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)

The hypothalamic paraventricular nucleus (PVN) has been implicated in a remarkable number of functions including control of pituitary-adrenocortical activity in response to stress, body fluid homeostasis, milk ejection reflex, prolactin secretion, thyroid hormone secretion, analgesia, food intake, gastrointestinal functions, cardiovascular functions, and control of pineal melatonin synthesis. Paraventricular neurons produce hormones of key importance in neuroendocrine regulation such as vasopressin (VP), oxytocin (OX), 41-residue corticotropin releasing factor (CRF), thyrotropin releasing hormone (TRH), somatostatin (SOM) and the putative prolactin releasing factor vasoactive intestinal polypeptide (VIP). Three recent advances pertinent to the organization of the PVN include: (1) the evidence that the structure of the PVN is compartmental in nature, topographically segregated cellular units seem to carry out different functions; (2) the discovery that paraventricular neurons are capable of expressing a multitude of neuromediators simultaneously, thus cellular units can be best specified by a certain combination of neuromediators; (3) evidence that the composition of the neuromediator "cocktail" in individual neurons is variable and depends on the physiological status of the animal. Hence, the PVN may be best considered as a dynamic mosaic of chemically specified subgroups of neurons. The flexibility of neurotransmitter status in paraventricular neurons may play a central role of a functional plasticity of fixed anatomical circuits.
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PMID:Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus. 304 19

The role of variation of venous return on baroreflex control of heart rate during lumbar epidural anesthesia was investigated in 12 unpremedicated patients. Group 1 patients (n = 6) received 8 ml of 0.5% plain bupivacaine in the epidural space (L3-4) (mean upper level of analgesia at T10). Group 2 patients (n = 6) received 8 ml of saline at the same level in the epidural space. Following the epidural injection, phenylephrine (PHE) and nitroglycerin (NTG) were employed to alter the stimulation of baroreceptor sites before and during application of lower body positive pressure (LBPP). Plasma bupivacaine, catecholamines, renin activity, and vasopressin were assayed. In contrast to saline, epidural bupivacaine induced a decrease in systolic arterial and right atrial pressures (-11 +/- 4 and -3.2 +/- 0.7 mmHg, respectively, mean +/- SEM) without change in heart rate, an increase in baroreflex slopes during PHE and NTG injections (+5.9 +/- 1.6 ms/mmHg and +2.8 +/- 0.9 ms/mmHg, respectively), and a decrease in plasma norepinephrine (-248 +/- 89 pg/ml). The application of LBPP restored hemodynamic and reflex variables to preepidural analgesia values, whereas plasma catecholamines decreased further. Plasma renin activity and vasopressin were not modified at any time in either groups. This study indicates that lumbar epidural anesthesia enhances cardiac vagal tone mainly through a decrease in venous return.
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PMID:Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans. 308 Sep 22

Whether plasma vasopressin (VP) mediates footshock-induced analgesia was examined in conscious rats. Footshocks significantly increased threshold temperature of tail flick and plasma VP as reported previously. Intravenous VP increased the threshold only in doses that are considered to elevate plasma VP to a level more than 500 times higher than that after footshocks. In addition, posterior pituitary stimulation increased plasma VP to a level ten times higher than that after footshocks but did not significantly change the threshold. It is therefore highly likely that plasma VP is not involved in footshock-induced analgesia.
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PMID:Plasma vasopressin is not involved in footshock-induced analgesia in rats. 322 26

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

Recent animal studies indicate that vasopressin has analgetic properties. The aim of this study was to find out if lypressin, a vasopressin analogue, produces analgesia in man. The effect of i.n. lypressin (5 and 10 I.U.) on experimental pain was tested in healthy humans. The lower dose proved high enough to produce a significant antidiuretic effect. Lypressin did not have any marked analgetic effect at these doses either on ischaemic, cutaneous thermal, or dental pain. The results indicate that lypressin cannot be used for pain relief in man at doses low enough not to produce a hazardous water retention.
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PMID:Human pain thresholds after the application of lypressin, a vasopressin analogue. 362 76

Several peptides, including arginine-vasopressin (AVP), neurotensin, and substance P, produce analgesia that is not mediated by opiate systems. Using the hot plate test, we studied the analgesic effects of intracisternal (i.c.) administration of various doses of the nonapeptide oxytocin (OXY) in Swiss-Webster mice. We found that OXY (1-4 micrograms) significantly increased the latency of animals to jump or lick their paws after placement on a hot plate. This effect was not blocked by naloxone pretreatment, which suggests that it is not opiate dependent. Using the hot plate test, we confirmed that AVP (1 and 4 micrograms) also produces analgesia. We then studied the analgesia produced by OXY and by AVP using 3 nonapeptide analogues with antagonist properties: [Pen1, LpMePhe2, Thr4, Orn8]OXY (PLMPTO-OXY) that has anti-oxytocic properties in the uterine contraction assay, d(CH2)5Tyr(Me)AVP(dTM-AVP) which antagonizes the antidiuretic properties of AVP and d(CH2)5D-Ile2,Abu4-AVP (dIA-AVP) which antagonizes the vasopressor effects of AVP. Simultaneous administration of PLMPTO-OXY completely blocked the analgesia produced by OXY whereas the antidiuretic antagonist dIA-AVP partially blocked OXY-induced analgesia and dTM-AVP had no effect. None of the antagonists used blocked AVP-induced analgesia. We concluded that the neural systems mediating the analgesic effects of i.c. OXY differ from those for AVP.
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PMID:Effects of nonapeptide antagonists on oxytocin- and arginine-vasopressin-induced analgesia in mice. 367 85

The purpose of this study is to analyze the causes of elevation of plasma antidiuretic hormone (ADH) level during surgery and the relationship between urinary volume and plasma ADH level by measuring plasma ADH level of patients undergoing operation for esophageal cancer. The results obtained were as follows: The plasma ADH level was 4.0 pg/ml before surgery, 59 pg/ml after skin incision, 190 pg/ml after thoracotomy, and 276 pg/ml after vagotomy (right esophageal branch). Elevation of the plasma ADH level was partially suppressed by epidural analgesia combined with GOF anesthesia. The main factors that elevate plasma ADH level during surgery were pain at the skin incision, the manipulation of the pleura and vagotomy. The plasma ADH level was high (114 pg/ml) just after surgery and decreased to a normal level (4.3 pg/ml) in the morning of the 2nd postoperative day. Urinary volume was 74 ml/h before surgery, 95 ml/h just after surgery and 40 ml/h in the morning of the 1st postoperative day, and then, continued to gradual increase. There was no correlation between urinary volume and plasma ADH level during surgery until the 1st postoperative day. Elevation of plasma ADH level was not a primary factor of oliguiria during and just after surgery.
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PMID:[Fluctuation in plasma ADH levels during and after surgery of esophageal cancer]. 378 29

Mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin changes induced by a 30-degree head-up tilt were studied before and during epidural anesthesia with bupivacaine in eight elderly patients (ages 58-82 yr). The tilt performed before epidural anesthesia did not modify mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin at 5 and 15 min. During epidural anesthesia, the superior level of analgesia ranged from T4 to T10. Epidural anesthesia induced significant (P less than 0.05) decreases from control values in mean arterial pressure and plasma norepinephrine (from 85 +/- 6 to 67 +/- 8 mmHg and from 600 +/- 108 to 307 +/- 77 pg/ml, respectively, mean +/- SEM) without significant changes in heart rate, plasma epinephrine, renin activity, and vasopressin. However 5 and 15 min after tilt, significant decreases from pretilt values were measured in mean arterial pressure (from 67 +/- 8 to 57 +/- 6 and 55 +/- 6 mmHg, respectively) and in heart rate (from 70 +/- 8 to 63 +/- 7 and 62 +/- 7 beats/min). Simultaneously, an increase in plasma vasopressin (from 14.8 +/- 5.5 to 36.2 +/- 10.3 and 40.0 +/- 10.5 pg/ml) was recorded, whereas plasma norepinephrine and epinephrine remained unchanged. Posttilt plasma renin activity values at 5 and 15 min were increased significantly when compared with the preepidural values (2,752 +/- 1,168, 2,410 +/- 1,214 and 713 +/- 190 pg X ml-1 X h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of epidural anesthesia on catecholamines, renin activity, and vasopressin changes induced by tilt in elderly men. 388 49

Vasopressin antiserum was given to two day old rats and the nociceptive thresholds were evaluated three months later. The rats were hypersensitive to pain when electrical current, but not heat, was used as the noxious stimulus. These animals were also insensitive to cold-water swim, a non-opioid form of stress analgesia. The vasopressin content in the pituitary or in the hypothalamus was not however modified by the neonatal treatment. The present results suggest a physiological role for vasopressin in non-opioid pain inhibitory systems.
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PMID:Long-term hyperalgesia in rats induced by neonatal administration of vasopressin antiserum. 394 58


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