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)

Animal studies have revealed two important aspects of vasopressin function which make this peptide a suitable candidate for involvement in complex behavioural syndromes: (1) vasopressin deficiency produces deficits of behaviour which are reversed by vasopressin; (2) well-developed systems exist for the distribution of vasopressin throughout the central nervous system (C.N.S.) via either peptidergic neurons or the cerebrospinal fluid (C.S.F.) and provide the means by which vasopressin may regulate cells controlling behavioural or physiological processes. Among the processes which vasopressin can influence are several of significance in the symptom-complex of affective illness, including alterations in memory, changes in pain sensitivity, synchronisation of biological rhythms, the timing and quality of R.E.M. sleep, and the regulation of fluid and electrolyte balance. In addition, vasopressin is functionally linked to monoamine neurotransmitter systems and, like them, is altered by pharmacological agents which affect mood. Some of the pharmacological and clinical data suggest that vasopressin function is diminished in depression and augmented in mania; sometimes, however, alterations in vasopressin function may be detectable only during crucial periods of the manic-depressive cycle. The hypothesis that vasopressin plays a role in disorders of human behaviour, particularly manic-depressive illness, can now be directly tested by radioimmunoassays of vasopressin in C.S.F. and plasma and by the administration of specific vasopressin analogues and inhibitors.
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PMID:Vasopressin in affective illness. 7 97

Mechanisms of possible pathophysiological importance in primary dysmenorrhea are discussed. Hyperactivity of the myometrium with accompanying uterine ischemia is considered to be of central importance in the causation of pain. Prostaglandins seem to be involved to a large extent in the development of the myometrial hyperactivity. Other mechanisms of possible importance such as ovarian hormones, cervical factors, vasopressin, nerves, and psychological factors can well act ultimately through prostaglandin release but an action directly on the myometrium and blood flow may also occur.
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PMID:Pathophysiology of dysmenorrhea. 38 Feb 50

Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling.
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PMID:The clinical physiology of water metabolism. Part I: The physiologic regulation of arginine vasopressin secretion and thirst. 39 80

Three children aged 2 1/2 to 5 1/2 yr, with burns covering 30%--45% of body surface area, developed hyponatremia and serum hypotonicity on the 5th--6th day following the burn injury. The hyponatremia persisted for 10--15 days. During this period, all three passed inappropriately concentrated urines. One child also demonstrated marked and inappropriate thirst. All three children demonstrated persistent respiratory alkalosis, which appeared and disappeared concomitantly with the hyponatremia. There were no signs of dehydration, and plasma volumes, measured in two children, were normal to high. These children are believed to show evidence of inappropriate antidiuretic hormone (ADH) secretion. In the absence of those conditions known to produce this syndrome, it is postulated that in these children it may have resulted from prolonged pain, anxiety, and/or pyrexia.
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PMID:Persistent hyponatremia and inappropriate antidiuretic hormone secretion in children with extensive burns. 45 38

Plasma vasopressin concentration was measured by radioimmunoassay before, during, and after anesthesia and surgery in ten subjects. During the short period between the onset of anesthesia and the start of operation, small elevations of vasopressin level were noted. Surgery itself was associated with significant elevations of up to 82 pg/ml. Highest levels of vasopressin were noted with major intra-abdominal surgery and lowest levels with limb surgery. The immediate postoperative period was marked by plasma vasopressin levels that were often higher than during surgery itself. Levels gradually fell to their preoperative state after three to four days. The elevated levels of vasopressin can be associated with oliguria and excessive water retention. Among the possible mechanisms for the stimulus to vasopressin secretion are pain, stress, positive pressure respiration and anoxia. This study confirms by radioimmunoassay the changes in plasma vasopressin level with surgery that have been previously described by bioassay.
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PMID:Radioimmunoassayable plasma vasopressin associated with surgery. 64 20

Intra-arterial injections of bradykinin into the hindlimb of the rabbit cause two types of cardiovascular reflex effects displayed in succession. The first-type effects appear early and are of inhibitory nature, being represented by systemic hypotension, contralateral hindlimb vasodilation and bradycardia; the second-type effects appear later and are excitatory in nature, consisting of hypertension, hindlimb vasoconstriction and tachycardia and occur closely associated with behavioral manifestations typical of the reaction to pain. Both the depressor and pressor effects are accompanied by hyperventilation. Analogous biphasic reflex responses may be caused by intraarterial injections of potassium ions. On the contrary, hypertonic solutions (NaCl, glucose) usually only produce second-type excitatory responses. No significant cardiocirculatory reflex effects are induced by even high doses of serotonin, nicotine, adenosine, adenosine triphosphate, adrenalin, noradrenalin, angiotensin, vasopressin and oxytocin. General anesthesia greatly inhibits the pressor reflexes and potentiates the depressor responses (to bradykinin and K ions) but does not appear to be a necessary condition for provoking depressor reflexes by chemical stimulation of somatic afferents. Both chemoreflex responses are prevented by sectioning the somatic nerves of the injected limb. Denervation of sinoaortic areas and of cardiopulmonary receptors by bilateral cervical vagotomy or complete removal of the skin from the injected limb does not prevent either type of chemoreflex response. These depressor and pressor chemoreflexes have been ascribed to activation of two functionally distinct types of sensory receptors in the skeletal muscle, differently sensitive to chemical substances and selectively concerned with different patterns of cardiocirculatory reflex response.
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PMID:Cardiovascular and respiratory chemoreflexes from the hindlimb sensory receptors evoked by intra-arterial injection of bradykinin and other chemical agents in the rabbit. 76 67

Bilateral electrolytic destruction of the paramedian midbrain caudal tegmentum caused the appearance in the internal part of the hypothalamic supraoptic nucleus of neurosecretory cells with low functional activity and degenerating forms (dark-stained and pycnomorphic cells); in the posterior hypophysis the destructed gigantic terminal varicosities (Herring bodies) were revealed; the posterior hypophysis contained a subnormal amount of neurosecret; the vasopressin-antidiuretic hormone level in blood plasma was reduced. Painful stimulation of animals with the destructed midbrain tegmentum revealed the functional insufficiency of the supraoptic hypophyseal neurosecretory system (SHNS). The results obtained permit considering that the paramedian midbrain tegmentum exerts a modulating influence upon the SHNS function during stress.
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PMID:[Functional relationships between the midbrain tegmentum and the supraoptico-hypophyseal neurosecretory system of the white rat hypothalamus]. 87 Aug 41

The treatment of a patient with diabetes insipidus (DI) is described, and the general treatment of the syndrome is reviewed. The patient was a 16-year-old male who had experienced pain, inflammation and tenderness in the left gluteal region owing to an abcess at the site of intramuscular injection of vasopressin tannate in oil (VTO). (He had been diagnosed as having DI at age 8. Since then, he had been maintained on VTO, lypressin and posterior pituitary snuff.) After the abscess healed during hospital treatment, VTO was stopped and the patient's urinary output increased sharply; urine specific gravity and osmolarity decreased correspondingly. Three days after stopping VTO, the investigational drug, 1-deamino-8-D-arginine vasopressin (DDAVP), was begun at 10 microgram every 12 hours. The dose was eventually increased to 20 microgram every 12 hours, and the patient was discharged on this regimen which controlled his urine output, specific gravity and osmolarity. Other treatments reviewed include antidiuretic-hormone-replacement agents (vasopressin, lypressin) and drugs used to potentiate low ADH levels (chlorpropamide, clofibrate and carbamazepine).
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PMID:Treatment of diabetes insipidus with DDAVP. 90 88

It has been demonstrated in animal model of somatic pain that hypothalamic paraventricular nucleus (PVN) participates in acupuncture analgesia, probably by mediation of vasopressin release. The role of PVN in acupuncture analgesia for experimental visceral pain in rats was further investigated in the present study. Experimental results demonstrated that electroacupuncture could inhibit the writhing response, produced by intraperitoneal injection of antimonium potassium tartrate and this inhibitory effect could be enhanced by electrical stimulation of PVN, but decreased by electrolytical lesion of PVN, intracerebroventricular injection of vasopressin antiserum (14 microliters) or the vasopressin antagonist, d(CH2)5Tyr(Me)-AVP (500 ng/5 microliters). Intraperitoneal administration of the latter drug (10 micrograms/kg), however, was ineffective. The above experimental results suggest that vasopressinergic neurons in PVN also participate in the inhibition of visceral pain by electroacupuncture.
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PMID:[Involvement of vasopressinergic neurons of paraventricular nucleus in the electroacupuncture-induced inhibition of experimental visceral pain in rats]. 129 59

Studies of renal afferent fibers and their functions have continued since the work of Pines in 1959 (Fiziol. Zh. SSSR Im. I M Sechenova 45: 1339-1347, 1959). The kidney contains mechanoreceptors and chemoreceptors that appear to have two major functions. First, renal mechano- and chemoreceptors evoke a variety of renorenal reflexes, while more global cardiovascular reflexes are primarily evoked by renal mechanoreceptors. A second function of renal afferent fibers is to cause the pain of renal disease. Recent studies suggest that renal afferent fibers may also regulate secretion of vasopressin from the pituitary gland. Substantial evidence indicates that, although most renal afferent fibers enter the spinal cord, their functions depend to a large extent on supraspinal circuitry. Thus our research has focused on defining characteristics of spinal neurons that relay renal information to the brain. In the cat, neurons in the L2-T11 segments with excitatory responses to renal A delta and C fiber input project to the medial medullary reticular formation and to the caudal and rostral ventrolateral medulla. Renal afferent information reaches these cells by way of the least splanchnic nerve and by way of more than one dorsal root. In the monkey spinothalamic neurons in the L3-T10 segments respond to renal nerve stimulation. Excitatory responses predominate, but inhibitory responses occur in L2 and L3. These cells also respond to renal A delta and C fibers. Stimulation of renal mechanoreceptors by occlusion of the ureteropelvic junction or renal vein excites feline spinoreticular neurons. Graded increases in renal vein pressure produce graded increases in cell responses. Activation of renal chemoreceptors increases activity of spinal interneurons. Within the L2-T11 segments, cells responding to ureteral occlusion are located caudally, cells with responses to renal artery occlusion are located rostrally, and cells responding to renal vein occlusion are located in between. The differential locations of cells with these inputs suggests the existence of a coding mechanism for different renal receptor populations. Distention of the renal pelvis is a potent stimulator of primate spinothalamic neurons. These neurons encode renal pelvic pressures in the noxious range and appear to be important in mechanisms of renal pain.
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PMID:Bowditch Lecture. Renal afferent inputs to ascending spinal pathways. 131 32


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