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

Effects of phenylephrine, vasopressin and angiotensin II on cytoplasmic free calcium concentration, [Ca2+]c, were examined by monitoring aequorin bioluminescence in isolated hepatocytes preloaded with aequorin. In the presence of 0.5 mM calcium in the medium, the pattern of changes in aequorin bioluminescence induced by phenylephrine was different from that induced by vasopressin or angiotensin II. When extracellular calcium concentration was reduced to 1 microM, however, these three agents induced identical changes in aequorin bioluminescence. These results suggest that the mode of action of phenylephrine on cytoplasmic free calcium concentration differs from that of either vasopressin or angiotensin II and that the difference in ability to increase calcium influx may account for the distinct patterns induced by these agents.
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PMID:Comparison of the changes in cytoplasmic free calcium concentration induced by phenylephrine, vasopressin and angiotensin II in hepatocytes. 377 38

The effects of the alpha 1-adrenergic agonist phenylephrine and the peptide hormones angiotensin II and arg8-vasopressin on cytoplasmic free calcium concentration were investigated in single rat hepatocytes microinjected with the photoprotein aequorin. Hepatocytes responded to physiological concentrations of the glycogenolytic agonists with a series of repetitive Ca transients. In each transient free Ca rose in 2-3s to above 600 nM from a resting level of 200 nM. Transient duration depended on the agonist and ranged from approximately 7s for phenylephrine to approximately 15s for angiotensin. Transient frequency, but not shape or size, depended on agonist concentration. The period ranged from less than 20s to several minutes. We suggest that the frequency of the Ca transients is the principal determinant of the amplitude of the cellular response to calcium-mobilizing agonists.
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PMID:Agonist-induced oscillations in cytoplasmic free calcium concentration in single rat hepatocytes. 382 23

In the stressed animal, the vasoactive hormones vasopressin and angiotensin-II and the neurotransmitter noradrenaline induce liver cells to release glucose from glycogen. The intracellular signal that links the cell-surface receptors for noradrenaline (alpha 1) and vasoactive peptides to activation of glycogenolysis is known to be a rise in the cytoplasmic concentration of free calcium ions (free Ca). The receptors for these agonists induce the hydrolysis of phosphatidylinositol 4,5-bisphosphate, a minor plasmalemma lipid, to produce inositol trisphosphate and diacylglycerol. Inositol trisphosphate has been shown to mobilize intracellular calcium in hepatocytes. We show here, by means of aequorin measurements in single, isolated rat hepatocytes, that the free Ca response to these agonists consists of a series of transients. Each transient rose within 3 s to a peak free Ca of at least 600 nM and had a duration of approximately 7 s. The transients were repeated at intervals of 0.3-4 min, depending on agonist concentration. Between transients, free Ca returned to the resting level of approximately 200 nM. Clearly, the mechanisms controlling free Ca in hepatocytes are more complex than hitherto suspected.
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PMID:Repetitive transient rises in cytoplasmic free calcium in hormone-stimulated hepatocytes. 394 48

The purpose of the present study was to determine the changes in intracellular ionized calcium concentration ([Ca2+]i) or [Ca2+]i sensitivity accompanying spontaneous and agonist-induced contraction of human myometrium at term pregnancy, as well as to quantify the response to three prototypical agonists: 1) oxytocin, 2) vasopressin, and 3) phenylephrine. Uterine biopsies were obtained at the time of cesarean section from patients who delivered at or near full-term gestation. These preparations were used to measure isometric force development and [Ca2+]i levels with the luminescent calcium indicator aequorin. Concentration-response relationships were determined with respect to isometric force development in the presence of the agonist. [Ca2+]i-force relationships were determined with respect to spontaneous phasic contractions, as well as agonist-induced phasic and tonic contractions. The results provide evidence that the phasic nature of term human myometrium is due to 1) the resting [Ca2+]i level being less than the calcium threshold for contractions and 2) the inability of the tissue to maintain high [Ca2+]i levels for prolonged periods of time. In addition, calcium-independent mechanisms of regulation were suggested by the relatively minor calcium sensitizing action of oxytocin and the observation that relaxation of tonic contractions preceded the fall in [Ca2+]i levels.
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PMID:[Ca2+]i signaling in pregnant human myometrium. 804 17

Single hepatocytes microinjected with aequorin generate free Ca oscillations when stimulated by agonists such as phenylephrine or vasopressin. Here we show that caffeine by itself does not elicit any significant change in free Ca, nor it does lower the threshold concentration of an agonist needed to induced spikes. In contrast, both caffeine and theophylline inhibit agonist-induced spikes. Since ryanodine inhibits vasopressin-induced spikes, but not phenylephrine-induced spikes, the actions of caffeine probably involve another target than the ryanodine receptor. This antagonistic action of caffeine on the hepatocyte calcium oscillator agrees with an inhibitory action of caffeine on the receptor for inositol 1,4,5-triphosphate.
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PMID:Caffeine inhibits agonists-induced cytoplasmic Ca2+ oscillations in single rat hepatocytes. 829 85

We show here, by aequorin measurements in single isolated rat hepatocytes, that elevation of cyclic AMP, by dibutyryl cyclic AMP, forskolin or glucagon, has different effects on oscillations in cytosolic concentration of free Ca2+ ('free Ca') induced by phenylephrine or vasopressin. Elevated cyclic AMP does not itself induce free Ca oscillations, but enhances both the peak free Ca and the frequency of spikes induced by phenylephrine. In contrast, elevated cyclic AMP has no effect on peak free Ca of vasopressin-induced spikes, but markedly prolongs the falling phase, with the result that spiking frequency (peak to peak) falls, although the period between spikes of resting free Ca is usually decreased. The data provide another example of receptor-specific information being retained in the oscillator mechanism, with implications for models of the hepatocyte calcium oscillator.
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PMID:Different modulatory effects of elevated cyclic AMP on cytosolic Ca2+ spikes induced by phenylephrine or vasopressin in single rat hepatocytes. 838 27

We investigated the effects of bovine GH (bGH) on Ca(2+) handling, phospholipase C (PLC) activation and inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)] formation in hepatocytes. bGH generates oscillations in cytosolic free Ca(2+) concentration ([Ca(2+)](i)) in single male rat hepatocytes microinjected with the photoprotein aequorin. In the absence of extracellular Ca(2+) these transients persisted for more than 10 min indicating a requirement for intracellular Ca(2+). Treatment of the hepatocyte with the phosphatidylinositol-specific phospholipase C (PI-PLC) inhibitor U-73122 removed the oscillations. These results suggest bGH-induced oscillations are due to PLC activation and generation of Ins(1,4,5)P(3). We measured the mass of Ins(1,4,5)P(3) in freshly isolated hepatocyte suspensions in response to bGH, and vasopressin as a control. Both agonists rapidly increased the levels of Ins(1,4,5)P(3). This is the first study to indicate that early events in the signal transduction pathways mediated by GH in hepatocytes involve intracellular Ca(2+) mobilization via activation of a PI-PLC and subsequent Ins(1,4,5)P(3) production.
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PMID:The phospholipase C-InsP3 pathway is involved in calcium mobilization induced by growth hormone in hepatocytes. 1512 67


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