Angiotensin II-induced calcium signalling in neurons and astrocytes of rat circumventricular organs

Gebke, E; Müller, Andreas R.; Jurzak, Mirek; Gerstberger, Rüdiger

doi:10.1016/s0306-4522(97)00601-5

Cited by 82 publications

(50 citation statements)

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“…Concerning the sources of Ca 2ϩ , our findings with thapsigargin suggest that Ca 2ϩ release from intracellular stores is needed for the full expression of the ROS increase. An involvement of Ca 2ϩ from intracellular stores is also suggested by the study of Gebke et al, 53 who showed in mixed cultures of subfornical organ and organum vasculosum of the lamina terminal neurons that Ang II increases intracellular Ca 2ϩ in the absence of extracellular Ca 2ϩ . Furthermore, Sumners et al 54 provided evidence that in hypothalamic neurons Ang II induces Ca 2ϩ release from intracellular stores.…”

Section: Discussionmentioning

confidence: 62%

Nox2, Ca ²⁺ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

et al. 2006

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Abstract-The dorsomedial portion of the nucleus tractus solitarius (dmNTS) is the site of termination of baroreceptor and cardiorespiratory vagal afferents and plays a critical role in cardiovascular regulation. Angiotensin II (Ang II) is a powerful signaling molecule in dmNTS neurons and exerts some of its biological effects by modulating Ca 2ϩ currents via reactive oxygen species (ROS) derived from reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase. We investigated whether a Nox2-containing NADPH oxidase is the source of the Ang II-induced ROS production and whether the signaling mechanisms of its activation require intracellular Ca 2ϩ or protein kinase C (PKC). Second-order dmNTS neurons were anterogradely labeled with 4-(4-[didecylamino]styryl)-N-methylpyridinium iodide transported from the vagus and isolated from the brain stem. ROS production was assessed in 4-(4-[didecylamino]styryl)-N-methylpyridinium iodide-positive dmNTS neurons using the fluorescent dye 6-carboxy-2Ј,7Ј-dichlorodihydro-fluorescein di(acetoxymethyl ester). Ang II (3 to 2000 nmol/L) increased ROS production in dmNTS neurons (EC 50 ϭ38.3 nmol/L). The effect was abolished by the ROS scavenger Mn (III) porphyrin 5,10,20-tetrakis (benzoic acid) porphyrin manganese (III), the Ang II type 1 receptor antagonist losartan, or the NADPH oxidase inhibitors apocynin or gp91ds-tat. Ang II failed to increase ROS production or to potentiate L-type Ca 2ϩ currents in dmNTS neurons of mice lacking Nox2. The PKC inhibitor GF109203X or depletion of intracellular Ca 2ϩ attenuated Ang II-elicited ROS production. We conclude that the powerful effects of Ang II on Ca 2ϩ currents in dmNTS neurons are mediated by PKC activation leading to ROS production via Nox2. Thus, a Nox2-containing NADPH oxidase is the critical link between Ang II and the enhancement of Key Words: arterial hypertension Ⅲ baroreflex Ⅲ calcium channels Ⅲ oxidative stress Ⅲ blood pressure Ⅲ autonomic nervous system A select group of brain stem nuclei regulates the systemic circulation by modulating cardiac output, vascular resistance, and fluid balance. 1,2 In particular, the dorsomedial region of the nucleus of the solitary tract (dmNTS), wherein vagal afferents from aortic baroreceptors and cardiorespiratory chemoreceptors terminate, plays a major role in cardiovascular regulation. [3][4][5] There is increasing evidence that angiotensin II (Ang II) is a critical neuromodulator in central autonomic nuclei, 6 -9 including the dmNTS. 10 -13 Within the dmNTS, activation of Ang II type 1 (AT 1 ) receptors alters cardiorespiratory reflexes including baroreceptor excitability and ion channel permeability. 10,14 These changes may contribute to Ang II-induced sympathoexcitation, 15-18 hypertension, 15,16 and heart failure. 17,18 Superoxide generated by the enzyme NADPH oxidase has emerged as a key intermediary in the central and peripheral effects of Ang II. 10,14 -16,18 -21 NADPH oxidase, initially described in neutrophils, 22,23 is now known to be present in diverse cell types, inc...

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Section: Discussionmentioning

confidence: 62%

Nox2, Ca ²⁺ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

et al. 2006

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“…The octapeptide angiotensin (ANG II) and other angiotensin fragments are considered to function in neurotransmitter or neuromodulatory roles mediated by AT 1, AT 2 , and AT 4 receptor subtypes (for reviews, see McKinley et al 2003;Phillips and Sumners 1998). A role for angiotensin receptors, in particular the AT 1 subtype, in regulating neuronal excitability can be inferred from electrophysiological and imaging observations of neuronal responsivity to exogenously applied angiotensin peptides in a variety of neurons (e.g., Bai and Renaud 1998;Barnes et al 2003;Ferguson and Washburn 1998;Gebke et al 1998;Li et al 2003;Oz and Renaud 2002;Shapiro et al 1994;Yang et al 1992). Binding studies and receptor-expression analyses also indicate a form of developmental plasticity within the central renin-angiotensin system with a high level of expression during the first and second postnatal week, changing during ontogeny (Milan et al 1991;Tsutsumi and Saavedra 1991).…”

Section: Introductionmentioning

confidence: 99%

Presynaptic Angiotensin II AT₁ Receptors Enhance Inhibitory and Excitatory Synaptic Neurotransmission to Motoneurons and Other Ventral Horn Neurons in Neonatal Rat Spinal Cord

Öz

Yang²,

O’Donovan³

et al. 2005

Journal of Neurophysiology

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“…It is interesting to note that hypertonicity and increased osmolality induce STC-1 in different tissues (52,57,58). Changes in plasma osmolality and hypertonicity, like ANG II, increase intracellular cytosolic calcium levels within SFO neurons (17,27,28). Chronic elevated levels of plasma osmolality, hypertonicity, or ANG II not only stimulate SFO neurons, but also increase discharge by these neurons.…”

Section: Perspectives and Significancementioning

confidence: 99%

“…On the other hand, blockade of the ANG II receptors within the SFO inhibits the dipsogenic and blood pressure response induced by ANG II (13,15,25,53). The neuronal depolarization of SFO neurons in response to endogenous ANG II is mediated by increases in intracellular calcium concentration, which can be inhibited by the specific blockade of the AT 1 R (17,26,48,66).As ANG II acts in the SFO to elicit drinking, this study was done to investigate the contribution of STC-1 in the SFO to the ANG II-induced drinking by the SFO. In the first series, STC-1 protein within the SFO was determined using Western blot analysis.…”

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confidence: 99%

“…The role of STC-1 within the SFO is not known, although it may function in modulating intracellular calcium concentrations within neurons, which could affect their excitability (17,(67)(68)(69). The SFO has been suggested to be one of the most important structures within the forebrain laminae terminalis in the regulation of electrolyte and body fluid homeostasis (1,3,7,12,13,25,31,36,37).…”

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confidence: 99%

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Stanniocalcin-1 in the subfornical organ inhibits the dipsogenic response to angiotensin II

Moreau

Iqbal

Turner

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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in the subfornical organ inhibits the dipsogenic response to angiotensin II. Am J Physiol Regul Integr Comp Physiol 303: R921-R928, 2012. First published August 29, 2012 doi:10.1152 doi:10. /ajpregu.00057.2012 for the calcium-regulating glycoprotein hormone stanniocalcin-1 (STC-1) have been found within subfornical organ (SFO), a central structure involved in the regulation of electrolyte and body fluid homeostasis. However, whether SFO neurons produce STC-1 and how STC-1 may function in fluid homeostasis are not known. Two series of experiments were done in Sprague-Dawley rats to investigate whether STC-1 is expressed within SFO and whether it exerts an effect on water intake. In the first series, experiments were done to determine whether STC-1 was expressed within cells in SFO using immunohistochemistry, and whether protein and gene expression for STC-1 existed in SFO using Western blot and quantitative RT-PCR, respectively. Cells containing STC-1 immunoreactivity were found throughout the rostrocaudal extent of SFO. STC-1 protein expression within SFO was confirmed with Western blot, and SFO was also found to express STC-1 mRNA. In the second series, microinjections (200 nl) of STC-1, ANG II, a combination of the two or the vehicle were made into SFO in conscious, unrestrained rats. Water intake was measured at 0700 for a 1-h period after each injection in animals. Microinjections of STC-1 (17.6 or 176 nM) alone had no effect on water intake compared with controls. However, STC-1 not only attenuated the drinking responses to ANG II for about 30 min, but also decreased the total water intake over the 1-h period. These data suggest that STC-1 within the SFO may act in a paracrine/autocrine manner to modulate the neuronal responses to blood-borne ANG II. These findings also provide the first direct evidence of a physiological role for STC-1 in central regulation of body fluid homeostasis. body fluid homeostasis; thirst; circumventricular organs; calciumregulating glycoprotein STANNIOCALCIN (STC) IS A GLYCOPROTEIN hormone first identified and characterized within bony fish corpuscles of Stannius, endocrine glands derived from renal tubular cells (18,24,29,63,64). These glands are thought to produce and release STC into the circulation in response to rising serum calcium levels (11,18,29,64). The STC then acts on the gills and gut epithelial cells to reduce calcium uptake, while STC within the kidney causes increases in reabsorption of phosphate (11,18,24), a mechanism that likely aids in chelating excess extracellular calcium (18,24). The net effect of these STC actions is the restoration of serum calcium levels (14,18,24,62).A mammalian homolog of STC has been identified that shares a 73% amino acid sequence homology with fish STC (41). Mammalian STC-1 is a disulfide-linked glycoprotein dimer of identical subunits (41), which is expressed in a variety of tissues, including heart, kidney, adipose tissue, skeletal muscle, lung, ovaries (18, 24), and brain (67-69). STC-1 functions in the cells of these tissues ...

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Angiotensin II-induced calcium signalling in neurons and astrocytes of rat circumventricular organs

Cited by 82 publications

References 51 publications

Nox2, Ca ²⁺ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

Nox2, Ca ²⁺ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

Presynaptic Angiotensin II AT₁ Receptors Enhance Inhibitory and Excitatory Synaptic Neurotransmission to Motoneurons and Other Ventral Horn Neurons in Neonatal Rat Spinal Cord

Stanniocalcin-1 in the subfornical organ inhibits the dipsogenic response to angiotensin II

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Angiotensin II-induced calcium signalling in neurons and astrocytes of rat circumventricular organs

Cited by 82 publications

References 51 publications

Nox2, Ca 2+ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

Nox2, Ca 2+ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

Presynaptic Angiotensin II AT1 Receptors Enhance Inhibitory and Excitatory Synaptic Neurotransmission to Motoneurons and Other Ventral Horn Neurons in Neonatal Rat Spinal Cord

Stanniocalcin-1 in the subfornical organ inhibits the dipsogenic response to angiotensin II

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About

Nox2, Ca ²⁺ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

Nox2, Ca ²⁺ , and Protein Kinase C Play a Role in Angiotensin II-Induced Free Radical Production in Nucleus Tractus Solitarius

Presynaptic Angiotensin II AT₁ Receptors Enhance Inhibitory and Excitatory Synaptic Neurotransmission to Motoneurons and Other Ventral Horn Neurons in Neonatal Rat Spinal Cord