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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultrastructure of collecting duct epithelia was studied with the osmium impregnation technique in renal cortical explants grown in culture in the form of globular bodies. When this technique was applied to 7-day-old globular bodies, the endoplasmic reticulum (ER) of the superficial layer cells was faintly impregnated in the presence or absence of arginine-vasopressin (AVP) in the incubation medium; the ER of the cells located in the core of the globular bodies was densely impregnated with osmium. When these globular bodies were sectioned in 2 fragments and one was incubated in AVP for 30 min while the other was used as a control, a marked increase in osmium impregnation occurred: osmium black deposits were then noted in the lumen of the endoplasmic reticulum of two-thirds of the cells in the superficial layer. Various patterns of impregnation were observed. Cryptlike formations gave rise to mature epithelial cells showing the same pattern of osmium impregnation. When cyclic adenosine monophosphate (cAMP) was substituted for AVP in the incubation medium, the treated globular bodies revealed the same ultrastructural characteristics. Our data suggest that this primary culture of collecting duct epithelia is made up of heterogeneous cells with characteristics of principal and intercalated cells and that the AVP has a stimulatory effect on ER maturation, which is mediated by the adenylate cyclase system.
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PMID:Vasopressin modifies osmium impregnation of the endoplasmic reticulum in cultured kidney collecting duct cells. 322 13

Neomycin was used to assess the involvement of Ins (1,4,5)P3 in the Ca2+ release from the endoplasmic reticulum induced by the bile acid taurolithocholate. In saponin-permeabilized rat hepatocytes, neomycin via its ability to bind Ins (1,4,5)P3 abolished the release of Ca2+ induced by added Ins (1,4,5)P3. In contrast, it did not alter the Ca2+ release initiated by the bile acid. In intact cells, neomycin had no effect on the [Ca2+]i rises promoted by taurolithocholate and vasopressin. It is suggested that the effect of taurolithocholate in liver is not mediated by Ins (1,4,5)P3 but results from a primary action on endoplasmic reticulum.
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PMID:Effect of the bile acid taurolithocholate on cell calcium in saponin-treated rat hepatocytes. 325 48

The effects of four bile acids on cell Ca2+ were examined in suspensions of isolated rat hepatocytes. Taurolithocholate and lithocholate which inhibit bile secretion increased the cytosolic Ca2+ concentration (ED50, 25 microM), as measured by the fluorescent indicator quin2, and promoted a net loss of Ca2+ from the cells. This effect resulted from rapid mobilization of Ca2+ from an intracellular Ca2+ store. This store corresponds to the one that is permeabilized by the inositol (1,4,5)trisphosphate-dependent hormone vasopressin. However, taurolithocholate and lithocholate, unlike the hormone, did not induce a significant accumulation of inositol trisphosphate fraction in isolated hepatocytes. In addition, these agents did not alter the cell and the mitochondria membrane permeability to ions. When applied to saponin-permeabilized cells, taurolithocholate and lithocholate released Ca2+ (ED50, 20 microM) from an ATP-dependent, nonmitochondrial pool which is sensitive to inositol (1,4,5)trisphosphate. In contrast, the bile acids taurocholate and cholate, which increase bile secretion, had no effect on cell Ca2+ in intact hepatocytes or in saponin-permeabilized hepatocytes. It is suggested that taurolithocholate and lithocholate permeabilize the endoplasmic reticulum to Ca2+ and that the resulting permeabilization of this compartment may be involved in the inhibition of bile secretion in mammalian liver.
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PMID:Release of calcium from the endoplasmic reticulum by bile acids in rat liver cells. 325 91

The effects of colchicine on neurosecretory neurons of the rat hypothalamus were studied by immunocytochemistry, high-resolution radioautography, and conventional electron microscopy. In control rats, intraneuronal immunocytochemical labeling of vasopressin, oxytocin and somatostatin occurred essentially in the Golgi apparatus, the neurosecretory granules and to a lesser extent, the endoplasmic reticulum. These immunostaining patterns were dramatically modified 24 h after the administration of colchicine: immunoreactive peptides were located in granular or tubular structures accumulated at the periphery of the perikarya, but the Golgi stacks were not immunostained. Two h after the administration of tritiated leucine, quantitative analysis of radioautographic labeling of supraoptic perikarya revealed large amounts of radioactive protein in the Golgi saccules of neurosecretory neurons in control rats, but in the neurons of colchicine-treated rats, radioautographic labeling was mainly located in granular structures accumulated at the periphery of the perikarya, with no significant labeling on the Golgi stacks. Lastly, 3 noteworthy effects of colchicine on the ultrastructural morphological features of these neurosecretory neurons consisted in: (1) a dramatic disorganization of the Golgi complexes, (2) an accumulation of electron-dense proteic material within the lumen of cisternae of both the rough and smooth endoplasmic reticulum and, (3) a marked depolymerization of perikaryal microtubules, specifically those associated with the Golgi stacks. Taken together, these data do not fit the prevailing concept that the colchicine-induced accumulation of secretory material within the perikarya of neurosecretory neurons essentially results from the blockade of axoplasmic transport mechanisms. Instead, they support the idea that the effects of colchicine are related to the inhibition of the intraneuronal transport of newly synthesized secretory material from the endoplasmic reticulum to the Golgi apparatus, suggesting that the microtubules associated with the Golgi stacks are possible sites of colchicine action.
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PMID:Effects of colchicine on the intraneuronal transport of secretory material prior to the axon: a morphofunctional study in hypothalamic neurosecretory neurons of the rat. 340 58

1. In hepatocytes, epidermal growth factor (EFG) (a) increased the rate of 45Ca2+ exchange in cells incubated at 1.3 mM extracellular Ca2+, (b) increased the activity of glycogen phosphorylase a and the intracellular free Ca2+ concentration (measured with quin2) in a process dependent on the concentration of extracellular Ca2+, and (c) enhanced the increase in glycogen phosphorylase activity which follows the addition of Ca2+ to cells previously incubated in the absence of Ca2+. It is concluded that EGF stimulates plasma-membrane Ca2+ inflow. 2. The effects of the combination of EGF and vasopressin on the rate of 45Ca2+ exchange and on the rate of increase in glycogen phosphorylase activity were the same as those of vasopressin alone. 3. The amount of 45Ca2+ released by EGF from internal stores was about 30% of that released by vasopressin. No detectable increase in [3H]inositol mono-, bis- or tris-phosphate was observed after the addition of EGF to cells labelled with myo-[3H]inositol. 4. In hepatocytes isolated from rats treated with pertussis toxin, the effects of EGF and vasopressin on phosphorylase activity (measured at 1.3 mM-Ca2+) and on the rate of Ca2+ inflow (measured with quin2) were markedly decreased compared with those in normal cells. 5. Treatment with pertussis toxin did not impair the ability of vasopressin to release Ca2+ from internal stores, but decreased vasopressin-stimulated [3H]inositol polyphosphate formation by 50%. 6. It is concluded that the mechanism(s) by which vasopressin and EGF stimulate plasma-membrane Ca2+-inflow transporters in hepatocytes involves a GTP-binding regulatory protein sensitive to pertussis toxin, and does not require an increase in the concentration of inositol trisphosphate comparable with that which induces the release of Ca2+ from the endoplasmic reticulum.
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PMID:Evidence that a pertussis-toxin-sensitive substrate is involved in the stimulation by epidermal growth factor and vasopressin of plasma-membrane Ca2+ inflow in hepatocytes. 350 16

The total Ca2+ content of the endoplasmic reticulum and the total Ca2+ and Mg2+ content of mitochondria were determined by electron probe microanalysis of rat liver rapidly frozen in vivo following brief (5-15 s) stimulation with vasopressin or prolonged (10-12 min) stimulation with vasopressin + glucagon. Brief vasopressin injection into the anterior mesenteric vein released 1.8 +/- 0.3 (S.D.) mmol of Ca2+/kg dry weight, from the rough endoplasmic reticulum (p less than 0.01), reducing Ca2+ content of the endoplasmic reticulum from 4.4 +/- 0.2 (S.E.) (controls) to 2.6 +/- 0.2 mmol of Ca2+/kg dry weight. Following vasopressin injection, endoplasmic reticulum Ca2+ was also significantly (p less than 0.025) lower than that in brief sham injected animals (3.5 +/- 0.2 mmol/kg dry weight). Mitochondrial Ca2+ was between 1.0 and 2.3 (+/-0.2) mmol/kg dry weight of mitochondrion, under all conditions studied, and no significant differences were observed. Both hormonal and brief sham injection into the anterior mesenteric vein increased mitochondrial Mg2+ from 42 (+/-0.8) to 49 (+/-1.8) mmol/kg dry weight (p less than 0.05). Hormonal stimulation of Mg2+ uptake was further confirmed by injection of vasopressin + glucagon into the jugular vein (to avoid any stimulation of the liver by the anterior mesenteric vein injection itself); mitochondrial Mg2+ increased from 43 (+/-0.9) (10-min sham) to 57 (+/-1.3) mmol/kg dry weight, with 10-min vasopressin + glucagon injection (p less than 0.01). These results demonstrate that hormones can release Ca2+ from the endoplasmic reticulum and modulate mitochondrial Mg2+ content in vivo without causing detectable changes in mitochondrial Ca2+.
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PMID:Subcellular calcium and magnesium mobilization in rat liver stimulated in vivo with vasopressin and glucagon. 368 Feb 16

The neurons of the supraoptic nucleus (SON) in the rat have been analysed by electron microscopy and morphometry, when the secretion of the antidiuretic hormone was fully suppressed by water loading. The water was supplied through a catheter inserted in the external jugular vein for 1.5, 2.5 and 24 h, respectively. The SON was also examined in normal rats and in rats that had been deprived of water for 72 h. The rats were fixed through chronically implanted catheters, so that at the time of fixation, the animal was uninfluenced by anaesthesia and surgery. The morphology of the granular endoplasmic reticulum and the Golgi complex showed that the water load suppressed the synthetic activity and the water deprivation stimulated it. The total volumes of the vasopressin-containing neurosecretory granules (NG) were 1.6, 2.8 and 5.0 X 10(4) micron3 after a 24-hour water load, in the normal state and after 72-hour water deprivation, respectively. In steady states there was a positive correlation between the secretory activity and the content of NG in the perikaryon.
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PMID:Morphometric electron-microscopic investigation of the neurons of the supraoptic nucleus in water-loaded, normal and water-deprived rats. 378 54

The effects of glucagon and vasopressin, singly or together, on cytosolic free Ca2+ concentration [( Ca2+]i) and on the 45Ca2+ efflux were studied in isolated rat liver cells. In the presence of 1 mM external Ca2+, glucagon and vasopressin added singly induced sustained increases in [Ca2+]i. The rate of the initial fast phase of the [Ca2+]i increase and the magnitude of the final plateau were dependent on the concentrations (50 pm-0.1 microM) of glucagon and vasopressin. Preincubating the cells with a low concentration of glucagon (0.1 nM) for 2 min markedly accelerated the fast phase and elevated the plateau of the [Ca2+]i increase caused by vasopressin. In the absence of external free Ca2+, glucagon and vasopressin transiently increased [Ca2+]i and stimulated the 45Ca2+ efflux from the cells, indicating mobilization of Ca2+ from internal store(s). Preincubating the cells with 0.1 nM-glucagon accelerated the rate of the fast phase of the [Ca2+]i rise caused by the subsequent addition of vasopressin. However, unlike what was observed in the presence of 1 mM-Ca2+, glucagon no longer enhanced the maximal [Ca2+]i response to vasopressin. In the absence of external free Ca2+, higher concentrations (1 nM-0.1 microM) of glucagon, which initiated larger increases in [Ca2+]i, drastically decreased the subsequent Ca2+ response to vasopressin (10 nM). At these concentrations, glucagon also decreased the vasopressin-stimulated 45Ca2+ efflux from the cells. It is suggested that, in the liver, glucagon accelerates the fast phase and elevates the plateau of the vasopressin-mediated [Ca2+]i increase respectively by releasing Ca2+ from the same internal store as that permeabilized by vasopressin, probably the endoplasmic reticulum, and potentiating the influx of extracellular Ca2+ caused by this hormone.
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PMID:Glucagon and vasopressin interactions on Ca2+ movements in isolated hepatocytes. 380 Sep 9

Lesions of the tissue surrounding the preoptic recess (anteroventral third ventricle (AV3V) region) have been shown to severely impair normal mechanisms of body fluid homeostasis, including the antidiuretic response. In an earlier investigation of the pathways affected by these lesions, coronal cuts were placed between the level of the organum vasculosum lamina terminalis in the AV3V region and the level of the supraoptic nuclei. Rats with such cuts exhibited hyperdipsia and polyuria, but their plasma levels of antidiuretic hormone (ADH) were elevated. The fine structure of the supraoptic nucleus, a major site of ADH production, and of the neural lobe of the hypophysis, where ADH is released, were observed in rats with similar cuts. Although neural lobes showed evidence of hormone depletion and degenerating axons and terminals were present in supraoptic nuclei, there was no morphological evidence that neurosecretory cell bodies in supraoptic nuclei were affected by these cuts. Therefore, in this investigation we observed the ultrastructural effects of such cuts on paraventricular nuclei, which are the other major source of ADH. Degenerating axons and terminals were common in paraventricular nuclei of lesioned rats, both in the major magnocellular subnucleus and in the periventricular region. Cell bodies and nuclei of neurosecretory cells were not significantly larger in lesioned animals, but morphometric evaluations revealed dispersion of the Golgi complex and alterations in the rough endoplasmic reticulum of the cells. In addition, more multiple nucleoli were present, and nucleoli tended to lie adjacent to the nuclear envelope more frequently. We conclude that the neurosecretory cells in the paraventricular nuclei become more active in rats with these knife cuts.
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PMID:The effects of transverse cuts caudal to the preoptic recess on the fine structure of paraventricular nuclei in rats. 398 97

Twenty-four hours after the injection of [35S]cysteine near either the rat paraventricular nuclei or the supraoptic nuclei, the [35S]neurophysin-like proteins of the brain stem were extracted, immunoprecipitated with anti-bovine neurophysins antibodies and analyzed. They consisted essentially of species behaving as neurophysin on sodium dodecyl sulfate--polyacrylamide gel electrophoresis. There was a very low percentage of neurophysins precursors which could be characterized in the paraventricular nuclei. In the rats pretreated by colchicine, the [35S]neurophysins were not detected in the brain stem, while they appeared in the paraventricular nuclei indicating that the precursors have been processed and the transport inhibited. These results suggest that: (i) both the biosynthetic and transport events in the hypothalamo-brain stem pathway are comparable to those occurring in the hypothalamo-neurohypophyseal tract; (ii) this pathway originates both from the supraoptic and paraventricular nuclei. Moreover, they indicate that processing is essentially complete in the hypothalamus of colchicine-pretreated animals. This provides further support to a model associating enzymes with both the endoplasmic reticulum membranes and the derived corresponding secretory vesicles.
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PMID:Hypothalamic biosynthesis and transport of neurophysins and their precursors to the rat brain stem. 399 5


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