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 phenomenon of involuntary dehydration, the delay in full restoration of a body water deficit by drinking, has been described extensively but relatively little is known about its physiological mechanism. It occurs primarily in humans when they are exposed to various stresses including exercise, environmental heat and cold, altitude, water immersion, dehydration, and perhaps microgravity, singly and in various combinations. The level of involuntary dehydration is approximately proportional to the degree of total stress imposed on the body. Involuntary dehydration appears to be controlled by more than one factor including social customs that influence what is consumed, the capacity and rate of fluid absorption from the gastrointestinal system, the level of cellular hydration involving the osmotic-vasopressin interaction with sensitive cells or structures in the central nervous system, and, to a lesser extent, hypovolemic-angiotensin II stimuli. Since humans drink when there is no apparent physiological stimulus, the psychological component should always be considered when investigating the total mechanisms for drinking.
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PMID:Problem: thirst, drinking behavior, and involuntary dehydration. 160 37

The effect of corticosterone injection and of acute and repeated stress on rat liver cytosol glucocorticoid receptor was studied to ascertain whether corticosterone-induced glucocorticoid receptor (GR) regulation also takes place in intact animals as it does in adrenalectomized ones. Adult male rats were exposed to six different stressors (swimming, 10 mg/kg histamine i.p., 500 mU/kg vasopressin s.c., heat, immobilization and cold) acutely or three times daily for 18 days (repeated stress). Each of the stressors applied acutely provoked a pronounced increase of plasma corticosterone with subsequent induction of hepatic tyrosine aminotransferase activity. Depletion of cytosol receptor was however only noticed after swimming and histamine injection. On the other hand, sustained hypersecretion of corticosterone evoked by repeated stress significantly reduced the number of GR in rat liver cytosol without any change in Kd. It is concluded that in the presence of intact adrenal glands cytosol receptors are more resistant to corticosterone-induced depletion than in their absence. Further, repeated stress causes down-regulation of GR in the liver, most probably by sustained corticosterone secretion, yet the effect of other stress factors cannot be excluded.
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PMID:Stress-induced changes of glucocorticoid receptor in rat liver. 161 78

In this paper, we present examples of some of the several behaviors which have been taken to indicate the reinforcing efficacy of drugs, including ethanol. Efforts to identify the genetic determinants of these behaviors have employed diverse pharmacogenetic methods. For example, we have used selective breeding to develop mice selected for severe or attenuated ethanol withdrawal and have found that Withdrawal Seizure Prone mice show a greater conditioned preference for ethanol-associated locations than the selected Withdrawal Seizure Resistant line. Similarly, HOT mice, selected for insensitivity to ethanol-induced hypothermia, had greater conditioned place preference after ethanol training than COLD mice, selected for ethanol hypothermic sensitivity. We have also developed selected mouse lines responsive or unresponsive to ethanol-stimulated locomotor activity. These FAST and SLOW lines develop sensitization rather than tolerance to ethanol-induced activity. Using inbred strains of mice, others had shown that strains differed in preference for drinking ethanol solutions. We found that these strains also differed in acceptance of ethanol. Single-gene techniques have been used to show that preference drinking is significantly altered in mutant rodent strains lacking hypothalamic vasopressin, or with nephrogenic diabetes insipidus. In a specific panel of Recombinant Inbred mouse strains, we found that a single gene appeared to control a significant portion of the variance in preference drinking. These examples show that traits putatively related to drug reinforcement show substantial genetic control. Specifically, single-gene methods show promise of identification and mapping of genes related to drug reinforcement.
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PMID:Genetic determinants of ethanol reinforcement. 163 89

Endothelin-1 (ET-1) is a potent, vasoconstrictive peptide isolated from culture media of vascular endothelial cells. The binding of ET-1 to membrane preparations from rat and bovine lung was studied using radioiodinated ET-1 (125I-ET-1). With both membrane preparations, 125I-ET-1 showed saturable binding to a single class of high affinity sites. Scatchard analysis of the binding data gave dissociation constants (Kd) for ET-1 of 0.22 nM and 0.15 nM, and receptor densities (Bmax) of 6.1 pmol/mg and 2.7 pmol/mg for rat and bovine lung membranes, respectively. Photo-reactive radioiodinated ET-1, N epsilon 9-azidobenzoyl-125I-ET-1, was synthesized and purified as a mono-reactive affinity labeling reagent. This reagent was used for affinity labeling of ET-1 receptor in bovine and rat lung membranes. Photoaffinity labeling followed by sodium dodecyl sulfate gel electrophoresis and autoradiography gave a radiolabeled protein band with an apparent Mr of 34,000 in both membrane preparations. The labeling of this protein band was inhibited by cold ET-1 in a concentration-dependent manner. Labeling was not abolished by unrelated peptides such as angiotensin II and [Arg8]-vasopressin, or by structurally related bee venom apamin. These results indicate that the ET-1 receptor or its ligand binding subunit consists of a 34,000 Da polypeptide.
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PMID:Affinity labeling of endothelin receptors in bovine and rat lung membranes by N epsilon 9-azidobenzoyl-125I-endothelin-1. 165 62

Glutamate microinjection (1 M, 250 nl) into the hypothalamic supraoptic nucleus (SON) stimulated heat production in brown adipose tissue (BAT) and caused a rapid and sustained increase in interscapular BAT and core temperatures in urethane-anaesthetized rats. This effect was blocked by intraperitoneal pretreatment with a sympathetic ganglionic blocker, chlorisondamine chloride (2.5 mg/kg), or a beta-adrenergic receptor blocker, propranolol (2.5 mg/kg), but not by prior hypophysectomy or intracerebroventricular pretreatment with specific receptor blockers to vasopressin (d(CH2)5[Tyr(Me)2]AVP, 5 micrograms) or oxytocin (d(CH2(5)[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT, 5 micrograms). The results demonstrate that stimulation of SON cells with glutamate elicits a non-vasopressinergic/non-oxytocinergic neural signal that can bring about a sympathetically-mediated increase in BAT thermogenesis. Heat production in BAT is an important mechanism of thermal protection during cold stimulation, and there is evidence that osmotic stimulation can influence thermoregulation. SON neurons play a major role in osmoregulation via release of the peptide hormones vasopressin and oxytocin. The present results suggest the possibility that apart from releasing peptide hormones for osmoregulation, SON neurons might be involved in mediating the effect of osmotic stimulation on thermoregulatory responses involved in thermal adaptation.
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PMID:Activation of brown adipose tissue thermogenesis by chemical stimulation of the hypothalamic supraoptic nucleus. 168 14

Evidence is given of cooperation between pituitary desensitization to the stimulatory action of corticotropin-releasing hormone (CRH) and glucocorticoid negative feedback in the modulation of the stress responsiveness. With regard to the former, we show that the pituitary becomes unresponsive to repeated CRH administration as soon as 15 min after the first one, while the adrenocortical effect of arginine-vasopressin (AVP) during this period is amplified, suggesting the involvement of AVP in the mechanism that permits repeated pituitary-adrenocortical axis activations. The activation of this axis is blocked by the glucocorticoid negative feedback induced by a previous stress. In fact, after a cold stress (4-6 degrees C for 90 min), the responsiveness to a subsequent psychic stressor (but not to a somatic one) is suppressed. Results after neurotoxic lesion of hippocampal and hypothalamic serotoninergic innervations, would indicate that the neurotransmitter is in some way involved in the accomplishment of this phenomenon.
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PMID:Mechanisms in the control of stress responsiveness. 169 50

A rare case of the inappropriate antidiuretic hormone syndrome after tuberculous epididymoorchitis in a renal transplant recipient is described. Orchiectomy was performed because of a cold abscess, following which clinical improvement was noted.
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PMID:Syndrome of inappropriate antidiuretic hormone following tuberculous epididymo-orchitis in renal transplant recipient: case report. 194 95

We assessed the effects of cold and isolation stress on arginine vasopressin (AVP) mRNA in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. Vasopressin mRNA levels were determined by in situ hybridization histochemistry at the cellular level. In posterior magnocellular neurons of the PVN isolation stress for 7 or 14 days increased vasopressin mRNA levels 28 and 29%, respectively, compared to group-housed controls. No significant alterations in vasopressin gene expression were observed in the SON after 7 or 14 days of isolation stress. Scattered magnocellular AVP mRNA-expressing cells of the medial parvocellular PVN showed increases of 19 and 34% after 7 and 14 days of isolation, respectively. We also studied the effect of cold or combined cold and isolation stress on vasopressin gene expression in the PVN and SON. Cold stress for 3 h daily for 4 consecutive days increased AVP mRNA levels in the posterior magnocellular PVN by 15%. Cold-isolated animals showed an increase of 21%. No significant effect on AVP mRNA levels in the SON was observed. In contrast to the posterior magnocellular PVN, cold or cold-isolation stress increased AVP mRNA in magnocellular neurons of the medial parvocellular region of the PVN by 25 and 43%, respectively, relative to control rats. These results suggest that psychological and metabolic stress may be added to the list of stressors that activate the hypothalamo-neurohypophysial system.
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PMID:Genomic effects of cold and isolation stress on magnocellular vasopressin mRNA-containing cells in the hypothalamus of the rat. 202 10

Frog, Rana esculenta, pituitary and testis gonadotropin-releasing hormone (GnRH) receptors were characterized by using 125I-chicken IIGnRH (cIIGnRH) as radiolabeled ligand. At 4 C equilibrium binding of 125I-cIIGnRH to pituitary homogenates was achieved after 90 min of incubation; binding of 125I-cIIGnRH to testis membrane fractions reached its maximum at 60 min of incubation. Binding of the radioligand was a function of tissue concentration, with a positive correlation over the range 0.5-2 tissue equivalents per tube. One pituitary and one testis per tube were used as standard experimental condition. Incubation of the pituitary homogenate with increasing concentrations of 125I-cIIGnRH indicated saturable binding at radioligand concentrations of 1 nM and above while for the testis membrane preparation saturation was achieved using 5 nM 125I-cIIGnRH. The binding of 125I-cIIGnRH was found to be reversible after addition of the cold analog and the displacement curves could be resolved into one linear component for both tissues. Scatchard analysis suggested the presence of one class of binding sites for both pituitary and testis (Pituitary: Kd = 1.25 +/- 0.14 nM and Bmax = 8.55 +/- 2.72 fmol/mg protein; testis: Kd = 2.23 +/- 0.89 nM and Bmax = 26.48 +/- 7.39 fmol/mg protein). Buserelin displaced the labeled 125I-cIIGnRH with a lower IC50 as compared with cIIGnRH cold standard, while Arg-vasopressin (AVP) was completely ineffective, confirming the specificity of binding.
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PMID:Characterization of gonadotropin-releasing hormone (GnRH) binding sites in the pituitary and testis of the frog, Rana esculenta. 216 Dec 25

Orthostatic dysregulation (OD), originally a German-Scandinavian term partially corresponding to an Anglo-American concept of sympathotonic orthostatic hypotension, is characterised by altered cardiovascular control on standing, and its clinical features include dizziness, palpitation and, occasionally, orthostatic hypotension. The symptomatology suggests presence of cardiovascular adrenoceptor dysfunction, although the aetiology of OD has not been elucidated. The above situation prompted us to investigate autonomic nervous function in OD. The subjects were 8 patients with OD (20 +/- 2 years old; mean +/- SD), all of them fulfilled the diagnostic criteria accepted in Japan, and 6 healthy controls (17 +/- 3 years old). Noradrenaline and isoproterenol infusion tests and conventional haemodynamic functional tests (70 degrees passive head-up tilt, cold pressor test, Valsalva manoeuvre and Aschner's eye-ball pressure test) were carried out upon the subjects under the continuous measurement of blood pressure, pulse rate and respiration. Plasma vasoactive substances (noradrenaline, adrenaline, arginine-vasopressin and renin activity) were also determined in supine position and at 15 minutes after the 70 degrees passive head-up tilt. In noradrenaline infusion test, different doses (0.01 microgram/kg, 0.02 microgram/kg, 0.05 microgram/kg and 0.1 microgram/kg) of noradrenaline were administered by means of intravenous bolus injection, and a degree of subsequent rise in blood pressure was used as an index for the cardiovascular alpha-adrenoceptor sensitivity. In isoproterenol infusion tests cardiovascular beta 1- and beta 2-adrenoceptor sensitivities were assessed, respectively, by a degree of an increase in pulse rate and a degree of a fall in blood pressure following bolus injection of the drug (0.001 microgram/kg, 0.002 microgram/kg, 0.005 microgram/kg and 0.01 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiovascular alpha- and beta-adrenoceptor sensitivities in orthostatic dysregulation]. 216 87


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