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)

Methods of blocker-induced noise analysis were used to investigate the way in which forskolin and vasopressin stimulate Na transport at apical membranes of short-circuited frog skin transporting Na at spontaneous rates of transport. Experiments were done under conditions where the apical Ringer solution contained either 100 mM Na or a reduced Na concentration of 5 or 10 mM Na and buffered with either HCO3 or HEPES. Reduction of apical solution Na concentration caused a large autoregulatory increase of Na channel density (NT) similar in magnitude to that observed previously in response to blocker (amiloride) inhibition of apical membrane Na entry. Forskolin at 2.5 microM caused maximal and reversible large increases of NT, which were larger than could be elicited by 30 mU/ml vasopressin. In both the absence and presence of the autoregulatory increase of NT (caused by reduction of apical Na concentration), forskolin caused large increases of NT. Although the fractional increases of NT in response to forskolin were roughly similar, the absolute increases of NT were considerably larger in those tissues studied at reduced Na concentration and where baseline values of NT were markedly elevated by reduction of apical Na concentration. Because the effects on NT were additive, it is likely that the cAMP-dependent and autoregulatory mechanism that lead to changes of NT are distinct. We speculate that autoregulation of NT may involve change of the size of a cytosolic pool of Na-containing vesicles that are in dynamic balance with the apical membranes. cAMP-dependent regulation of NT may involve change of the dynamic balance between vesicles and the apical membranes of these epithelial cells. Alternative hypotheses cannot at present be ruled out, but will require incorporation of the idea that regulation of NT can occur both by hormonal and nonhormonal (autoregulatory) mechanisms of action.
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PMID:Activation of epithelial Na channels by hormonal and autoregulatory mechanisms of action. 166 57

Isolated rat neurohypophyses were fixed by their stalks to a platinum wire electrode and superfused with Krebs-HEPES solution. Vasopressin and oxytocin released into the medium were determined by specific radioimmunoassays. Hormone secretion was increased by electrical stimulation of the pituitary stalk at different frequencies. The effects of several potassium channel blockers, tetraethyl-ammonium (TEA) ions, 4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP) were tested. The release of vasopressin and oxytocin evoked by electrical stimulation with 900 pulses at 15 Hz (about 900 and 1,000 microU, respectively) was about 10 times higher than that evoked by 900 pulses at 3 Hz. Both 10 and 30 mmol/l TEA enhanced the release of vasopressin evoked by stimulation at 3 and 15 Hz, by 25- and 2-fold, respectively, to attain a maximum release of about 1,800 microU per stimulation. The stimulated release of oxytocin attained a maximum of about 9,000 microU at 15 Hz in the presence of 10 mmol/l TEA or at 3 Hz with 30 mmol/l TEA. Thus, in the presence of maximally effective concentrations of TEA both stimulation frequencies (3 and 15 Hz) were equieffective in evoking release of vasopressin and oxytocin. 4-AP or 3,4-DAP enhanced the release of vasopressin evoked by 15 Hz stimulation maximally to about 1,600 microU. In the presence of 4-AP or 3,4-DAP the release of oxytocin evoked by stimulation at 15 Hz increased maximally to about 8,000 microU and that evoked by stimulation at 3 Hz to about 1,500 microU.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of potassium channel blockers on neurohypophysial release of oxytocin and vasopressin. Evidence for frequency-dependent interaction with the endogenous opioid inhibition of oxytocin release. 285 13

1. Isolated rat neurohypophyses were fixed by their stalks to a platinum wire electrode and superfused with oxygenated Krebs-HEPES solution. Vasopressin release into the medium was determined by radioimmunoassay. Vasopressin secretion was increased by electrical stimulation at different frequencies (3-30 Hz) and different train lengths (75-900 pulses). The effects of tetraethylammonium (TEA) ions and of enhanced calcium were tested. 2. Electrical stimulation at 7.5 or 15 Hz evoked a markedly larger release of vasopressin than stimulation at 3 Hz. During continuous stimulation at 7.5 and 15 Hz the evoked vasopressin release per pulse declined rapidly, but with similar time constants for both frequencies indicating that the fatigue of the release process was strongly time dependent. The kinetic analysis showed also that the initial release per pulse was identical for 7.5 and 15 Hz stimulation. Nevertheless, with increasing duration, stimulation at 7.5 Hz became less efficient (in terms of release per total stimulus) than stimulation at 15 Hz and this was due to the time-dependent fatigue. 3. TEA (10 mM) increased the release of vasopressin evoked by 3 Hz stimulation much more than that evoked by 15 Hz stimulation resulting in an equieffective activation of release by both stimuli. On the other hand, elevation of the extracellular calcium from 1.2 to 3 mM did not alter the different efficiency of stimuli of 3 and 15 Hz. In the presence of TEA the time-dependent fatigue of the release during continuous stimulation was prevented, but an additional, slower component of the fatigue became apparent which was release or impulse dependent. 4. As prolongation of the action potential by TEA facilitates preferentially the hormone release evoked by low (ineffective) frequencies, it is suggested that a frequency-dependent broadening of action potentials which reportedly occurs on neurosecretory neurones may play an important role in the frequency-dependent facilitation of hormone release from the rat neurohypophysis.
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PMID:Effects of tetraethylammonium ions on frequency-dependent vasopressin release from the rat neurohypophysis. 341 19

Single rat neurointermediate lobes (n.i.l.s) were fixed by their stalks to a platinum wire clip electrode and incubated in oxygenated Krebs-HEPES medium. Vasopressin release int the medium was determined by radioimmunoassay. Vasopressin secretion was increased by different stimuli and the effects of gadolinium (Gd3+) were tested. Electrical stimulation (15 Hz, three times 1 min with 1 min intervals) increased vasopressin release in a calcium-dependent manner. Gd3+ (10 microM to 3 mM) inhibited the evoked release of vasopressin in a concentration-dependent fashion; at 3 mM the inhibition was 98%. The inhibitory effect of Gd3+ up to 300 microM was antagonized by increasing the calcium concentration in the medium up to 6 mM. The effects of 1 and 3 mM-Gd3+ were unaffected by increasing the calcium concentration. Exposure of n.i.l.s to depolarizing concentrations of potassium (high K+, 60 mM, 30 min) increased the vasopressin release more than 33-fold. The elevated vasopressin release remained constant during six consecutive 5 min periods. In the initial 5 min period 300 microM-Gd3+ reduced the evoked vasopressin release by 80% but during the last 5 min period only by 30%. At 3 mM-Gd3+ vasopressin release was completely blocked during the whole time of incubation with high K+. Vasopressin release induced by exposure of n.i.l.s to cold (4 degrees C, 20 min) was completely inhibited by 3 mM-Gd3+, but reduced by only 25% in the presence of 300 microM-Gd3+. Vasopressin release induced by incubation of n.i.l.s with the ionophore X-537A (lasalocid) (10 microM, 30 min) was reduced by 90% in the presence of 300 microM-Gd3+ and completely prevented by 3 mM-Gd3+. 300 microM-Gd3+, added to the incubation medium, had no significant effect on the vasopressin release from crude synaptosomal preparations evoked by high K+. However, when 300 microM-Gd3+ was already present during the tissue homogenization, the evoked vasopressin release from the synaptosomes was completely blocked. It is concluded that Gd3+ inhibits exocytotic vasopressin release at two different sites. First, Gd3+ may block voltage-regulated calcium channels. Secondly, Gd3+ may inhibit the exocytotic release mechanism by an intracellular site of action. It is speculated that contractile proteins may be the intracellular target for Gd3+.
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PMID:Gadolinium ions inhibit exocytotic vasopressin release from the rat neurohypophysis. 405 5

The purpose of this study was to determine whether human vasoactive intestinal peptide (VIP) aggregates in aqueous solution and, if so, whether the peptide interacts with a biomimetic phospholipid monolayer and increases surface pressure. Using a custom-made Teflon trough containing HEPES buffer (pH 7.4) at room temperature and a surface tensiometer, we found that the critical micellar concentration (CMC) of VIP is 0.4 microM. Surface pressure of a dipalmitoylphosphatidylcholine (DPPC) monolayer spread over the HEPES buffer declined significantly over 120 min because of phospholipid decomposition. However, injection of VIP at concentrations above CMC into the subphase of the monolayer elicited a significant concentration-dependent increase in surface pressure that persisted for 120 min (P < 0.05). Unlike VIP, injection of [(8)Arg]-vasopressin at an equimolar concentration only prevented the time-dependent decline in DPPC monolayer surface pressure. Taken together, these data indicate that human VIP aggregates in aqueous solution and expresses surface-active properties at physiological concentrations in vitro. We suggest that these attributes could have a role in modulating the bioactive effects of the peptide in vivo.
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PMID:Surface-active properties of vasoactive intestinal peptide*. 1079 26