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)

Recently, we have shown that angiotensin II-induced AT1 receptor-mediated vasopressin release can be potentiated by blockade of periventricular AT2 receptors. In the present study, we investigated whether the AT2 receptor also exerts an inhibitory effect on osmotically induced vasopressin release. In addition, we tested the effect of the muscarinic receptor antagonist, atropine, on hyperosmolar saline-induced vasopressin release. Plasma vasopressin levels were determined 90 s after intracerebroventricularly applied hyperosmolar saline (0.2, 0.3 and 0.6 M, 5 microliters) with or without intracerebroventricular pretreatment with 1 nmol of the selective AT2 receptor antagonist, PD 123177 (1-(4-amino-3-methylphenyl)methyl-5-diphenylacetyl-4,5,6,7-tetrahy dro- 1H-imidazo[4,5-c]pyridine-6-carboxylic acid-2HCl), or with 15 nmol of the muscarinic receptor antagonist, atropine. PD 123177 potentiated 0.2 M saline-induced vasopressin release (4.7 +/- 0.8 pg/ml vs. 2.2 +/- 0.3 in vehicle-pretreated controls, P < 0.05), did not affect 0.3 M saline-induced vasopressin release (4.3 +/- 0.7 pg/ml vs. 5.4 +/- 0.6 pg/ml in vehicle-pretreated controls) and reduced 0.6 M saline-induced vasopressin release (10.0 +/- 2.3 pg/ml vs. 17.9 +/- 1.8 pg/ml in vehicle-pretreated controls, P < 0.05). Pretreatment with atropine reduced 0.3 M (2.3 +/- 0.6 pg/ml vs. 5.4 +/- 0.9 pg/ml in vehicle-pretreated controls, P < 0.05) and 0.6 M saline-induced AVP release (4.0 +/- 1.5 pg/ml vs. 18.4 +/- 2.4 pg/ml in vehicle-pretreated controls, P < 0.05) but did not affect 0.2 M saline-induced vasopressin release (2.1 +/- 0.4 pg/ml vs. 3.2 +/- 0.8 pg/ml in vehicle-pretreated controls). Our results suggest that the low saline concentration-induced, AT1 receptor-mediated, vasopressin release is under inhibitory control by periventricular AT2 receptors. Following high saline concentrations, a muscarinic mechanism seems to be predominant on which AT2 receptor stimulation acts in a facilitating manner.
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PMID:Effect of angiotensin AT2 and muscarinic receptor blockade on osmotically induced vasopressin release. 874 Nov 76

Magnocellular hypothalamo-neurohypophysial neurones display characteristic firing patterns, related to the hormone they release. To identify the membrane currents that may underlie these firing patterns, we performed whole-cell recording of freshly dissociated magnocellular neurones from the supraoptic nucleus. After recording, cells were immunocytochemically identified by using highly selective monoclonal antibodies raised respectively against vasopressin (AVP) and oxytocin (OT) neurophysin. In 64 out of 131 neurones (48.8%), we detected the presence of a transient potassium current whose kinetic properties were characteristic of an A-current. The A-current was activated by depolarisation over -40 mV, and inactivated rapidly with a monoexponential decay (tau = 28 +/- 2.7 ms; n = 33 at 0 mV). Using conditioning prepulses of 50 ms, the voltage dependence of the inactivation was determined, and the data were adequately fit with a Boltzman equation (half-maximal inactivation: -42.5 mV). The steady-state time-dependent inactivation curve was determined using a prepulse potential at -40 mV, and data were best described with a mono-exponential equation (tau = 89.7 ms). The sensitivity to 1 mM 4-amino-pyridine (63 +/- 9% inhibition, n = 6), and a reversal potential close to the theoretical Nernst equilibrium for potassium (-56.3 +/- 1 mV, n = 6, vs. -58 mV) confirmed that the transient current studied was indeed an A-type potassium current. Immunocytochemical identification revealed that the A-current was selectively expressed in OT-neurophysin-positive cells. As previous work in hypothalamic slice preparations suggests that the A-current is expressed by both AVP cells and OT cells, the present data suggest that whereas the A-current is expressed in the soma of OT cells, it may be expressed only on the dendritic tree of AVP cells, which is truncated in the dispersed cell preparation used here. This distribution may play a role in the specific firing characteristics of magnocellular neurones.
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PMID:Differential distribution of a potassium current in immunocytochemically identified supraoptic magnocellular neurones of the rat. 914 94

As first observed in rat adrenal glomerulosa cells, cytoplasmic Ca(2+) signal, induced by K(+), angiotensin II or vasopressin, evokes an increase in the level of reduced mitochondrial pyridine nucleotides, NADH and NADPH. Prostaglandin F(2)alpha and extracellular ATP exert similar effects in rat ovarian luteal cells. This coupling of cytoplasmic Ca(2+) concentration and mitochondrial metabolism occurs also when the stimuli are applied at physiological concentration and under conditions when no formation of high-Ca(2+) perimitochondrial microdomains may be presumed. We present evidence that low submicromolar Ca(2+) signals in the cytoplasm can increase mitochondrial Ca(2+) concentration and activate mitochondrial dehydrogenation processes. Several observations support the assumption that intramitochondrial Ca(2+) signals play a significant role in the stimulation of steroid hormone production.
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PMID:The effect of cytoplasmic Ca2+ signal on the redox state of mitochondrial pyridine nucleotides. 1502 83

A series of fluorescent ligands designed for vasopressin and oxytocin G protein-coupled receptors was synthesized and characterized to develop fluorescence polarization or homogeneous time-resolved fluorescence (HTRF) binding assays. These ligands, labeled with europium pyridine-bis-bipyridine cryptate or with Alexa 488,546,647 selectively bound to the vasopressin V1a and oxytocin receptors with high affinities and exhibited antagonistic properties. The affinities of several unlabeled ligands determined by our homogeneous assays on membrane preparations or on intact cells into 96- and 384-well plate formats were similar to those determined by usual radioligand binding methods. Compared to other binding assays, the polarization and HTRF binding assays are nonradiaoactive, therefore safer to perform, yet very sensitive and homogeneous, therefore easier and faster to automate. These methods are thus suitable for efficient drug high-throughput screening procedures and can easily be applied to other G protein-coupled receptor models.
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PMID:Toward efficient drug screening by homogeneous assays based on the development of new fluorescent vasopressin and oxytocin receptor ligands. 1785 55


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