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 present study was designed to investigate the effect of fluid percussion brain injury (FPI) on vasopressin-induced pial artery vasodilation and the role of superoxide anion generation in those observed effects. In the piglet, it was observed previously the FPI produces pial artery constriction associated with free radical generation. Anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. FPI of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Vasopressin in physiological and pharmacological concentrations (10 and 1,000 microU/ml) produced vasodilation that was reversed to constriction after FPI (15 +/- 1 vs. -8 +/- 1 and 25 +/- 1 vs. 13 +/- 1% for 10 and 1,000 microU/ml before and after injury, respectively). Vasopressin-induced dilation was associated with increased cerebrospinal fluid guanosine 3', 5'-cyclic monophosphate, and these biochemical changes were blunted by FPI (407 +/- 12 and 720 +/- 28 vs. 4 and 272 +/- 5 fmol/ml for control and 10 microU/ml before and after injury, respectively). In contrast, polyethylene glycol superoxide dismutase (PEG-SOD) and catalase pretreatment 30 min before FPI partially restored vasopressin-induced pial artery dilation (14 +/- 1 vs. 3 +/- 1 and 22 +/- 1 vs. 2 +/- 4% for 10 and 1,000 microU/ml before and after FPI, respectively). Similarly, biochemical changes associated with vasopressin dilation were also partially restored by PEG-SOD and catalase after FPI. These data show that vasopressin is reversed from a dilator to a vasoconstrictor after FPI and suggests the superoxide anion generation contributes to the alteration of vasopressin cerebrovascular effects after injury and that such altered vasopressin cerebrovascular effects contribute to pial vasoconstriction after FPI.
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PMID:Influence of brain injury on vasopressin-induced pial artery vasodilation: role of superoxide anion. 896 66

In isolated hamster hepatocytes, the Ca2+ ionophore A-23187 immediately decreased the uptake rate of taurocholic acid (TCA) by 60-70%, whereas it slowly inhibited that of ursodeoxycholic acid (UDCA) by a maximum of 35-45%, with an inhibition constant (Ki) of 0.36 and 1.93 microM, respectively. In contrast to ionomycin, which mimicked the effect of A-23187, vasopressin inhibited the bile acid uptake rate by 40 and 45%, respectively, only after a 5- to 10-min preincubation. The Na(+)-dependent bile acid transport was exclusively inhibited by these agents, and this inhibition was independent of extracellular Ca2+. However, intracellular Ca2+ depletion with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid or chelation with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid resulted in 40-50% inhibition of the uptake rate of both bile acids. The exogenous protein kinase C activator, phorbol 12-myristate 13-acetate (PMA), but not the nonactive 4 alpha-phorbol, significantly inhibited TCA uptake rate. Although both A-23187 and ionomycin immediately increased and decreased the cellular Na+ and K+ concentration, respectively, neither vasopressin nor PMA had a significant effect on the cellular concentration of these cations, even after a 10-min incubation. Furthermore, the effect of A-23187 and ionomycin on TCA uptake and Na+ flux, respectively, disappeared after a 40-min preincubation, and additional ionophore remained without effect. However, after a 40-min incubation with A-23187, PMA was still able to inhibit TCA uptake. Therefore, A-23187 and ionomycin transiently inhibited Na(+)-dependent uptake of both TCA and UDCA, in part because of transient alteration of the cellular Na+ and K+ concentration. Vasopressin and PMA inhibited Na(+)-dependent bile acid uptake, at least in part, through protein kinase C activation.
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PMID:Regulation of taurocholate and ursodeoxycholate uptake in hamster hepatocytes by Ca(2+)-mobilizing agents. 899 53

Using as models the neurohypophyseal nonapeptide hormone oxytocin and its analogue deaminooxytocin, several directed routes to formation of sulfur-sulfur bridges have been developed and evaluated. The linear sequences (through common octapeptide-resin intermediates) were assembled smoothly on tris(alkoxy)benzylamide (PAL) poly(ethylene glycol)-polystyrene (PEG-PS) graft supports, using stepwise Fmoc solid-phase chemistry. Side-chain protection of beta-mercaptopropionic acid (Mpa) and/or cysteine (Cys) was provided by S-2,4,6-trimethoxybenzyl (Tmob), S-acetamidomethyl (Acm), and/or a series of sulfenyl thiocarbonate and carbamoylsulfenyl protecting/activating groups: S-(methoxycarbonyl)sulfenyl (Scm), S-(methoxycarbonyl)disulfanyl (Sscm), S-(N-methyl-N-phenylcarbamoyl)sulfenyl (Snm), and S-(N-methyl-N-phenylcarbamoyl)disulfanyl (Ssnm). Thiolytic displacement of S-Snm (preferred) or S-Scm provided intramolecular cyclized peptide disulfides, and homologation of the chemistry with S-Ssnm (again preferred) and S-Sscm provided the corresponding trisulfides along with smaller amounts of disulfides and tetrasulfides. These chemistries could be implemented both in solution and in solid-phase modes. Various parameters were studied systematically and optimized, and the novel trisulfides of oxytocin and deaminooxytocin were synthesized and purified to homogeneity. The trisulfide compounds were evaluated in three assays: uterotonic in vitro, uterotonic in vivo, and pressor tests, and they showed substantial potencies, ranging from 5% to 40% of the parent (disulfide) activities, as well as protracted actions. The affinities of the peptide trisulfides to uterine membrane receptors were only 3.3-3.6-fold lower than those of the parent disulfides. Possible explanations of the biological results are discussed.
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PMID:Synthesis and pharmacology of novel analogues of oxytocin and deaminooxytocin: directed methods for the construction of disulfide and trisulfide bridges in peptides. 908 75

The role of superoxide in sepsis-altered hepatocyte Ca2+i regulation was studied by examining the effect of treatment of septic rats with superoxide dismutase-polyethylene glycol (SOD-PEG) on hepatocyte Ca2+ influx and efflux, and cytosolic [Ca2+]. Rats were implanted with sterile or bacteria-laden (Escherichia coli and Bacteroides fragilis) fecal pellets into the abdominal cavity. Eight hours after the implantation, rats were treated with SOD-PEG or its vehicle PEG. Septic and sterile implanted rats were killed 24 h postimplantation, and their livers were removed to isolate viable hepatocytes. Isolated hepatocytes were incubated with traces of 45Ca to assess Ca2+ influx and efflux. The 45Ca exchange assessments also allowed calculation of the intracellular exchangeable Ca2+ contents. [Ca2+]i was quantified by the use of fluorescent dye indo-1 and microfluorometric techniques. There were no differences in the Ca2+ influx, Ca2+ efflux, intracellular exchangeable Ca2+, or [Ca2+]i between the treated or untreated sterile and unoperated controls. However, compared with the nonseptic groups, the septic rats with or without administration of the vehicle (PEG) showed marked increases in Ca2+ influx, intracellular exchangeable Ca2+ and [Ca2+]i but not Ca2+ efflux. When challenged with vasopressin, the hepatocytes from septic rats, administered with PEG alone, did not elevate their [Ca2+]i as was characteristic of the hepatocytes from the nonseptic rats. The treatment of septic rats with SOD-PEG was effective in restoring Ca2+ influx, cellular exchangeable Ca2+, [Ca2+]i, and the [Ca2+]i response to vasopressin to levels found in the control and sterile groups. These findings support the concept that the generation of the superoxide free radical leads to Ca2+i-related derangements and related cell/organ dysfunction in sepsis.
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PMID:Superoxide radical scavenging prevents cellular calcium dysregulation during intraabdominal sepsis. 911 Apr 11

We infused arginine vasotocin, the natural avian antidiuretic hormone, and two antidiuretic hormone analogues into house sparrows (Passer domesticus) to evaluate the vascular and tubular components of antidiuresis in a small (25-g) bird. During control infusion of 25 mmol L-1 NaCl (0.6 mL h-1), urine flow rate was 0.73 mL h-1, glomerular filtration rate was 10.0 mL h-1, the ratio of polyethylene glycol (PEG) in the urine relative to that in the plasma was 16.4, and urine osmolality was 279 mOsmol kg-1. Infusion of arginine vasotocin (0.4 ng kg-1 min-1) decreased urine flow rate by 50% and glomerular filtration rate by 27%, while urine osmolality and the ratio of urine PEG to plasma PEG rose to 150% and 140% of control values, respectively. A higher dose of arginine vasotocin (1.6 ng kg-1 min-1) accentuated these changes. Infusion of the antidiuretic hormone analogue dPTyr(Me)AVT, designed as an antagonist to the V1 (mammalian vascular) receptors for arginine vasopressin, by itself (4.0 ng kg-1 min-1) had no effect on any measured variable (P > or = 0.1). Infusion of the analogue along with arginine vasotocin (0.4 ng kg-1 min-1) abolished the effect of arginine vasotocin on glomerular filtration rate, which suggests that this analogue blocked vascular receptors for arginine vasotocin in house sparrows. Under these circumstances, changes in urine flow rate, the ratio of urine PEG to plasma PEG, and urine osmolality were reduced to nonsignificance. The analogue d(CH2)5[D-Ile2,Ile4,Ala-MH2]AVP, designed as an antagonist to the effects of arginine vasopressin at V2 (mammalian renal tubular) receptors, also was without effect by itself. However, in the presence of this analogue, the effects of arginine vasotocin on urine flow rate and the ratio of urine PEG to plasma PEG were significantly enhanced, and this occurred without any enhanced diminution of glomerular filtration rate. Thus, this analogue appeared to activate a tubular mechanism of antidiuresis. Overall, the data suggest that action of arginine vasotocin at renal vascular receptors plays an important role in effecting antidiuresis in house sparrows. Blockade of renal vascular actions of arginine vasotocin by a V1 antagonist suggest that these receptors may be similar to the mammalian vascular (V1) receptor. The data also suggest a separate action of arginine vasotocin at the renal tubules, but the receptors there apparently differ from the mammalian tubular (V2) receptor.
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PMID:Renal glomerular and tubular effects of antidiuretic hormone and two antidiuretic hormone analogues in house sparrows (Passer domesticus). 923 2

When toadfish are made ureotelic by a crowding/confinement protocol, they excrete approximately 90 % of their urea nitrogen (urea-N) production in large, irregular pulses (1-2 pulses per day) from the gill region. We investigated three hypotheses as to the mechanism of pulsatile excretion: (i) the presence of an active reabsorptive 'back-transport' mechanism that is periodically inhibited to allow urea-N excretion to occur; (ii) the periodic occurrence of a generalized, non-specific increase in gill permeability; and (iii) the presence of a specific facilitated diffusion transport system that is periodically activated. Exposure of toadfish during non-pulse periods to treatments designed to block a 'back-transport' mechanism (Na+-free sea water or the urea analogues 30 mmol l-1 thiourea or 30 mmol l-1 acetamide in the external water) did not stimulate a leakage of urea-N, thereby opposing the first hypothesis. The second hypothesis was opposed by several results. Neither injection of the potent branchial vasodilator L-isoprenaline (10(-5) mol l-1) nor infusion of NH4Cl, the latter at levels known to stimulate urea-N efflux in perfused gills, had any effect on urea-N excretion. Furthermore, during natural pulse events, when the normally very low gill permeability to urea (3x10(-7) cm s-1) increased at least 35-fold, there was no accompanying increase in permeability to either 3H2O (1.5x10(-5) cm s-1) or the paracellular marker [14C]PEG-4000 (10(-8) cm s-1). However [14C]thiourea permeability (1.5x10(-7) cm s-1) increased approximately fivefold, in support of the third hypothesis. Furthermore, when 30 mmol l-1 urea was placed in the external water, a concentration (60 000 micromol-N l-1) approximately three times that of blood (20 000 micromol-N l-1), each efflux pulse event (measured with [14C]urea) was accompanied by a net uptake, such that blood urea-N levels rose rather than fell. A proportional 1:1 relationship between influx per unit external concentration and efflux per unit internal (i.e. plasma) concentration indicated a fully bidirectional transport system. The simultaneous presence of 60 mmol l-1 thiourea in the external water inhibited the influx component by 73 %, further supporting this conclusion. These data, together with recent molecular, morphological and endocrinological evidence, strongly suggest that pulsatile urea-N excretion is caused by the periodic activation of a facilitated urea transporter in the gills, similar to the vasopressin-regulated urea transporter in the mammalian kidney.
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PMID:Pulsatile urea excretion in gulf toadfish (Opsanus beta): evidence for activation of a specific facilitated diffusion transport system. 946 61

Arginine vasopressin (AVP) has recently been shown to exist in and to be released from airway epithelial cells, but the physiologic role of this hormone in airway epithelial function is unknown. To determine whether AVP affects ciliary motility, and if so, to elucidate the mechanism of action and the subtype of AVP receptors involved, we measured ciliary beat frequency (CBF) and the intracellular Ca2+ concentration ([Ca2+]i) of cultured rabbit tracheal epithelium with a photoelectric method and the fura-2 fluorescence method, respectively. Addition of AVP caused a rapid increase in CBF, followed by a decline and a subsequent sustained response. The ciliary stimulatory action was dose dependent, the maximal peak increase from the baseline CBF being 20.6 +/- 4.7% (mean +/- SE, P < 0.001), and this effect was reduced to 5.9 +/- 2. 0% by the V1 receptor antagonist OPC-21268 (P < 0.01), but not by the V2 receptor antagonist OPC-31260. The AVP-induced increase in CBF was not altered by the protein kinase A (PKA) inhibitor Rp-adenosine-3',5'-cyclic monophosphorothioate triethylamine (Rp-cAMPS) or by Ca2+-free solution containing ethylene glycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA), but was abolished by pretreatment with thapsigargin. Exposure of cells to AVP elicited a transient increase in [Ca2+]i, an effect that was likewise abolished by thapsigargin. The rank-order potency of AVP analogues to increase [Ca2+]i was AVP = [deamino1, D-3-(pyridyl) Ala2-Arg8] vasopressin (DP-VP), a specific V1b receptor agonist > [Phe2, Ile3, Orn8] vasopressin (PO-VT), a V1a agonist > 1-desamino-8-D-arginine vasopressin (dDAVP), a V2 agonist. Moreover, OPC-21268 greatly attenuated the action of AVP, whereas OPC-31260 was without effect. These results suggest that AVP stimulates ciliary motility of rabbit tracheal epithelium through mobilization of Ca2+ from thapsigargin-sensitive stores, and that this effect may be mediated by V1b receptors.
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PMID:Vasopressin stimulates ciliary motility of rabbit tracheal epithelium: role of V1b receptor-mediated Ca2+ mobilization. 969 2

Cardiac vagal afferents terminating in the nucleus of the solitary tract (NTS) are believed to participate in stimulating neurohypophysial secretion of vasopressin as well as increased ingestion of water and NaCl solution in response to decreased blood volume. However, we recently reported that chronic lesions of NTS, which eliminate neural input from cardiac and arterial baroreceptors, do not impair hypovolemia-induced vasopressin secretion in rats. In the present investigation we sought to determine whether those sensory signals were necessary for hypovolemia-induced thirst and salt appetite. Rats with chronic lesions of the NTS increased consumption of water and NaCl solution normally when plasma volume was reduced isosmotically by subcutaneous injection of polyethylene glycol solution. These results were obtained whether rats were allowed to drink water or 0.15 M NaCl in one-bottle tests or water and 0.5 M NaCl in two-bottle tests. The induction of thirst and salt appetite by hypovolemia despite the apparent loss of neural input to the brain from cardiac volume-sensitive receptors indicates that other signals generated by plasma volume deficits can stimulate these behavioral responses in rats.
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PMID:Thirst and salt appetite elicited by hypovolemia in rats with chronic lesions of the nucleus of the solitary tract. 988 3

1. The effects of injections i.c.v. of quipazine, (2 micromol kg-1) and 1-(2,5-di-methoxy-4-iodophenyl)-2-aminopropane (DOI; 2 micromol kg-1) on renal sympathetic and phrenic nerve activity, mean arterial blood pressure (MAP) and heart rate were investigated in alpha-chloralose anaesthetized rats pretreated with a peripherally acting 5-HT2 receptor antagonist. 2. Quipazine or DOI caused a rise in MAP which was associated with a tachycardia and renal sympathoinhibition in rats pretreated (i.c.v.) with the antagonist vehicle 10% PEG. These effects of quipazine were completely blocked by pretreatment with cinanserin (a 5-HT2 receptor antagonist) and attenuated by spiperone (a 5-HT2A receptor antagonist). However, pretreatment with SB200646A (a 5-HT2B/2C receptor antagonist) only blocked the sympathoinhibition, while pretreatment with SB204741 (a 5-HT2B receptor antagonist) reversed the sympathoinhibition to excitation as it also did for DOI. Quipazine also caused renal sympathoexcitation in the presence (i.v.) of a vasopressin V1 receptor antagonist. 3. Injection (i.v.) of the V1 receptor antagonist at the peak pressor response evoked by quipazine alone and in the presence of SB204741 caused an immediate fall in MAP. For quipazine alone the renal sympathoinhibition was slowly reversed to an excitation, while the renal sympathoexcitation observed in the presence of SB204741 was potentiated. In both, the quipazine-evoked tachycardia was unaffected. 4. The data indicate that cardiovascular responses caused by i.c.v. quipazine and DOI are primarily due to activation of central 5-HT2A receptors, which causes the release of vasopressin and a tachycardia. This released vasopressin appears to suppress a 5-HT2A receptor-evoked central increase in sympathetic outflow, which involves the activation of central 5-HT2B receptors indirectly by the released vasopressin.
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PMID:Evidence for a role for central 5-HT2B as well as 5-HT2A receptors in cardiovascular regulation in anaesthetized rats. 1051 29

OBJECTIVES: This study was undertaken to investigate the effects of hypovolemic and hypertonic treatments on plasma vasopressin (AVP) levels and fluid balance in thyroidectomy-induced hypothyroidism in the rat. The influence of hypothyroidism on AVP responsiveness to hypertonic and hypovolemic stimuli were compared. MATERIALS & METHODS: Adult male rats were divided into two groups. The rats were surgically thyroidectomized (hypothyroid) or sham-operated (euthyroid). Two weeks later these groups were further divided in three subgroups each containing six rats. The first subgroup consisted of unchallenged rats. The second group underwent hypovolemic treatment by using I.P. 700 mg polyethylene glycol. The third subgroup consisted of hypertonic (1.5 M NaCl; 1 ml/100 g) stimulated animals. All rats were decapitated and trunk blood collected in heparinized tubes. Plasma samples were stored at -20 degrees C until assayed. Plasma AVP, T3 and T4 levels were measured by radioimmunoassay. Hematocrit values and plasma Na and K concentrations were also determined. RESULTS: In the hypothyroid rats, hypovolemic treatment significantly reduced the expected increases in plasma AVP levels (p<0.05) compared to the respective intact animals. In the hypertonic group, similar increases occurred in plasma AVP levels of hypothyroid and euthyroid rats. Hematocrit values and plasma Na concentrations were not significantly different in the hypothyroid rats compared to euthyroid rats. CONCLUSION: In conclusion, thyroidectomy-induced hypothyroidism may affect AVP response to hypovolemic stimulus although it has no important effect on basal AVP levels nor AVP response to hypertonic stimulus.
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PMID:Influence of hypovolemic and hypertonic treatments on plasma vasopressin levels and fluid balance in the thyroidectomy-induced hypothyroid rats. 1145 27


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