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)

In an attempt to test the possibility that sino-aortic baroreceptors may mediate the previously reported stress response in hypothalamic magnocellular neurosecretory cell activity in rats, effects of deafferentation of sino-aortic baroreceptors on plasma levels of vasopressin and oxytocin after fear-related emotional stress were studied in male rats 28-33 days after the surgery. An alpha 1-adrenergic receptor agonist, phenylephrine (1 mg/kg) injected i.p. under anesthesia increased arterial blood pressure in the rats that had received surgical operation of sino-aortic denervation (SAD) and in the rats of sham-operation control (SHAM). Reflex bradycardia after phenylephrine occurred in the SHAM but not in the SAD group. These results indicate that afferent signals originating from sino-aortic baroreceptors were effectively blocked by the SAD surgery. In the similarly prepared SAD group, plasma level of vasopressin was decreased and plasma level of oxytocin was increased significantly to the same extent as in the SHAM group after low-frequency shocks (0.05 Hz, 5 min) or environmental cue signals previously paired with shocks. It is therefore suggested that afferent neural signals originating from sino-aortic baroreceptors are not primarily involved in the suppressive vasopressin or the facilitatory oxytocin response to fear-related emotional stress in rats.
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PMID:Neurohypophysial responses to emotional stress after deafferentation of sino-aortic baroreceptors in rats. 131 20

The effects of intracerebroventricularly (i.c.v.) administered histaminergic receptor antagonists on plasma levels of vasopressin, oxytocin, prolactin and adrenocorticotrophic hormone (ACTH) after fear-related emotional stress were investigated in the male rat. Pyrilamine, a histaminergic H1-receptor antagonist did not significantly alter the suppressive vasopressin or the facilitative prolactin response to nonassociatively applied emotional stress. On the other hand, i.c.v. administered ranitidine, a histaminergic H2-receptor antagonist, blocked these responses to stress. Pyrilamine again did not significantly change the suppressive vasopressin response to the associatively applied emotional stress. However, the drug attenuated the prolactin response slightly but significantly. Ranitidine blocked the suppressive vasopressin and the facilitative prolactin responses to the associatively applied emotional stress, but the drug did not change the facilitative oxytocin or ACTH response to the stress. Suppression of motor activity during the associatively applied emotional stress was not significantly changed by either of these antagonists. These results suggest that histaminergic H2 receptors are selectively involved in the neural pathways which mediate the suppressive vasopressin and the facilitative prolactin responses to fear-related emotional stress.
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PMID:A histaminergic H2-receptor antagonist, ranitidine, blocks the suppressive vasopressin response to fear-related emotional stress in the rat. 136 4

Effects of a dopamine D1 receptor antagonist, SCH 23390, were investigated on plasma level of vasopressin after stressful stimuli in rats. The antagonist markedly attenuated the increase in plasma level of vasopressin after electric footshocks but not after s.c. injected hypertonic saline. The antagonist, however, did not significantly change the suppressive vasopressin response to fear-related emotional stress, though the drug suppressed motor behavior of the rat during testing period. These data suggest that dopamine D1 receptors play an important role selectively in the facilitatory vasopressin response to noxious stimuli in rats.
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PMID:A dopamine D1 receptor antagonist, SCH 23390, selectively blocks vasopressin release after noxious stimuli in the rat. 138 18

The effects of emotional stress (ES) corresponding to conditioned fear on colonic motility and its antagonism by [deamino-Pen1, Val4, D-Arg8]vasopressin, a vasopressin antagonist, were investigated by electromyography in conscious fasted rats fitted with chronically implanted electrodes. A 117% increase (19.6 +/- 2.1 vs. 9.0 +/- 0.9 cycles/10 min during the control period) in the frequency of colonic spike bursts was observed when rats were placed for 30 min in a box in which they had previously received electric foot shocks. Intracerebroventricular (icv) administration of corticotropin-releasing hormone (CRH; 0.5 micrograms/kg) mimicked the effects of ES and increased the spike burst frequency of the colon by 88.6% from 5 to 15 min after its administration. At doses between 5 and 20 micrograms/kg the antagonist [deamino-Pen1, Val4, D-Arg8]vasopressin significantly reduced or abolished the effects of ES and CRH administration on colonic motility. Injected icv at doses of 2.5 and 5 ng/kg [Arg8]vasopressin dose dependently increased the frequency of colonic spike bursts. These effects were not reproduced by similar or higher (50 ng/kg) doses given intraperitoneally, and the effects were abolished after previous administration of vasopressin at a dose of 20 micrograms/kg. It is concluded that the effects of ES on colonic motility in rats previously shown to be linked to the central nervous system (CNS) release of CRH are in turn mediated through the central release of vasopressin.
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PMID:CNS vasopressin mediates emotional stress and CRH-induced colonic motor alterations in rats. 155 Feb 33

Interactions between emotional stress due to fear and hypovolemic stimuli on vasopressin secretion were studied in rats. Intraperitoneally injected dextran did not significantly change plasma osmolality and arterial blood pressure but increased blood hemoglobin and plasma vasopressin level. An i.v. infused physiological solution reversed these changes. Emotional stress due to fear acquired by learning suppressed plasma vasopressin level in dextran-injected rats. Emotional stress due to fear produced by low-frequency footshocks also suppressed the increased plasma vasopressin level. These results suggest that emotional stress due to fear interacts with afferent neural signals originating from cardio-vascular volume receptors in the control of vasopressin secretion.
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PMID:Interactions between emotional stress due to fear and hypovolemic stimuli in the control of vasopressin secretion in rats. 170 80

Arginine-8-vasopressin (AVP) was administered subcutaneously on postnatal days 3-7 in a high (10 micrograms/100 g b.wt.) or a low dose (1 microgram/100 g b.wt.) to male Wistar rats. Control pups were untreated or saline injected. Behavioral observations in a complex maze after maturation indicated that neonatal administration of AVP increases exploratory behavior in this novel environment in a dose-dependent way. Cardiac monitoring during the conditioned emotional stress of fear of inescapable electric footshock showed that only the high dose of AVP attenuates the bradycardiac stress response. The analysis of cardiac responses also suggested an adult hyposensitivity to AVP in rats treated neonatally with AVP. In addition, the low dose of neonatal AVP was impairing the retention of a passive avoidance behavior. The data indicate that the neonatal administration of AVP exerts long-term effects upon the behavioral adaptation to novelty and memory processes related to emotional stress. That neonatal AVP is less effective in influencing adult vagally mediated cardiac stress responses suggests differences in the developmental sensitivity ("critical periods") of the central vasopressinergic systems involved in the regulation of behavior and autonomic functioning.
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PMID:Effects of neonatal administration of vasopressin on cardiac and behavioral responses to emotional stress in adult male rats. 180 83

The effects of various stressful conditions on the levels of oxytocin (OT) and vasopressin (VP) in plasma and cisternal cerebrospinal fluid (CSF) of male rats were investigated. Three experimental models were used: exposure to a novel environment for 5 min, immobilization for 15 min, and ether inhalation for 10 min resulting in anaesthesia. Novelty and immobilization induced a slight but significant increase in OT levels in the CSF immediately after the stress. The effect of ether was considerably more pronounced. The concentration of VP in the CSF was elevated only by ether stress. In plasma, the level of OT was increased immediately following immobilization and ether stress but not after novelty stress, whereas VP only showed a delayed response 20 min after immobilization. These results indicate a rapid preferential release of OT in the periphery in response to physical and pharmacological stress. In addition, they provide evidence that release of OT into the CSF is triggered by physical, pharmacological as well as emotional stress, while the central release of VP is rather resistant to emotional stress. The data suggest that OT is a stress hormone in the central nervous system.
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PMID:Differential effects of emotional and physical stress on the central and peripheral secretion of neurohypophysial hormones in male rats. 200 57

The effects of an opioid receptor antagonist, naloxone (NAL), were studied on the changes in pituitary hormone secretion induced by emotional stress. Male Wistar rats were trained with tone stimuli paired with electric footshocks and tested with the tone and environmental cue signals for emotional stress of fear acquired by learning as described previously (Onaka et al. 1988). Rats received s.c. injected NAL 30 min before testing at doses of 0, 0.2, 1.0, 5.0 and 25.0 mg/kg b.w. Half the rats were injected with 0.5 M NaCl (20 ml/kg b.w.) together with NAL. In these hypertonic rats plasma vasopressin level was slightly increased after NAL. The increment was statistically significant in control groups but not in experimental groups. However the suppression of vasopressin secretion by emotional stimuli was not changed by NAL. Plasma oxytocin levels were extremely high and not significantly different among experimental, unshocked control and untested control groups. NAL further increased the oxytocin level dose-dependently. NAL did not significantly change plasma adrenocorticotrophic hormone (ACTH) levels and hence did not modify the augmentative response in ACTH secretion to emotional stimuli. Plasma prolactin level was significantly elevated after emotional stimuli and NAL depressed the prolactin level in each of experimental and control groups. After NAL, the magnitude of the facilitatory response in prolactin secretion to emotional stimuli was decreased. Motor activity and its suppressive response to emotional stimuli were not influenced by NAL. In another half of rats under a normal osmotic condition the vasopressin response to emotional stimuli was not affected by NAL. NAL further augmented potentiation of oxytocin secretion after emotional stimuli dose-dependently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of naloxone on neuroendocrine responses to fear-related emotional stress. 216 20

In an attempt to find whether vasopressin (VP) secretion is suppressed by learned emotional stress, we have given rats under a hypertonic condition simultaneously applied light and tone that had been paired previously with footshocks and have quantified immunoreactive VP (ir-VP) in the plasma. In a training session light (60 watt) and tone (2 kz) of 3-s duration which were paired with electric footshocks (50 Hz, 1-s duration) were given to rats 11 times at an interval of 30 s. Various lengths of time after the training, the rats were tested with light and tone, which were unpaired with footshocks and repeatedly applied every 15 s for 3 min in the box used for training. Hypertonic NaCl (0.5 M, 2 ml/100 g b.w.) was injected s.c. 30 min before testing to increase the basal level of plasma VP. After testing, plasma ir-VP was significantly less in the experimental group than in the 0-mA control group of rats that were trained without FS. The values for the experimental group were also significantly less than those of untested control rats that had been trained with FS but were not tested. Plasma osmolality and blood haemoglobin concentration were not significantly different between control and experimental groups. Plasma immunoreactive adrenocorticotrophic hormone (ir-ACTH) level was higher and motor activity as expressed by cumulative time period of body movement during testing was lower in the experimental group than in either of the control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin secretion: suppression after light and tone stimuli previously paired with footshocks in rats. 284 77

Effects of footshocks (FS) on antidiuretic hormone (vasopressin, VP) in the plasma were studied in rats. Continuously applied FS of 60 s period with 5 ms pulses at 50 Hz frequency significantly increased VP as well as adrenocorticotrophic hormone (ACTH) in the plasma in a time- and shock intensity-dependent manner. Contrarily, the 50 Hz FS of 2 s period as repeated intermittently at every 15 s for over the period of 2, 10, and 30 min were much less effective for increasing plasma VP, whereas these intermittent FS increased plasma ACTH to an extremely high level. During the inter-shock intervals of 13 s between successive two shock periods rats exhibited a "freezing" behavior. Hypertonic saline or urethane injected I.P. immediately after termination of the intermittent FS significantly increased VP as well as ACTH in the plasma. These data clearly indicate that FS potentiate VP secretion and suggest the possibility that emotional stress may suppress the noxious stimuli-induced VP secretion.
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PMID:Potentiation of vasopressin secretion by footshocks in rats. 303 42


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