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PubMed1984

Vasopressin effect on learning in 6-hydroxydopamine-pretreated rats: correlation with caudate vasopressin levels.

Conditioned avoidance learning was studied at 2 months of age in rats treated with intracisternal 6-OH dopamine (DA) at 5 days of life after desipramine pretreatment. Subcutaneous DDAVP 20 micrograms/rat or LVP 1 microgram/rat improved conditioned avoidance learning in the 6-OH DA-treated rats at least as much as in control rats. Caudate vasopressin levels significantly correlated with learning ability in the shuttle box in control rats (r = 0.69, n = 8), 6-OH DA-treated rats (r = 0.64, n = 8), 6-OH DA plus DDAVP-treated rats (r = 0.60, n = 9), or in the total sample (r = 0.59, n = 25, p less than 0.01).

Animals↗
PubMed1996

[The ultrastructural characteristics of the epithelial cells in the frog bladder under the action of vasopressin and in a vasopressin-independent increase in permeability for water].

In experiments on isolated frog urinary bladders it has been found that the low basal level of water permeability in the absence of arginine-vasopressin (AVP) could be significantly increased when the serosal solution was changed several times every 15 min for a fresh Ringer solution. The electron microscopic study of these cells by the freeze-fracture technique showed that the enhancement of water permeability by AVP-independent manner was related to the appearance of intramembranous particle aggregates in luminal membrane of granular cell, that are usually observed only under the action of AVP. The immunocytochemical experiments with monoclonal antibodies against actin revealed the similarity in intracellular actin distribution under the action of AVP and AVP-independent increase of water permeability.

Animals↗
PubMed1998

Vasopressin regularizes the phasic firing pattern of rat hypothalamic magnocellular vasopressin neurons.

Vasopressin (AVP) magnocellular neurons of hypothalamic nuclei express specific phasic firing (successive periods of activity and silence), which conditions the mode of neurohypophyseal vasopression release. In situations favoring plasmatic secretion of AVP, the hormone is also released at the somatodendritic level, at which it is believed to modulate the activity of AVP neurons. We investigated the nature of this autocontrol by testing the effects of juxtamembrane applications of AVP on the extracellular activity of presumed AVP neurons in paraventricular and supraoptic nuclei of anesthetized rats. AVP had three effects depending on the initial firing pattern: (1) excitation of faintly active neurons (periods of activity of <10 sec), which acquired or reinforced their phasic pattern; (2) inhibition of quasi-continuously active neurons (periods of silences of <10 sec), which became clearly phasic; and (3) no effect on neurons already showing an intermediate phasic pattern (active and silent periods of 10-30 sec). Consequently, AVP application resulted in a narrower range of activity patterns of the population of AVP neurons, with a Gaussian distribution centered around a mode of 57% of time in activity, indicating a homogenization of the firing pattern. The resulting phasic pattern had characteristics close to those established previously for optimal release of AVP from neurohypophyseal endings. These results suggest a new role for AVP as an optimizing factor that would foster the population of AVP neurons to discharge with a phasic pattern known to be most efficient for hormone release.

Action Potentials↗
PubMed1998

Effects of the vasopressin V1a receptor antagonist, SR 49059, on the response of human uterine arteries to vasopressin and other vasoactive substances.

BACKGROUND: Arginine vasopressin (AVP) activates the uterus via V1a receptors and is apparently an important factor for the myometrial hyperactivity, uterine ischemia and pain of primary dysmenorrhea. The orally active and selective, non-peptide AVP1a receptor antagonist, SR 49059, has been shown to inhibit the myometrial action of AVP, but the specific influence of this substance on the effects of AVP and other vasoactive agents on human uterine arteries is unknown. METHODS: Concentration-responses of AVP on isolated medium-sized human uterine arteries were studied after incubation with only vehicle (DMSO, 0.1%) and with SR 49059 in concentrations of 0.5, 2.5 and 10 nmol/L. Furthermore, the concentration-responses of AVP were investigated without and with SR 49059 (2 and 10 nmol/L) on small and medium-sized arteries. Finally, the influence of 2.5 nmol/L of SR 49059 on concentration-responses of endothelin-1, noradrenaline and prostaglandin F2 alpha was studied. RESULTS: The EC50 for AVP on medium-sized arteries was 0.53 +/- 13 nmol/L. SR 49059 caused a competitive, dose-dependent inhibition of AVP-responses, the highest concentration giving an EC50 of 460 nmol/L. The pA2 value was 9.84. The responses of the small artery preparations to AVP, both without and with the antagonist, were more pronounced than those of the medium-sized ones. The vasoconstrictive effects of endothelin-1, noradrenaline and prostaglandin F2 alpha were less pronounced than those of AVP and unaffected by pre-exposure to SR 49059. CONCLUSIONS: The high potency of AVP on human uterine arteries, particularly those of small size, supports an involvement of the peptide in the regulation of uterine blood flow in both physiological and pathophysiological condition. SR 49059 is a potent and selective AVP V1a receptor antagonist in the smooth muscle of human uterine arteries.

Adult↗
PubMedDate not supplied

Vasopressin release, water channels, and vasopressin antagonism in cardiac failure, cirrhosis, and pregnancy.

Vasopressin (AVP) is released in response to both osmotic and nonosmotic stimuli. Nonosmotic-stimulated AVP release occurs in cardiac failure, cirrhosis, and pregnancy in response to alterations in arterial circulatory integrity. Cardiac failure in rats is associated with increased plasma AVP and hypothalamic AVP mRNA, and in humans, it is associated with cardiac failure. Plasma AVP concentrations are elevated when measured with a sensitive radioimmunoassay. Urinary concentrations of AVP-responsive aquaporin-2 water channels are also elevated in cardiac failure. V2 receptor antagonists correct the impaired solute-free water excretion seen in rats with low-output cardiac failure and reverse the upregulation of renal aquaporin-2 water channels. Orally active non-peptide-selective V2 receptor antagonists administered to patients with congestive cardiac failure decrease urinary concentrations of aquaporin-2, increase solute-free water clearance, and correct the hyponatremia. Cirrhosis of the liver results in splanchnic arterial vasodilation and increased vascular capacity, most likely secondary to increased nitric oxide production. This relative underfilling of the arterial circulation stimulates nonosmotic AVP release with resultant water retention. Aquaporin-2 gene expression is upregulated in the kidneys of rats with cirrhosis of the liver. AVP-2 receptor antagonists administered to animals with cirrhosis reverse the water retention. Human studies using orally active, non-peptide-selective V2 receptor antagonists in patients with cirrhosis are currently underway. Pregnancy is another state of nitric oxide-mediated arterial vasodilation that is associated with plasma AVP concentrations that are relatively high for the degree of hypoosmolality. Upregulation of the water channel aquaporin-2 in the renal papillae of pregnant rats has also been demonstrated, and this effect is reversed by administration of a V2 receptor antagonist.

Animals↗
PubMed1980

Long term stability of lysine vasopressin and of specifically tritiated lysine vasopressin in weakly acidic aqueous solutions.

Lysine vasopressin tritiated at meta position of tyrosine (1.9 Ci/mmole) decomposes during a long storage period, mainly as a result of radiolysis. The loss of specific activity by isotopic exchange with water is slow. The nonlabelled peptide undergoes only very minute decomposition (polymerization). Specific radioactivity declines with a half life of 47.4 months.

Animals↗
PubMed1991

Chronic treatment with vasopressin analogues alters affinity of vasopressin receptors in the septum and amygdala of the rat brain.

Accurel devices were used to administer AVP or AVP-antagonist into the lateral ventricle of the rat brain for 7 days. Neither AVP nor antagonist altered total binding site concentration in either septum or amygdala. However, treatment with antagonist caused a marked decrease in the affinity of the receptor for agonist in both the septum and amygdala.

Amygdala↗
PubMed1992

Microdialysis administration of vasopressin and vasopressin antagonists into the septum during pole-jumping behavior in rats.

Wistar rats (n = 95) were trained in a pole-jumping apparatus (10 trials/session/day) to investigate the involvement of centrally and peripherally released endogenous AVP in their acquisition rate and to examine the feasibility of the microdialysis technique for the administration of peptides during a behavioral test. After session 1, a microdialysis probe was implanted into the septum; during sessions 2 and 3 the probe was perfused with artificial cerebrospinal fluid (aCSF) alone or containing either AVP (delivered amount via the probe: 0.2 ng) or the V1 (d(CH2)5Tyr(Me)AVP, 5.0 ng) or the V2/V1 (d(CH2)5-D-Tyr(Et)VAVP, 5.0 ng) antagonist. Administration of AVP via microdialysis into the septum failed to alter the acquisition rate of pole jumping. Also, ip application of both hypertonic saline and the AVP V1 antagonist (10 micrograms) in another experiment failed to show a significant effect upon behavior. Septal administration of the V1 or the V2/V1 antagonist via microdialysis, however, produced a significantly impaired performance. The results indicate that AVP release within the septum is involved in the acquisition of pole-jumping behavior probably mediated by the V1 receptor subtype. An additional involvement of the V2 receptor subtype, however, cannot be entirely excluded. The microdialysis technique proved to be a potent tool to administer substances concomitantly with behavioral tests.

Animals↗