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 release of adrenocorticotropin (ACTH) from the corticotrophs is controlled principally by vasopressin and corticotropin-releasing hormone (CRH). Oxytocin may augment the release of ACTH under certain conditions, whereas atrial natriuretic peptide acts as a corticotropin release-inhibiting factor to inhibit ACTH release by direct action on the pituitary. Glucocorticoids act on their receptors within the hypothalamus and anterior pituitary gland to suppress the release of vasopressin and CRH and the release of ACTH in response to these neuropeptides. CRH neurons in the paraventricular nucleus also project to the cerebral cortex and subcortical regions and to the locus ceruleus (LC) in the brain stem. Cortical influences via the limbic system and possibly the LC augment CRH release during emotional stress, whereas peripheral input by pain and other sensory impulses to the LC causes stimulation of the noradrenergic neurons located there that project their axons to the CRH neurons stimulating them by alpha-adrenergic receptors. A muscarinic cholinergic receptor is interposed between the alpha-receptors and nitric oxidergic interneurons which release nitric oxide that activates CRH release by activation of cyclic guanosine monophosphate, cyclooxygenase, lipoxygenase and epoxygenase. Vasopressin release during stress may be similarly mediated. Vasopressin augments the release of CRH from the hypothalamus and also augments the action of CRH on the pituitary. CRH exerts a positive ultrashort loop feedback to stimulate its own release during stress, possibly by stimulating the LC noradrenergic neurons whose axons project to the paraventricular nucleus to augment the release of CRH.
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PMID:Role of the hypothalamic pituitary adrenal axis in the control of the response to stress and infection. 1100 12

We compared menstrual pain, uterine contractility and blood circulation, and plasma concentrations of vasopressin and prostaglandin F(2alpha) metabolite in women with versus without primary dysmenorrhea, and determined the effects of a vasopressin antagonist, 1-deamino-2-D-Tyr(OEt)-4-Thr-8-Orn-oxytocin (Atosiban), on these parameters. Our results do not support the contention that vasopressin is involved in the etiology of dysmenorrhea, plasma concentrations of vasopressin being similar in dysmenorrheic women and controls, and the vasopressin antagonist Atosiban having no effect on menstrual pain, intrauterine pressure or uterine artery pulsatility index in dysmenorrheic women.
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PMID:Effects of a vasopressin antagonist in women with dysmenorrhea. 1101 49

This short review summarizes the effect of various stressful stimuli on the expression of neuropeptides which co-localize in corticotrophin releasing hormone (CRH)-synthesizing neurons in the hypothalamic paraventricular nucleus, as well as in oxytocin and vasopressin neurons in the supraoptic nucleus. Stress-induced changes failed to act on CRH neurons in the central amygdaloid nucleus but formalin-evoked pain enhanced galanin mRNA expression in the medial subdivision of this nucleus. Changes in the expression of enkephalin, galanin, dynorphin and cholecystokinin mRNA in response to restraint and formalin-induced pain are documented in hypothalamic and amygdaloid nuclei by in situ hybridization histochemical technique.
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PMID:Stress-induced expression of co-localized neuropeptides in hypothalamic and amygdaloid neurons. 1103 23

The development of adrenergic sensitivity in nociceptors has been suggested as a mechanism of neuropathic pain. We sought to determine if nociceptors in the skin of normal subjects exhibit adrenergic sensitivity. We investigated the effects of intradermal administration of norepinephrine, phenylephrine, and brimonidine on heat pain sensitivity. Norepinephrine and phenylephrine (in concentrations ranging from 0.1 to 10 microM by factors of 10), brimonidine (at 0.01-1 microM), and saline were injected (30 microl volume) in a random, double-blind manner to different sites on the volar surface of the forearm in ten subjects. Before and after the injections, heat testing was performed with a non-contact laser thermal stimulator. Heat pain threshold was measured by means of a 'Marstock' technique in which subjects pressed a reaction time key when they perceived that a slowly increasing heat stimulus (1 degrees C/s ramp from a 36 degrees C base) was painful. In addition, the subjects used magnitude estimation techniques to rate the intensity of pain to a suprathreshold heat stimulus (47 degrees C, 2 s). Mechanical testing was done using 200-microm diameter probes attached to calibrated weights that provided forces over the range of 16-512 mN. The intradermal injections of norepinephrine, phenylephrine and brimonidine produced little evoked pain. However, a dose-dependant decrease in heat pain threshold, but not mechanical pain threshold, was observed. At the highest drug dose injected, all three adrenergic compounds produced a significant decrease in heat pain threshold compared to the saline injection. A significant increase in response to the suprathreshold heat stimulus was also found. One possible explanation for this apparent heat hyperalgesia is that the decrease in perfusion due to the localized vasoconstriction may alter the heat response. However, in control studies we found that the non-adrenergic vasoconstrictors, angiotensin II and vasopressin did not produce heat hyperalgesia at doses that produced comparable decreases in blood flow. In addition, occlusion of blood flow with a blood pressure cuff did not lead to heat hyperalgesia. Thus, the heat hyperalgesia observed with the adrenergic agonists is not due to a decrease in perfusion associated with the injection. These results indicate that alpha(1)- and alpha(2)-adrenoceptor-mediated mechanisms may play a role in sensitization of nociceptors to heat stimuli in normal skin.
Pain 2001 Feb 01
PMID:Heat, but not mechanical hyperalgesia, following adrenergic injections in normal human skin. 1116 66

In mammalian organisms were found composed systems controlling the transmission and perception of nociceptive impulses. The present review focuses on clinical and laboratory studies that are aimed at identifying the role of AVP, known antidiuretic hormone in the mechanism of pain phenomenon.
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PMID:[The role of arginine vasopressin (AVP) in pain transmission and perception]. 1187 80

A 43-year-old woman with advanced pulmonary blastoma was admitted for worsening back pain. Her drug regimen included hydromorphone and benazepril. On admission, hydromorphone patient-controlled analgesia (PCA) was started for acute pain control and dexamethasone for possible cord compression. Baseline laboratory tests were unremarkable, but magnetic resonance imaging revealed T3 and L3 lesions. Irradiation was started with improvement in her pain. In anticipation of discharge, a fentanyl transdermal patch was given, and PCA was tapered. Two days later, the patient became progressively confused and fell. Neurologic examination and computed brain tomography were normal. Her serum sodium was 119 mEq/L (normal 136-144 mEq/L) and was confirmed on repeat testing, urine sodium was 194 mEq/L, and urine and serum osmolalities were 554 mOsm/kg (normal 300-900 mOsm/kg) and 245 mOsm/kg (normal 280-300 mOsm/kg), respectively, consistent with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Fluids were restricted, hydromorphone PCA was started again, and fentanyl was discontinued. After 36 hours, her serum sodium increased to 136 mEq/L. Because we were unsure whether the fentanyl or her cancer was causative and were unable to find any published reports of fentanyl-associated SIADH, we readministered the fentanyl patch 2 days later. Within 48 hours, serum sodium dropped to 123 mEq/L. Fentanyl was discontinued, fluids were restricted, and 3% saline was started. Her serum sodium increased to 132 mEq/L in 48 hours. The patient was prescribed oral hydromorphone and benazepril and was discharged. The repeated temporal relationship between the administration of fentanyl and the onset of SIADH strongly implicates fentanyl as the causative agent in this case. To our knowledge, this is the first report of fentanyl-associated SIADH.
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PMID:Fentanyl-associated syndrome of inappropriate antidiuretic hormone secretion. 1222 57

Nausea is an unpleasant sensation usually referred to the stomach and sometimes followed by vomiting. Little is known about the subjective aspects of nausea because like pain and fatigue, it is a private sensation. We conceive of nausea as a complex control mechanism that signals us when not to eat. Our research in the areas of motion sickness and chemotherapy has led us to propose that we each have a dynamic threshold for nausea, which depends on the interaction of inherent factors and more changeable psychological factors, and that this threshold effects the individual's cognitive appraisal of both the nauseogenic stimulus and his/her bodily change in response to the nauseogenic stimulus. Inherent factors that are described are age, gender and race; psychological factors that are included are anxiety, expectation, anticipation and adaptation. The physiological responses that have been found to accompany nausea include an increase in sympathetic nervous system activity, a decrease in parasympathetic activity, an increase of abnormal dysrhythmic gastric activity, and an increase in plasma vasopressin. It is concluded that beneficial selective reduction of nausea will depend on a greater knowledge of the interaction of the psychological and physiological variables.
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PMID:The psychophysiology of nausea. 1250 40

Vasovagal syncope is defined as a reflex loss of consciousness related to reaction to various stimuli as orthostatic stress, pain or emotions connected with loss of muscle postural tone. The aetiology of this disorder is still unknown. The imbalance between the parts of autonomic nervous system and other homeostasis-related systems as renin-angiotensin-aldosterone system, peptides as endothelin, neuropeptide Y, vasopressin, adrenomedullin and cAMP, adenosine and AMP can play an important role in the development of vasovagal syncope. In the first part of the paper the authors describe the mechanisms involved in the development of vasovagal reaction, pathophysiology of the head-up tilt test and the role of autonomic nervous system.
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PMID:[Neurohumoral mechanisms for vasovagal syncopes. Part I]. 1286 5

The actions of bradykinin, angiotensin, oxytocin, vasopressin and substance P have been examined both on isolated smooth muscle preparations and in vivo. It was found that the isolated rat uterus and guinea-pig ileum can be used to distinguish between oxytocin and bradykinin and that the isolated rat colon and hen rectal caecum are almost specific test preparations for substance P. All the peptides were active on peripheral blood vessels, bradykinin, substance P and oxytocin causing vasodilatation and vasopressin and angiotensin vasoconstriction; bradykinin, substance P and angiotensin also caused an increase in capillary permeability in guinea-pigs. Only bradykinin and substance P were active in low concentrations in producing pain when applied to an exposed blister base. These two peptides were also active in causing bronchoconstriction. Oxytocin and vasopressin were the only peptides having milk-ejecting or antidiuretic activity which could be dissociated from cardiovascular effects. The spectrum of activity displayed by these peptides is in agreement with those functions which have been established for vasopressin and oxytocin and with those suggested, but not yet fully accepted, for bradykinin and angiotensin. It also indicates a possible function for substance P based on its vascular and permeability effects.
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PMID:A spectrum of pharmacological activity in some biologically active peptides. 1386 27

The use of intrathecal clonidine as an adjunct for the management of chronic pain, intra- and postoperative analgesia is gaining an increase in popularity. However, antinociceptive doses of intrathecal clonidine may produce pronounced hemodynamic side effects, including hypotension and bradycardia. In this report, we present a case of severe hypotension after cardiopulmonary bypass in a patient with intrathecal clonidine infusion. We postulate that the intrathecally administered alpha 2-agonist clonidine reduced our patient's ability to tolerate the hemodynamic lability that is present during the separation from cardiopulmonary bypass by potentially inhibiting sympathetic nervous system activity, renin-angiotensin system, or vasopressin release. The authors report a case of severe hypotension after cardiopulmonary bypass in a patient receiving intrathecal clonidine infusion for chronic neuropathic pain.
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PMID:Intrathecal clonidine and severe hypotension after cardiopulmonary bypass. 1457 Jun 31


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