Endothelin-1, superoxide and adeninediphosphate ribose cyclase in shark vascular smooth muscle

Fellner, Susan K.; Parker, Laurel

doi:10.1242/jeb.01506

Cited by 11 publications

(7 citation statements)

References 67 publications

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“…RyRs are generally considered downstream targets for the products of ADPR cyclase in other vascular beds (1,21,24). cADPR activates RyRs by removing FK506 binding proteins (FKBPs) that associate with the receptor (44,61).…”

Section: Discussionmentioning

confidence: 99%

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ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivo

Thai

Fellner²,

Arendshorst

2007

American Journal of Physiology-Renal Physiology

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An important role for the enzyme ADP-ribosyl cyclase (ADPR cyclase) and its downstream targets, the ryanodine receptors (RyR), is emerging for a variety of vascular systems. We hypothesized that the ADPR cyclase/RyR pathway contributes to regulation of renal vasomotor tone in vivo. To test this, we continuously measured renal blood flow (RBF) in anesthetized Sprague-Dawley rats. Infusion of the ADPR cyclase inhibitor nicotinamide intrarenally at low doses inhibits angiotensin II (ANG II)- and norepinephrine (NE)-induced vasoconstriction by 72 and 67%, respectively (P < 0.001). RBF studies in rats were extended to mice lacking the predominant form of ADPR cyclase (CD38). Acute renal vasoconstrictor responses to ANG II and NE are impaired by 59 and 52%, respectively, in anesthetized CD38-/- mice compared with wild-type controls (P < 0.05). Intrarenal injection of the RyR activator FK506 decreases RBF by 22% (P > 0.03). Furthermore, RyR inhibition with ruthenium red attenuates ANG II and NE responses by 50 and 59%, respectively (P < or = 0.01). Given at higher doses, nicotinamide increases basal RBF by 22% (P > 0.001). Non-receptor-mediated renal vasoconstriction by L-type voltage-gated Ca(2+) channels is also dependent on ADPR cyclase and RyRs. Nicotinamide and ruthenium red inhibit constriction by the L-type channel agonist BAY K 8644 by 59% (P > 0.02) and 63% (P > 0.001). We conclude that 1) ADPR cyclase activity contributes to regulation of renal vasomotor tone under resting conditions, 2) renal vasoconstriction induced by G protein-coupled receptor agonists ANG II and NE is mediated in part by ADPR cyclase and RyRs, and 3) ADPR cyclase and RyRs participate in L-type channel-mediated renal vasoconstriction in vivo.

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Section: Discussionmentioning

confidence: 99%

“…Multiple doses of these agonists were tested in the same animal. Concentrations of ruthenium red and nicotinamide were based on in vitro published concentrations (19,21) and calculated as estimated final renal arterial concentration. Concentrations that altered MAP or RBF were not used to inhibit vasoconstrictive agents.…”

Section: Methodsmentioning

confidence: 99%

ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivo

Thai

Fellner²,

Arendshorst

2007

American Journal of Physiology-Renal Physiology

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“…These effects were also reversed by reducing agents such as DTT. In addition, endothelin-1 (ET-1) that activates IP3R also increases the ROS generation (78). Whether ET-1 induced IP3R and enhanced ROS generation are linked is not known (78).…”

Section: A Ip3r Receptorsmentioning

confidence: 99%

“…In addition, endothelin-1 (ET-1) that activates IP3R also increases the ROS generation (78). Whether ET-1 induced IP3R and enhanced ROS generation are linked is not known (78). The effect of ROS on IP3R in cardiac myocytes needs further investigation, and if that has any influence on the cardiac excitability is to be determined.…”

Section: A Ip3r Receptorsmentioning

confidence: 99%

Redox Control of Cardiac Excitability

Aggarwal

Makielski

2013

Antioxidants & Redox Signaling

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Reactive oxygen species (ROS) have been associated with various human diseases, and considerable attention has been paid to investigate their physiological effects. Various ROS are synthesized in the mitochondria and accumulate in the cytoplasm if the cellular antioxidant defense mechanism fails. The critical balance of this ROS synthesis and antioxidant defense systems is termed the redox system of the cell. Various cardiovascular diseases have also been affected by redox to different degrees. ROS have been indicated as both detrimental and protective, via different cellular pathways, for cardiac myocyte functions, electrophysiology, and pharmacology. Mostly, the ROS functions depend on the type and amount of ROS synthesized. While the literature clearly indicates ROS effects on cardiac contractility, their effects on cardiac excitability are relatively under appreciated. Cardiac excitability depends on the functions of various cardiac sarcolemal or mitochondrial ion channels carrying various depolarizing or repolarizing currents that also maintain cellular ionic homeostasis. ROS alter the functions of these ion channels to various degrees to determine excitability by affecting the cellular resting potential and the morphology of the cardiac action potential. Thus, redox balance regulates cardiac excitability, and under pathological regulation, may alter action potential propagation to cause arrhythmia. Understanding how redox affects cellular excitability may lead to potential prophylaxis or treatment for various arrhythmias. This review will focus on the studies of redox and cardiac excitation. Antioxid. Redox Signal. 18, 432-468.

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“…cADPR sensitizes the ryanodine receptor (RyR) to Ca 2ϩ (calcium-induced calcium release) to enhance Ca 2ϩ release from the SR (8,10). One of us (S. K. F.) has shown that ET-1 utilizes the NAD(P)H oxidase, superoxide, and ADPR cyclase pathway in VSMC of the anterior mesenteric artery of Squalus acanthias (12).…”

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confidence: 99%

Endothelin-A and -B receptors, superoxide, and Ca²⁺signaling in afferent arterioles

Fellner

Arendshorst

2007

American Journal of Physiology-Renal Physiology

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It is unknown if endothelin-A and -B receptors (ET(A)R and ET(B)R) activate the production of superoxide via NAD(P)H oxidase and subsequently stimulate the formation of cyclic adenine diphosphate ribose (cADPR) in afferent arterioles. Vessels were isolated from rat kidney and loaded with fura 2. Endothelin-1 (ET-1) rapidly increased cytosolic Ca(2+) concentration ([Ca(2+)](i)) by 303 nM. The superoxide dismutase mimetic tempol, the NAD(P)H oxidase inhibitor apocynin, and nicotinamide, an inhibitor of ADPR cyclase, diminished the response by approximately 60%. The ET(B)R agonist sarafotoxin 6c (S6c) increased peak [Ca(2+)](i) by 117 nM. Subsequent addition of ET-1 in the continued presence of S6c caused an additional [Ca(2+)](i) peak of 225 nM. Neither nicotinamide or 8-bromo- (8-Br) cADPR nor apocynin decreased the [Ca(2+)](i) response to S6c, but inhibited the subsequent [Ca(2+)](i) response to ET-1. The ET(B)R blockers BQ-788 and A-192621 prevented the S6c [Ca(2+)](i) peak and reduced the ET-1 response by more than one-half, suggesting an ET(B)R/ET(A)R interaction. In contrast, the ET(A)R blocker BQ-123 had no effect on the S6c [Ca(2+)](i) peak and obliterated the subsequent ET-1 response. ET-1 immediately stimulated superoxide formation (measured with TEMPO-9-AC, 68 arbitrary units) that was inhibited 95% by apocynin or diphenyl iodonium. S6c or IRL-1620 increased superoxide by 8% of that caused by subsequent ET-1 addition. We conclude that ET(A)R activation of afferent arterioles increases the formation of superoxide that accounts for approximately 60% of subsequent Ca(2+) signaling. ET(B)R activation appears to result in only minor increases in superoxide production. Nicotinamide and 8-Br-cADPR results suggest that ET-1 (and primarily ET(A)R) causes the activation of vascular smooth muscle cell-ADPR cyclase.

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Endothelin-1, superoxide and adeninediphosphate ribose cyclase in shark vascular smooth muscle

Abstract: In vascular smooth muscle (VSM) of

Cited by 11 publications

References 67 publications

ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivo

ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivo

Redox Control of Cardiac Excitability

Endothelin-A and -B receptors, superoxide, and Ca²⁺signaling in afferent arterioles

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Endothelin-1, superoxide and adeninediphosphate ribose cyclase in shark vascular smooth muscle

Abstract: In vascular smooth muscle (VSM) of

Cited by 11 publications

References 67 publications

ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivo

ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivo

Redox Control of Cardiac Excitability

Endothelin-A and -B receptors, superoxide, and Ca2+signaling in afferent arterioles

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Endothelin-A and -B receptors, superoxide, and Ca²⁺signaling in afferent arterioles