4 pg/ml in the 6 jerboas producing hypoosmotic urine (157 +/- 6 mosmol/liter). In vitro biochemical experiments were performed on the kidney medullas from two groups of 5 jerboas fed a dry diet (group I) or a water-enriched diet (group II), respectively, for 4 to 7 weeks. Compared to group II, group I animals exhibited (a) higher plasma ADH values, 372 +/- 86 versus 76 +/- 25 pg/ml; (b) higher urine osmolarities (3817 +/- 638 versus 647 +/- 90 mosmol/liter); (c) some decrease in [3H]lysine-vasopressin (LVP) binding capacity to kidney membrane fractions (maximal binding: 0.4 versus 0.6 pmol [3H]LVP bound/mg protein); d) decreased adenylate cyclase responses to arginine-vasopressin, lysine-vasopressin, and oxytocin in kidney membrane fractions; and (e) weaker adenylate cyclase responses to arginine-vasopressin in microdissected pieces of the medullary thick ascending limb of Henle's loop. The values found for (a) the dissociation constant of [3H]lysine-vasopressin binding to membranes (KD); (b) adenylate cyclase sensitivity to the three neurohypophyseal hormones (KA); and (c) adenylate cyclase sensitivity to arginine-vasopressin (KA) in medullary collecting tubules and medullary thick ascending limbs are similar in the two groups of jerboas and roughly comparable to those previously reported for the rat kidney medulla. The reduced maximal adenylate cyclase responses to vasopressin in the jerboas fed a dry diet might indicate some physiological "down regulation" of the number of vasopressin-specific receptors in the kidney as a result of the huge ADH concentration present in blood plasma under these conditions. However, this desensitization is not sufficient to account for the production of hypoosmotic urine in spite of the relatively high ADH plasma levels which persisted after acute overhydration.

Adenylyl Cyclases↗
PubMed1990

Dopamine antagonism does not potentiate the effects of oxytocin and vasopressin on prolactin secretion.

The roles of oxytocin and vasopressin on prolactin secretion were studied. Adult female Sprague-Dawley rats ovariectomized for two weeks and treated with a long-acting estrogen, polyestradiol phosphate for one week were used. Hormone administration and serial blood sampling were accomplished through indwelling intra-atrial catheters which were implanted two days before the experiment. Both oxytocin (20 micrograms/rat) and vasopressin (5 micrograms/rat) stimulated prolactin secretion within 10 min after injection and the effects were diminished by 30 min. In animals pretreated with a small dose of dopamine antagonist, sulpiride (1 microgram/rat), the effect of TRH on prolactin secretion was repeatedly shown to be potentiated. Same pretreatments with two different time intervals (30 and 60 min) between sulpiride and oxytocin/vasopressin administration, however, had no effect on oxytocin- or vasopressin-stimulated prolactin secretion. A vasopressin analog, 1-deamino-[D-Arg8]-vasopressin (dDAVP), with antidiuretic but no vasopressor activity was also used in the study. It was found that unlike vasopressin, dDAVP had no effect on prolactin secretion. In conclusion, both oxytocin and vasopressin can have a stimulatory effect on prolactin secretion when given in vivo. Unlike TRH, however, the action of oxytocin or vasopressin was not augmented by pretreatments of dopamine antagonist. The action of vasopressin on prolactin secretion may be a side effect of its vasopressor activity.

Animals↗
PubMed1990

Desmopressin, but not vasopressin, decreases activity of the hypothalamo-neurohypophysial system in Brattleboro rats.

The pituitary neural lobe of homozygous Brattleboro rats has high rates of glucose utilization not affected by chronic treatment with exogenous vasopressin, despite attenuation of polydipsia and polyuria. We evaluated whether this effect may result from the inability of vasopressin to affect the hypothalamo-neurohypophysial metabolism or from the development of resistance to chronic vasopressin treatment. We used the [14C]deoxyglucose method to compare 28-h effects of vasopressin treatment (5 U/kg, i.m., twice a day) with that of desmopressin (100 micrograms/kg, i.p., once a day), a long-lasting antidiuretic hormone, on glucose utilization of the hypothalamo-neurohypophysial system and related structures in conscious homozygous Brattleboro rats. Vasopressin and desmopressin reduced water intake, plasma osmolality and plasma Na+ concentration similarly. Vasopressin decreased glucose utilization in the supraoptic nucleus, subfornical organ and median preoptic nucleus, but did not alter activity in the paraventricular nucleus and neural lobe. Desmopressin decreased glucose utilization in all these structures. The results indicate that desmopressin has a more potent inhibitory action on the hypothalamo-neurohypophysial system than vasopressin over this short duration of treatment. The lack of response in the neural lobe from chronic treatment with vasopressin seems to be due to its inability to affect the paraventricular nucleus metabolism. The maintenance of metabolic activity in the paraventricular nucleus of vasopressin-treated Brattleboro rats suggests that this structure contributes importantly to the metabolism of neural lobe.

Animals↗
PubMed1996

Circadian rhythm of neuronal activity in suprachiasmatic nucleus slices from the vasopressin-deficient Brattleboro rat.

In vitro extracellular recordings were made from tissue slices of suprachiasmatic nucleus from homozygous Brattleboro rats which are deficient in vasopressin. A high proportion (56%) of neurons were excited by application of exogenous vasopressin, indicating that the V1 receptors expressed by these neurons were functional. Basal activity of these vasopressin-sensitive neurons showed a marked circadian variation (higher during the subjective light phase) while vasopressin-insensitive neurons showed no significant variation, suggesting the presence of the V1 receptor identifies a population of highly circadian neurons. Suprachiasmatic neurons from both homozygous rats and their heterozygous (vasopressin-containing) litter mates displayed a circadian rhythm of spontaneous (basal) activity, with firing rates declining during the subjective dark phase, indicating that the endogenous pacemaker driving the circadian rhythm was not dependent upon the presence of vasopressin. However, the peak of spontaneous activity displayed during the subjective light phase was significantly lower in the vasopressin-deficient animals. These data show that the presence of endogenous vasopressin within the suprachiasmatic nucleus is not necessary for the generation of the circadian pattern of activity. However, vasopressin does function to amplify the rhythm by its excitatory effect during the light phase.

Animals↗
PubMed2005

Enhanced reactivity to vasopressin in rat basilar arteries during vasospasm after subarachnoid hemorrhage.

Subarachnoid hemorrhage increases the plasma level of vasopressin, a well-known vasoconstrictor. We examined the sensitivity to vasopressin in rat basilar artery after subarachnoid hemorrhage using a rat subarachnoid hemorrhage model. Vasospasm was observed 1-2 days after subarachnoid hemorrhage induction, and the contractile response to vasopressin in rat basilar arteries was assessed. The concentration-response curve for vasopressin in subarachnoid hemorrhage (1 day) rats shifted leftward compared with that of control rats. The concentration-response curve for vasopressin V(1) receptor agonist also shifted leftward and upward compared with that of control rats. The concentration-response curve for vasopressin was inhibited not by vasopressin V(2) receptor antagonist but by vasopressin V(1) receptor antagonist. Thus, it was demonstrated that the vasoconstricting effect of vasopressin was significantly enhanced in the vasospasm phase after subarachnoid hemorrhage.

Animals↗