Formation and Actions of Cyclic ADP-Ribose in Renal Microvessels

Li, N; Teggatz, Eric G.; Li, P L; Allaire, R; Zou, Ai-Ping

doi:10.1006/mvre.2000.2255

Cited by 29 publications

(22 citation statements)

References 44 publications

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“…The superfusate (PSS) in the bath was bubbled with 95% O 2-5% CO2 and maintained at pH 7.4 and 37°C. This condition for isolated artery preparation was chosen based on a number of previous studies (3,34,43,47,59). Because there is no hemoglobin in the superfusate, enough O 2 supply is needed to maintain tissue PO2 for normal endothelial and VSM function.…”

Section: Microdissection and Microperfusion Of Small Coronary Arterymentioning

confidence: 99%

“…Because there is no hemoglobin in the superfusate, enough O 2 supply is needed to maintain tissue PO2 for normal endothelial and VSM function. By adjusting bubbling rate, an appropriate balance of O 2 supply and consumption could be reached, which maintains an appropriate environment for studies of vasomotor responses in this isolated artery preparation (34,43,59). The internal diameter of arteries was measured with a video system composed of a stereomicroscope (Leica MZ8), a charge-coupled device camera (KP-MI AU, Hitachi), a video monitor (VM-1220U, Hitachi), a video measuring apparatus (VIA-170, Boeckeler Instrument), and a video printer (UP890 MD, Sony).…”

Section: Microdissection and Microperfusion Of Small Coronary Arterymentioning

confidence: 99%

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Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Guo¹,

Teggatz²,

Zhang³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Cyclic ADP ribosemediated Ca 2ϩ signaling in mediating endothelial nitric oxide production in bovine coronary arteries. Am J Physiol Heart Circ Physiol 290: H1172-H1181, 2006. First published October 21, 2005 doi:10.1152/ajpheart.00441.2005.-The present study tested the hypothesis that cyclic ADP ribose (cADPR) serves as a novel second messenger to mediate intracellular Ca 2ϩ mobilization in coronary arterial endothelial cells (CAECs) and thereby contributes to endothelium-dependent vasodilation. In isolated and perfused small bovine coronary arteries, bradykinin (BK)-induced concentrationdependent vasodilation was significantly attenuated by 8-bromocADPR (a cell-permeable cADPR antagonist), ryanodine (an antagonist of ryanodine receptors), or nicotinamide (an ADP-ribosyl cyclase inhibitor). By in situ simultaneously fluorescent monitoring, Ca 2ϩ transient and nitric oxide (NO) levels in the intact coronary arterial endothelium preparation, 8-bromo-cADPR (30 M), ryanodine (50 M), and nicotinamide (6 mM) substantially attenuated BK (1 M)-induced increase in intracellular [Ca 2ϩ ] by 78%, 80%, and 74%, respectively, whereas these compounds significantly blocked BKinduced NO increase by about 80%, and inositol 1,4,5-trisphosphate receptor blockade with 2-aminethoxydiphenyl borate (50 M) only blunted BK-induced Ca 2ϩ -NO signaling by about 30%. With the use of cADPR-cycling assay, it was found that inhibition of ADP-ribosyl cyclase by nicotinamide substantially blocked BK-induced intracellular cADPR production. Furthermore, HPLC analysis showed that the conversion rate of ␤-nicotinamide guanine dinucleotide into cyclic GDP ribose dramatically increased by stimulation with BK, which was blockable by nicotinamide. However, U-73122, a phospholipase C inhibitor, had no effect on this BK-induced increase in ADP-ribosyl cyclase activity for cADPR production. In conclusion, these results suggest that cADPR importantly contributes to BK-and A-23187-induced NO production and vasodilator response in coronary arteries through its Ca 2ϩ signaling mechanism in CAECs.nucleotide; vasodilation; endothelium; endothelium-derived relaxing factor CYCLIC ADP RIBOSE (cADPR), endogenously generated from nicotinamide (Ni) adenine dinucleotide, has emerged as a novel intracellular Ca 2ϩ -mobilizing second messenger in a wide variety of mammalian cells. The actions of this signaling nucleotide are completely independent of the inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ]-signaling pathway, but it exerts its action by targeting ryanodine (Ry) receptors (RyRs) (8,15,16,(31)(32)(33)44). Elevation of intracellular cADPR levels followed by Ca 2ϩ mobilizition and activation of Ca 2ϩ -dependent effects within cells has been found to be essential for versatile physiological processes, such as cell cycle regulation, cell proliferation, gene expression, egg fertilization, neurotransmitter release, muscle contraction, and nitric oxide signaling (10,29,55). Recent studies (17,35,36,52,55,57) in our laboratory and by others have reported that in va...

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Section: Microdissection and Microperfusion Of Small Coronary Arterymentioning

confidence: 99%

Section: Microdissection and Microperfusion Of Small Coronary Arterymentioning

confidence: 99%

Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Guo¹,

Teggatz²,

Zhang³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

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“…This delay was attributed to the time required for the SR Ca 2+ content to be increased following SERCA activation by cADPR (Lukyanenko et al, 2001). This proposal could explain the frequently observed pronounced delay in the onset of cADPR activity (Cui et al, 1999;Aarhus et al, 1995;Li et al, 2000).…”

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confidence: 95%

Cyclic ADP-ribose increases Ca2+ removal in smooth muscle

Bradley

Currie

MacMillan

et al. 2003

Journal of Cell Science

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Ca2+ release via ryanodine receptors (RyRs) is vital in cell signalling and regulates diverse activities such as gene expression and excitation-contraction coupling. Cyclic ADP ribose (cADPR), a proposed modulator of RyR activity, releases Ca2+ from the intracellular store in sea urchin eggs but its mechanism of action in other cell types is controversial. In this study, caged cADPR was used to examine the effect of cADPR on Ca2+ signalling in single voltage-clamped smooth muscle cells that have RyR but lack FKBP12.6, a proposed target for cADPR. Although cADPR released Ca2+ in sea urchin eggs (a positive control), it failed to alter global or subsarcolemma [Ca2+]c, to cause Ca2+-induced Ca2+ release or to enhance caffeine responses in colonic myocytes. By contrast, caffeine (an accepted modulator of RyR) was effective in these respects. The lack of cADPR activity on Ca2+ release was unaffected by the introduction of recombinant FKBP12.6 into the myocytes. Indeed in western blots, using brain membrane preparations as a source of FKBP12.6, cADPR did not bind to FKBPs, although FK506 was effective. However, cADPR increased and its antagonist 8-bromo-cADPR slowed the rate of Ca2+ removal from the cytoplasm. The evidence indicates that cADPR modulates [Ca2+]c but not via RyR; the mechanism may involve the sarcolemma Ca2+ pump

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“…In membrane preparations of aorta (13,53), renal microvessels (39), coronary arteries (31,52,55), and pulmonary artery (16), evidence for ADPR cyclase activity has been demonstrated. Measurement of changes in [Ca 2ϩ ] i in response to cADPR has been made in permeabilized renal VSM cells (39). To our knowledge, there have been no Ca 2ϩ studies examining the activation of the cADPR pathway in intact fresh afferent arterioles and no studies exploring the effect of ANG II on this particular pathway in VSM of any origin.…”

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confidence: 99%

Angiotensin II Ca²⁺signaling in rat afferent arterioles: stimulation of cyclic ADP ribose and IP₃pathways

Fellner¹,

Arendshorst²

2005

American Journal of Physiology-Renal Physiology

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(24,36). Only recently, however, has a role for cADPR been investigated in vascular smooth muscle (VSM). In membrane preparations of aorta (13, 53), renal microvessels (39), coronary arteries (31, 52, 55), and pulmonary artery (16), evidence for ADPR cyclase activity has been demonstrated. Measurement of changes in [Ca 2ϩ ] i in response to cADPR has been made in permeabilized renal VSM cells (39). To our knowledge, there have been no Ca 2ϩ studies examining the activation of the cADPR pathway in intact fresh afferent arterioles and no studies exploring the effect of ANG II on this particular pathway in VSM of any origin.The ADPR cyclase of VSM has several unique properties that distinguish it from the CD38 ADPR cyclase of nonvascular cells. In contrast to the CD38 enzyme of sea urchin eggs, aplysia, and HL-60 cells, in which Zn 2ϩ enhances the activity of the enzyme, Zn 2ϩ inhibits the cyclase of rat aortic VSM cells (13). Nitric oxide (NO) inhibits the VSM enzyme, whereas it is stimulatory in macrophages, neurons, pancreatic cells, and sea urchin eggs (52). Recently, it has been shown that oxidative stress increases [Ca 2ϩ ] i in fresh bovine coronary VSM cells through a pathway that involves cADPR (55) and that NO inhibits ADPR cyclase in coronary artery VSM (52).Only one study investigated the effect of ANG II on the activity of ADP-ribosyl cyclase (27). This laboratory found that in membrane preparations of neonatal but not older cardiac myocytes, ANG II increased cyclase activity in a dose-dependent fashion (27). The mechanism by which ANG II stimulated an increase in ADPR cyclase activity is unknown, but these investigators speculated that a G protein-coupled process is involved (27). Because of the crucial importance of afferent arterioles in regulating glomerular filtration and sodium balance, we investigated the effects of ANG II on Ca 2ϩ signaling in freshly isolated afferent arterioles using inhibitors of IP 3 R, RyR, and ADPR cyclase. METHODSAll studies were performed in compliance with the guidelines and practices of the University of North Carolina at Chapel Hill Institutional Animal Care and Use Committee.

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Formation and Actions of Cyclic ADP-Ribose in Renal Microvessels

Cited by 29 publications

References 44 publications

Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Cyclic ADP-ribose increases Ca2+ removal in smooth muscle

Angiotensin II Ca²⁺signaling in rat afferent arterioles: stimulation of cyclic ADP ribose and IP₃pathways

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Formation and Actions of Cyclic ADP-Ribose in Renal Microvessels

Cited by 29 publications

References 44 publications

Cyclic ADP ribose-mediated Ca2+signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Cyclic ADP ribose-mediated Ca2+signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Cyclic ADP-ribose increases Ca2+ removal in smooth muscle

Angiotensin II Ca2+signaling in rat afferent arterioles: stimulation of cyclic ADP ribose and IP3pathways

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Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Angiotensin II Ca²⁺signaling in rat afferent arterioles: stimulation of cyclic ADP ribose and IP₃pathways