Angiotensin II Ca2+ signaling in rat afferent arterioles:: stimulation of cyclic ADP ribose and IP3 pathways

被引:52
作者
Fellner, SK [1 ]
Arendshorst, WJ [1 ]
机构
[1] Univ N Carolina, Dept Cell & Mol Physiol, Chapel Hill, NC 27599 USA
关键词
calcium-induced calcium release; ryanodine; vascular smooth muscle; nicotinamide;
D O I
10.1152/ajprenal.00372.2004
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
ANG II induces a rise in cytosolic Ca2+ ([Ca2+](i)) in vascular smooth muscle (VSM) cells via inositol trisphosphate receptor (IP3R) activation and release of Ca2+ from the sarcoplasmic reticulum (SR). The Ca2+ signal is augmented by calcium-induced calcium release (CICR) and by cyclic adeninediphosphate ribose (cADPR), which sensitizes the ryanodine-sensitive receptor (RyR) to Ca2+ to further amplify CICR. cADPR is synthesized from beta-nicotinamide adenine dinucleotide (NAD(+)) by a membrane-bound bifunctional enzyme, ADPR cyclase. To investigate the possibility that ANG II activates the ADPR cyclase of afferent arterioles, we used inhibitors of the IP3R, RyR, and ADPR cyclase. Afferent arterioles were isolated from rat kidney with the magnetized microsphere and sieving technique and loaded with fura-2 to measure [Ca2+](i). In Ca2+-containing buffer, ANG II increased [Ca2+](i) by 125 +/- 10 nM. In the presence of the IP3R antagonists TMB-8 and 2-APB, the peak responses to ANG II were reduced by 74 and 81%, respectively. The specific antagonist of cADPR 8-Br ADPR and a high concentration of ryanodine (100 muM) inhibited the ANG II-induced increases in [Ca2+](i) by 75 and 69%, respectively. Nicotinamide and Zn2+ are known inhibitors of the VSM ADPR cyclase. Nicotinamide diminished the [Ca2+](i) response to ANG II by 66%. In calcium-free buffer, Zn2+ reduced the ANG II response by 68%. Simultaneous blockade of the IP3 and cADPR pathways diminished the [Ca2+](i) response to ANG II by 83%. We conclude that ANG II initiates Ca2+ mobilization from the SR in afferent arterioles via the classic IP3R pathway and that ANG II may lead to activation of the ADPR cyclase to form cADPR, which, via its action on the RyR, substantially augments the Ca2+ response.
引用
收藏
页码:F785 / F791
页数:7
相关论文
共 55 条
  • [1] The role of cyclic-ADP-ribose-signaling pathway in oxytocin-induced Ca2+ transients in human myometrium cells
    Barata, H
    Thompson, M
    Zielinska, W
    Han, YS
    Mantilla, CB
    Prakash, YS
    Feitoza, S
    Sieck, G
    Chini, EN
    [J]. ENDOCRINOLOGY, 2004, 145 (02) : 881 - 889
  • [2] Novel isoforms of NADPH oxidase in vascular physiology and pathophysiology
    Bengtsson, SH
    Gulluyan, LM
    Dusting, GJ
    Drummond, GR
    [J]. CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 2003, 30 (11) : 849 - 854
  • [3] The endoplasmic reticulum: a multifunctional signaling organelle
    Berridge, MJ
    [J]. CELL CALCIUM, 2002, 32 (5-6) : 235 - 249
  • [4] INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING
    BERRIDGE, MJ
    [J]. NATURE, 1993, 361 (6410) : 315 - 325
  • [5] CARMINES OK, 1993, AM J PHYSIOL-RENAL, V265, pF677
  • [6] DISPARATE EFFECTS OF CA CHANNEL BLOCKADE ON AFFERENT AND EFFERENT ARTERIOLAR RESPONSES TO ANG-II
    CARMINES, PK
    NAVAR, LG
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 256 (06): : F1015 - F1020
  • [7] INTERDEPENDENCE OF RYANODINE BINDING, OLIGOMERIC RECEPTOR INTERACTIONS, AND CA2+ RELEASE REGULATION IN JUNCTIONAL SARCOPLASMIC-RETICULUM
    CARROLL, S
    SKARMETA, JG
    YU, X
    COLLINS, KD
    INESI, G
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1991, 290 (01) : 239 - 247
  • [8] Integrin mobilizes intracellular Ca2+ in renal vascular smooth muscle cells
    Chan, WL
    Holstein-Rathlou, NH
    Yip, KP
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2001, 280 (03): : C593 - C603
  • [9] Angiotensin II triggers EGFR tyrosine kinase-dependent Ca2+ influx in afferent arterioles
    Che, Q
    Carmines, PK
    [J]. HYPERTENSION, 2002, 40 (05) : 700 - 706
  • [10] KCL AND ANGIOTENSIN RESPONSES IN ISOLATED RAT RENAL ARTERIOLES - EFFECTS OF DILTIAZEM AND LOW-CALCIUM MEDIUM
    CONGER, JD
    FALK, SA
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (01): : F134 - F140