Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PMS is probably a group of entities which include various symptoms that occur during the 7 to 10 days before menstruation and disappear a few hours after the onset of menstruation. The definition of PMS lacks objective criteria. The most common symptoms are irritability, bloating, aggressiveness, mastodynia, and headaches. The prevalence of PMS is estimated at 30 to 40 per cent. PMS is more prevalent among women working outside the home, alcoholics, women of high parity, and women with toxemic tendency; it probably runs in families. The etiology of PMS is no less obscure to us than when it was first described by Frank in 1931. No single theory has been established to explain the entire diversity of PMS symptomatology. The multitude of possible etiologic factors includes psychosocial bases, progesterone deficiency, prolactin excess, thyroid hypofunction, renin angiotensin alternations, antidiuretic hormone excess, decreased colloidosmotic pressure, endorphin activity alternations, serotonin metabolism alternations, prostaglandin action, vitamin deficiency, and such unconventional theories as the ovarian infection or the "yeast overgrowth" theory. A partial resolution of this divergence of hypotheses comes from the biopsychosocial model developed by Keye and Trunnel. According to this model, a biologic, perhaps genetically determined, predisposition to PMS is realized when past and present life experiences, attitudes, beliefs, coping styles, and social forces interact to stress a woman. The diagnosis of PMS is based on establishing a relationship between the luteal phase of the cycle and the symptoms. The evaluation of PMS patients includes the use of a monthly diary to scale the symptoms, a physical examination, and biochemical studies to rule out other disorders. Management includes education, reassurance, and drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The premenstrual syndrome. 218 58

A study was undertaken on the effects of kainic acid lesioning on the nodulus of the rat cerebellum on behavior and various brain receptors in conscious, freely moving rats. The basis for the study was the observation that barrel rotation and other motor effects induced by intraventricular administration of vasopressin and nicotine could be elicited by their administration into the nodular area of the cerebellum. Histology revealed a marked destruction of Purkinje, stellate, and Golgi cells in the area surrounding the site of kainate administration, with little effect on the granular cells. Immediately after administering 4-12 ng of kainic acid into the nodular cerebellum, rats exhibited circling movements, barrel rotation, and clonic convulsions accompanied by stereotypic head movements, aggressiveness, and gnawing-biting; effects gradually diminishing over 3 days. Receptor binding studies 4-14 days after kainate lesioning revealed a marked increase in 3H-nicotine and 3H-QNB binding in the surrounding cerebellar region, caudate nucleus, and hypothalamus, with no change in 3H-dihydromorphine binding. The findings are consistent with the hypothesis that nicotinic and muscarinic pathways in the vestibular cerebellum, along with its connection to nigrostriatal dopaminergic systems, are involved in the mediation of barrel rotation, ataxia, and other motor disturbances resulting from administration of vasopressin on nicotine intraventricularly.
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PMID:Behavior and receptor changes after kainate lesioning of nodular cerebellum. 302 7

The neurochemical and behavioural effects of a novel stereotaxic surgical method developed for interrupting the nerve fibres running through the rat pituitary stalk to the posterior pituitary gland was studied. The cerebrospinal fluid (CSF) vasopressin (AVP) and oxytocin (OT) content as well as changes in aggressiveness were measured in rats one week and one month after the surgical intervention. The main results are as follows: (1) the compression of the pituitary stalk elicits a chronic increase in water consumption, as well as in CSF vasopressin and oxytocin content; (2) the surgical intervention increased the frequency of clinch fighting after one week. The increase in aggressiveness accentuated after one month and, in addition, operated animals showed reduced scores of resting while exploratory and social behaviours increased; (3) there was a strong positive correlation between water consumption, vasopressin, and aggressiveness; (4) oxytocin changes showed a positive correlation with variation in social behaviour. The surgical intervention may serve as a model for lesions of the pituitary stalk and formation of ectopic neurohypophyses in humans.
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PMID:Compression of the pituitary stalk elicits chronic increases in CSF vasopressin, oxytocin as well as in social investigation and aggressiveness. 873 35

The brain systems that motivate humans to form emotional bonds with others probably first evolved to mobilize the high-quality maternal care necessary for reproductive success in placental mammals. In these species, the helplessness of infants at birth and their dependence upon nutrition secreted from their mothers' bodies (milk) and parental body heat to stay warm required the evolution of a new motivational system in the brain to stimulate avid and sustained mothering behavior. Other types of social bonds that emerged subsequently in placental mammals, in particular monogamous bonds between breeding pairs, appear to have evolved from motivational brain systems that stimulate maternal behavior. This chapter focuses on aspects of the evolution and neurobiology of maternal and pair bonding and associated behavioral changes that may provide insights into the origins of human violence. The roles of the neuropeptides oxytocin and vasopressin as well as the neurotransmitter dopamine will be emphasized. Maternal and pair bonding are accompanied by increased aggressiveness toward perceived threats to the object of attachment as well as diminished fear and anxiety in stressful situations. The sustained closeness with mother required for the survival of infant mammals opened a new evolutionary niche in which aspects of the mother's care became increasingly important in regulating development in offspring. The quantity and quality of maternal care received during infancy determines adult social competence, ability to cope with stress, aggressiveness, and even preference for addictive substances. Indeed, the development of neurochemical systems within the brain that regulate mothering, aggression, and other types of social behavior, such as the oxytocin and vasopressin systems, are strongly affected by parental nurturing received during infancy. Evidence will be reviewed that the neural circuitry and neurochemistry implicated in studies of lower mammals also facilitate primate/human interpersonal bonding. It is hypothesized that neural bonding systems may also be important for the development in individuals of loyalty to the social group and its culture. Neglect and abuse during early life may cause bonding systems to develop abnormally and compromise capacity for rewarding interpersonal relationships and commitment to societal and cultural values later in life. Other means of stimulating reward pathways in the brain, such as drugs, sex, aggression, and intimidating others, could become relatively more attractive and less constrained by concern about violating trusting relationships. The ability to modify behavior based on negative experiences may be impaired. Unmet needs for social bonding and acceptance early in life might increase the emotional allure of groups (gangs, sects) with violent and authoritarian values and leadership. Social neurobiology has the potential to provide new strategies for treating and preventing violence and associated social dysfunction.
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PMID:Biological aspects of social bonding and the roots of human violence. 1581 33

Since vasopressin has been shown to be critical for adaptation of the hypothalamo-pituitary-adrenal axis during stress through its ability to potentiate the stimulatory effect of CRF, it has been hypothesized that this peptide may provide a good opportunity for pharmacological treatment of stress-related disorders. The availability of the first orally active non-peptide V(1b) receptor antagonist, SSR149415, opened a new era for examining the role of vasopressin in animal models of anxiety and depression. In rats, SSR149415 blocked several endocrine (i.e. ACTH release), neurochemical (i.e. noradrenaline release) and autonomic (i.e. hyperthermia) responses following various stress exposures. Moreover, the drug was able to attenuate some but not all stress-related behaviors in rodents. While the antidepressant-like activity of the compound was comparable to that of reference antidepressants, the overall profile displayed in anxiety tests was different from that of classical anxiolytics, such as benzodiazepines. These latter were highly effective and reliably produced robust effects in most anxiety tests, while SSR149415 showed clear-cut effects only in particularly stressful situations. Experiments with mice or hamsters indicated that V(1b) receptor blockade is associated with reduced aggressiveness, suggesting that SSR149415 could prove useful for treating aggressive behavior. It is important to note that SSR149415 is devoid of adverse effects on motor functions or cognitive processes, and it did not produce tolerance to its anxiolytic- or antidepressant-like activity. Altogether, these findings suggest that V(1b) receptor antagonists represent a promising alternative to agents currently used for the treatment of depression and some forms of anxiety disorders.
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PMID:Non-peptide vasopressin V1b receptor antagonists as potential drugs for the treatment of stress-related disorders. 1589 61

The vasopressin peptide analog desmopressin has been used during surgery to prevent bleeding in patients with coagulation defects. Recent experimental and clinical data revealed that perioperative desmopressin therapy can minimize the spread and survival of residual cancer cells. Here, we explored the antitumor effects of desmopressin in combination with chemotherapeutic agents using the F3II mammary carcinoma in syngeneic Balb/c mice. Intravenous administration of desmopressin at a dose of 2 microg/kg together with weekly cycles of carmustine (20 mg/kg) prevented primary tumor infiltration of the skin. Combination of desmopressin with paclitaxel (25 mg/kg) significantly reduced metastatic progression to the lung. Although desmopressin had an antiproliferative effect on F3II cells, in vitro studies did not demonstrate an enhanced cytotoxicity with chemotherapy. Our results suggest that desmopressin may contribute to impair aggressiveness of residual mammary tumors during chemotherapy.
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PMID:Antitumor effects of desmopressin in combination with chemotherapeutic agents in a mouse model of breast cancer. 1903 85

Vasopressin (AVP) is a hormone with antidiuretic properties that is also involved in cellular proliferation of breast, pulmonary, and pancreatic neoplasias, attributable to the interaction with specific receptors, among which is the V2-R. Using a culture model of CAKI-2 and A498 cancer cells, our study aimed to verify if renal carcinoma cells also express V2-R and whether receptor activation modulates their proliferation. Immunofluorescence and RT-PCR showed that both CAKI-2 and A498 cells effectively synthesize and express the V2-R. Administration of the vasopressin analogue DDAVP induced an evident growth in both CAKI-2 and A498 cell lines. However, this proliferative effect was completely avoided by the preventive addition of the V2-R antagonist SR121463B (satavaptan). Our study shows for the first time that renal cancer may effectively synthesize and express the V2-R. Furthermore, AVP exerts in vitro a proliferative effect by acting on this receptor, as the selective V2-R blockage is able to completely prevent the cellular growth. A validation of these findings with in vivo models is required to ascertain if the eventual presence of V2-R could influence the aggressiveness of human renal neoplasias. From this point of view, a new, interesting therapeutical application of V2-R antagonists in the treatment of renal cancer could also be proposed, similar to that successfully described in the treatment of autosomal polycystic kidney disease (ADPKD).
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PMID:Aquaretic inhibits renal cancer proliferation: Role of vasopressin receptor-2 (V2-R). 1921 6

Recently, several studies have shown different conclusions regarding the effect of oxytocin (OT) on the social behaviors of male mice. Most of these studies used exogenous OT, but currently, investigations of the neural bases of social behavior are increasingly employing gene inactivation. This study aimed to analyze the role of OT in the modulation of social behaviors (i.e., sexual and social interaction behaviors) in male mice with selective deletions of the OT gene (OTKO) and the influence of this deletion in basal vasopressin (AVP) plasma concentrations. Our results showed that in the social interaction test, OTKO mice exhibited lower levels of social behaviors and higher levels of non-social behaviors compared to the wild type (WT) group. Additionally, the OTKO group showed a decrease in the number of agonistic behaviors delivered, and consequently, their dominance score was lower than that of the WT group. In the ethological analysis, the OTKO group had a lower aggressive performance and increased social investigation than the WT group. No significant differences were observed in the sexual behavior between groups. Finally, we found lower AVP plasma concentrations in the OTKO compared with the WT group. In conclusion, our data suggest that OT modulates social investigation behavior and the aggressiveness of male mice. The decrease in AVP concentrations in the OTKO group allows us to infer that AVP is physiologically relevant to these behavioral modulations. However, sexual behaviors do not seem to be affected by the lack of OT or by a decrease in the AVP concentration.
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PMID:Oxytocin modulates social interaction but is not essential for sexual behavior in male mice. 2337

The present study investigated the long-lasting effects of prenatal repeated restraint stress on social behavior and anxiety, as well as its repercussions on oxytocin (OT) and vasopressin (VP)-positive neurons of the paraventricular (PVN) and supraoptic (SON) nuclei from stressed pups in adulthood. Female Wistar rats were exposed to restraint stress in the last 7 days of pregnancy. At birth, pups were cross-fostered and assigned to the following groups: prenatally non-stressed offspring raised by prenatally non-stressed mothers (NS:NS), prenatally non-stressed offspring raised by prenatally stressed mothers (S:NS), prenatally stressed offspring raised by prenatally non-stressed mothers (NS:S), prenatally stressed offspring raised by prenatally stressed mothers (S:S). As adults, male prenatally stressed offspring raised both by stressed mothers (S:S group) and non-stressed ones (NS:S group) showed impaired social memory and interaction. In addition, when both adverse conditions coexisted (S:S group), increased anxiety-like behavior and aggressiveness was observed in association with a decrease in the number of OT-positive magnocellular neurons, VP-positive magnocellular and parvocellular neurons of the PVN. The NS:S group exhibited a reduction in the amount of VP-positive magnocellular neurons compared to the S:NS. Thus, the social behavior deficits observed in the S:S and NS:S groups may be only partially associated with these alterations to the peptidergic systems. No changes were shown in the OT and VP cellular composition of the SON nucleus. Nevertheless, it is clear that a special attention should be given to the gestational period, since stressful events during this time may be related to the emergence of behavioral impairments in adulthood.
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PMID:Prenatal stress produces social behavior deficits and alters the number of oxytocin and vasopressin neurons in adult rats. 2362 43

The role of vasopressin in aggression received much attention in recent years. However, vasopressin has complex roles on social behavior, which are affected by social experience, motivation and hormonal background, suggesting that its effects depend on the condition of subjects. This hypothesis was tested here by studying the impact of vasopressin deficiency on aggressiveness in reproductively naive and reproductively experienced males, as well as in lactating females, with special reference to the patterns and contexts of attack behavior. We also studied effects on impulsiveness, a behavioral feature strongly related to aggression. Vasopressin deficiency did not affect aggressiveness in reproductively experienced males, decreased the share of violent attacks in reproductively inexperienced males without affecting total attack counts, and suppressed maternal aggression in both early and late phases of lactation; violent forms of attack were decreased in the latter but not the former phase. Changes in aggression appeared unrelated to general changes in maternal behaviors. Impulsivity in the delay discounting task was markedly decreased by vasopressin deficiency in lactating females but not males. Taken together, our findings confirm that vasopressin has an impact on aggressiveness, but show that this impact depends on the condition of subjects, and suggest that the effects of vasopressin on maternal aggression develop in conjunction with impulsivity. Interestingly, overall effects on aggression and specific effects on violent attacks dissociated in both males and females, which hints to the possibility that vasopressin has distinct roles in the development of escalated forms of aggression.
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PMID:The effects of vasopressin deficiency on aggression and impulsiveness in male and female rats. 2500 64


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