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)

This study was undertaken to investigate the effects of hypovolemic and hypertonic treatments on plasma vasopressin (AVP) levels and fluid balance in propylthiouracil (PTU)-induced hypothyroidism in the rat. The influence of hypothyroidism on AVP responsiveness to hypertonic and hypovolemic stimuli were compared. Adult male rats were divided into two groups. Groups I and II were intraperitoneally (i.p.) injected with saline (1ml/250g) and PTU (10mg/kg/day), respectively, for a period of two weeks. These groups were further divided in three subgroups each containing six rats. The first subgroup consisted of unchallenged rats. I.P. 700 mg polyethylene glycol was used for hypovolemic treatment. The third subgroup consisted of hypertonic (1.5 M NaCl; 1ml/100 g) stimulated animals. All rats were decapitated and trunk blood collected in hep-arinized tubes. Plasma samples were stored at -20 degrees C until assayed. Plasma AVP, T3 and T4 levels were measured by radioimmunassay. Hematocrit values and plasma Na concentrations were also determined. In the PTU-induced hypothyroid rats, hypertonic treatment caused lower increase in plasma AVP levels (p<0.05) compared to the respective control animals. In the hypovolemic group, decreases in AVP responses were not found to be statistically significant. In conclusion, although hypothyroidism does not statistically change basal AVP levels, it may affect AVP response to hypertonic stimulus. It is not clear whether changes in fluid-electrolyte balance cause disturbance in AVP release in hypothyroidism or vice versa. Therefore, these preliminary findings need to be confirmed by further investigations.
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PMID:Influence of hypovolemic and hypertonic treatments on plasma vasopressin levels and fluid balance in the propylthiouracil-induced hypothyroid rat. 1146 93

Enzymatic cleavage of some peptide hormones, neurotransmitters and neuromodulators could be implicated in the regulation of extra- and intracellular fluid volume and osmolality. Prolyl endopeptidase is known to hydrolyze several peptides, which act on hydromineral balance, such as angiotensins, bradykinin, vasopressin, oxytocin, thyrotropin-releasing hormone, neurotensin and opioids. In this work, we analyzed the effects of certain volume and/or osmotic changes in the activity of the soluble and membrane-bound prolyl endopeptidase in several brain areas, heart, lungs, kidney and adrenal and pituitary glands of the rat. Soluble prolyl endopeptidase activity was higher in the renal cortex of the chronic salt-loaded rats than in the control rats. In the water-deprived and polyethylene glycol-treated rats, heart particulate prolyl endopeptidase was lower than in the control rats. Particulate prolyl endopeptidase was also lower in the adrenal gland of the acute salt-loaded rats and in the brain cortex of the water-loaded rats than in the control rats. Data suggest that tissue-dependent peptide hydrolysis evoked by prolyl endopeptidase activity is involved in the water-electrolyte homeostasis.
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PMID:Effects of hydrosaline treatments on prolyl endopeptidase activity in rat tissues. 1149 89

To date, glucagon-like peptide 1(7-36) amide (tGLP-1) has been found to affect the neurohypophysial and cardiovascular functions in normotensive and normovolaemic rats. The aim of the present study was to investigate possible effects of tGLP-1 on the mean arterial blood pressure and the release of vasopressin and oxytocin under conditions of blood volume depletion in the rat. In the first series of experiments, the animals were injected i.p. with either 0.15 M saline or 30% polyethylene glycol (PEG). PEG caused an 18% reduction of blood volume 1 h after injection. No significant changes in the mean arterial blood pressure were found in either normo- or hypovolaemic rats during the experiment. tGLP-1 injected i.c.v. at a dose of 1 microg/5 microl 1 h after the i.p. injection increased similarly the arterial blood pressure in normo- and hypovolaemic rats. The plasma vasopressin/oxytocin concentrations were markedly elevated in hypovolaemic animals and tGLP-1 further augmented the release of both hormones. In the second study, hypovolaemia was induced by double blood withdrawal. The haemorrhage resulted in a marked decrease of the mean arterial blood pressure and in the elevated plasma vasopressin/oxytocin concentrations. tGLP-1 injected immediately after the second blood withdrawal increased the arterial blood pressure. In parallel, tGLP-1 enhanced significantly vasopressin and oxytocin secretion when compared with haemorrhaged, saline-injected rats. The results of this study indicate that tGLP-1 may affect the arterial blood pressure and the secretion of neurohypophysial hormones under pathological conditions brought about by blood volume depletion.
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PMID:Effects of glucagon-like peptide-1(7-36) amide on neurohypophysial and cardiovascular functions under hypo- or normotensive hypovolaemia in the rat. 1183 48

Chondroitin 4-sulphate (CS) hydrogels were examined as potential matrices for the electro-controlled delivery of peptides and proteins. A CS hydrogel, cross-linked with ethylene glycol diglycidyl ether, and with a swelling ratio of 20, was used to study the influence of molecular size and shape of guest molecules on loading and release rates. Three positively charged molecules of different molecular weights (vasopressin MW 1084, aprotinin MW 6512 and lysozyme MW 14,400), and one negatively charged protein (bovine serum albumin MW 67,000) were used as model solutes. The hydrogels were loaded by equilibrium swelling. As a result, the three positively charged peptide and proteins were found to be concentrated in the gels, most likely due to ionic attraction between the negative charges in the gel polymeric backbone and the positively charged solutes. No such concentration of solute in the gel was seen for the negatively charged albumin. The latter is presumably loaded passively by diffusing in the water phase of the gel. The loading efficiency (indicated by the loading rate and the total amount of solute loaded in the gel) was found to increase with decreasing molecular size of solute. Electro-stimulated release of the loaded peptide and proteins was followed for 3 h during which an electric field was applied in pulses of 5 V (pulse duration and pulse interval were both of 20 min). The release of lysozyme and aprotinin from CS hydrogels responded to electrical pulses. On the other hand, vasopressin and albumin were largely released by passive diffusion and their release could not be electrically controlled. This work shows that the size of the guest molecule is an important parameter when electrically-stimulated drug release is desired, but further work obviously needs to be carried out with a larger range of molecular weights and conformations.
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PMID:Loading into and electro-stimulated release of peptides and proteins from chondroitin 4-sulphate hydrogels. 1184 10

This study examined the role of the diagonal band of Broca (DBB) in drinking behaviour and vasopressin release. Adult male rats were anaesthetized (pentobarbital 50 mg/kg) and received DBB injections of either ibotenic acid (0.5 microl of 5 micro g/ microl) or vehicle (0.5 microl of phosphate-buffered saline). Although baseline drinking and urine output were not affected, drinking to 30% polyethylene glycol (MW 8000; 1 ml/100 g s.c.) and angiotensin II (0, 1.5 and 3.0 mg/kg s.c.) were significantly increased in ibotenic acid in phosphate-buffered saline (DBBX) rats. Drinking to hypertonic saline (0.9, 4 and 6%; 1 ml/100 g), and water deprivation were not significantly affected. DBBX rats had significantly lower basal heart rates than controls but the cardiovascular responses to infusions of angiotensin II (100 ng/kg/min i.v. for 45 min) were not affected. DBBX rats had significantly higher basal vasopressin, but angiotensin-stimulated vasopressin release was not significantly different. Although the DBB is not involved in basal water intake, it is involved in dipsogenic responses to hypovolemic stimuli and possibly basal autonomic function and basal vasopressin release.
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PMID:Lesions of the diagonal band of broca enhance drinking in the rat. 1296 34

Oestrogen receptor (ER)-beta expression correlates inversely with osmotic control of arginine vasopressin (AVP) release such that cellular dehydration induced by 72 h of 2% saline consumption depletes ER-beta in the magnocellular AVP neurones in the supraoptic (SON) and paraventricular nuclei (PVN). The current studies were performed to determine whether other pathways that stimulate AVP release, such as hypovolaemia, also regulate ER-beta expression in these nuclei, and to evaluate the time course of the change in ER-beta expression during water deprivation and subsequent rehydration. ER-beta expression was evaluated immunocytochemically. In rats made hypovolaemic with a subcutaneous injection of 40% polyethylene glycol (PEG), a significant depletion of ER-beta in both SON and magnocellular PVN (P </= 0.001) was evident 8 h post PEG injection. ER-beta was also significantly depleted following 20 h and 26 h of water deprivation in SON (P = 0.003) and magnocellular PVN (P < 0.001). Six hours of rehydration in rats that had been water deprived for 26 h induced recovery of expression that was statistically significant, although not complete (P </= 0.015 in PVN). Thus, for the first time, the present studies demonstrate that haemodynamic in addition to osmotic influences are capable of regulating ER-beta expression in the magnocellular system, and that the combination of these factors induced by a physiological manipulation (e.g. 20 h of water deprivation) can eliminate ER-beta expression. Because ER-beta has been shown to mediate inhibition of AVP secretion in explants of the hypothalamic-neurohypophyseal system, these data suggest that down-regulation of ER-beta may contribute to stimulated AVP release during hypovolaemic states such as fluid deprivation and haemorrhage.
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PMID:Depletion of oestrogen receptor-beta expression in magnocellular arginine vasopressin neurones by hypovolaemia and dehydration. 1518 29

Pediatric incontinence is a bothersome symptom for children and their parents. It can have a profound influence on a child's social and psychologic development and well-being. It is important to understand the different disorders that result in incontinence and also to understand the neural influences and development on urinary control. Urinary leakage can be a functional or organic disorder, with many possible etiologies. The most common group of pediatric patients with incontinence are those with overactive bladder disorder. Pharmacologic therapy centers on the blockage of muscarinic receptors by the tertiary amines such as oxybutynin, tolterodine, trospium chloride, and propiverine. Although most novel anticholinergic medications are effective and well tolerated in children, in our experience oxybutynin extended release provides superior relief for urge urinary incontinence in children. Other agents such as alpha-adrenoceptor antagonists have been used with success to improve bladder empyting and decrease outlet resistance. Night-time voiding disorders such as primary monosymptomatic nocturnal enuresis tend to be symptomatically treated. One of the mainstays of pharmacotherapy is desmopressin, an analog to antidiuretic hormone, which decreases night-time urine production. Tricyclic antidepressants such as imipramine have also been used successfully through a combined mechanism of action believed to be the result of anticholinergic, antispasmodic, and sympathomimetic effects. Often the successful treatment of constipation also treats urinary incontinence or at least the symptoms of urinary leakage are improved. The new non-absorbable, tasteless, and odorless PEG-3350 (polyethylene glycol 3350) powder has quickly become a mainstay of the pharmacologic treatment for constipation because of its ease of preparation and favorable adverse effect profile. A better understanding of the physiologic control, cellular interactions, and second messenger signal transduction pathways has led to the development of many new potential target sites for pharmacologic intervention. The advancement of new uroselective muscarinic antagonists is currently under investigation for agents such as darifenacin and temiverine, which have the potential to improve efficacy without increasing unwanted adverse effects. New pharmacologic delivery systems are also being developed ranging from intravesical to transdermal applications to change biodistribution and improve selectivity. Incontinence is a significant problem for children, their parents, and their physicians. The changing and advancing field of pharmacotherapy has made big strides for symptom control in this patient population.
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PMID:Contemporary and emerging drug treatments for urinary incontinence in children. 1597 61

Central 5-HT2A receptors have been implicated in central volume control by activating a central angiotensinergic pathway to cause the release of vasopressin. Interestingly, to induce DOCA-salt hypertension in rats vasopressin release is required. Thus the present experiments were carried out to determine whether continuous blockade of these receptors over 20 days, with the non-selective 5-HT2 receptor antagonist mianserin would prevent the development of deoxycorticosterone acetate (DOCA)-salt hypertension. Mianserin, given i.c.v. 90 or 60 microg twice daily for 20 days prevented the development of hypertension in conscious rats receiving DOCA-salt but did not affect blood pressure in rats on salt alone. Further, the dose of 30 microg given i.c.v. twice daily had no effect nor did the vehicle, polyethylene glycol (PEG), on the development of the hypertension. Mianserin 90 microg twice daily i.c.v. was also shown to prevent the increase in fluid intake, urinary flow and sodium excretion caused by DOCA-salt treatment. These data indicate that this action of mianserin is not due to an intrinsic hypotensive action but an action which involves interference with the mechanism by which DOCA-salt treatment causes hypertension. Thus the data overall support the view that to induce hypertension with DOCA-salt a central 5-HT-containing pathway needs to be activated, which then activates 5-HT2 receptors to cause the release of vasopressin which has previously been shown to be responsible for the initiation of DOCA-salt treatment hypertension.
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PMID:Chronic treatment with mianserin prevents DOCA-salt hypertension in rats--evidence for the involvement of central 5-HT2 receptors. 1601 6

Using nystatin-perforated patch-clamp and whole cell recording, we tested the hypothesis that K(ATP) channels contribute to resting conductance of rat descending vasa recta (DVR) pericytes and are modulated by vasoconstrictors. The K(ATP) blocker glybenclamide (Glb; 10 microM) depolarized pericytes and inhibited outward currents of cells held at -40 mV. K(ATP) openers pinacidil (Pnc; 10 microM) and P-1075 (1 microM) hyperpolarized pericytes and transiently augmented outward currents. All effects of Pnc and P-1075 were fully reversed by Glb. Inward currents of pericytes held at -60 mV in symmetrical 140 mM K(+) were markedly augmented by Pnc and fully reversed by Glb. Ramp depolarizations in symmetrical K(+), performed in Pnc and Pnc + Glb, yielded a Pnc-induced, Glb-sensitive K(ATP) difference current that lacked rectification and reversed at 0 mV. Immunostaining identified both K(IR)6.1, K(IR)6.2 inward rectifier subunits and sulfonurea receptor subtype 2B. ANG II (1 and 10 nM) and endothelin-1 (10 nM) but not vasopressin (100 nM) significantly lowered holding current at -40 mV and abolished Pnc-stimulated outward currents. We conclude that DVR pericytes express K(ATP) channels that make a significant contribution to basal K(+) conductance and are inhibited by ANG II and endothelin-1.
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PMID:KATP channel conductance of descending vasa recta pericytes. 1604 5

The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30-40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na(+) concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.
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PMID:Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat. 1720 93


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