Regular ArticleActivation of Calcium Sparks by Angiotensin II in Vascular Myocytes
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Presenilin 1 mutation decreases both calcium and contractile responses in cerebral arteries
2017, Neurobiology of AgingCitation Excerpt :This discrepancy suggests that the putative stimulatory RyR-PS interaction does not occur in VSMC of PS1dE9 mice. In addition, we did not observe any modification in the shape and frequency of Ca2+ sparks which are specific elementary RyR-dependent Ca2+ signals (Arnaudeau et al., 1996; Macrez and Mironneau, 2004). Since Ca2+ sparks reflect transient activation of small clusters of RyR1 and RyR2 channels (Coussin et al., 2000), our results suggest that the spontaneous gating of these RyR channels is not directly affected by the PS1dE9 mutation.
BK Channels in the Vascular System
2016, International Review of NeurobiologyCitation Excerpt :The local transient action of Ca2 + sparks and activation of BK channels drives a global change in membrane potential and global Ca2 +, which ultimately relaxes smooth muscle and increases arterial diameter (Fig. 1). Ca2 + sparks have since been characterized in SMCs of nearly every organ blood vessel, including coronary arteries (Porter et al., 1998), mesenteric arteries (Krishnamoorthy, Sonkusare, Heppner, & Nelson, 2014; Miriel, Mauban, Blaustein, & Gil Wier, 1999), rat portal vein (Arnaudeau, Macrez-Leprêtre, & Mironneau, 1996), unpressurized cerebral arteries (Jaggar, Stevenson, & Nelson, 1998), and unpressurized spiral modiolar artery (Krishnamoorthy, Regehr, Berge, Scherer, & Wangemann, 2011), making it, along with BK channels STOCs (Jaggar et al., 2000), a universal regulator of vascular myogenic tone. The importance of such a negative feedback mechanism for the regulation of myogenic tone in muscular arteries and arterioles is evident from observations that pharmacological inhibition of BK channels by low concentrations of TEA, paxilline or iberiotoxin, or genetic manipulation of BK channel α, β, or γ subunit expression leads to the loss of this potent hyperpolarizing signal, leading to membrane depolarization, increase in VDCC activation, increase in Ca2 + influx, vasoconstriction and increase in myogenic tone (Brenner et al., 2000; Evanson et al., 2014; Knot et al., 1998; Krishnamoorthy et al., 2014; Nelson et al., 1995).
TRPP2 modulates ryanodine- and inositol-1,4,5-trisphosphate receptors-dependent Ca<sup>2+</sup> signals in opposite ways in cerebral arteries
2015, Cell CalciumCitation Excerpt :We have evaluated if the basal calcium level remained unchanged by following the basal fluorescence emitted by fluo8 one hour after the beginning of the loading, assuming an equivalent fluo8-AM desesterification in both mouse strains. Similarly, we performed the evaluation of basal Ca2+ concentration by the co-loading of fluo4-AM and Calcium crimsom-AM and probe calibration, as described previously [31]. The basal Ca2+ concentration expressed as R − Rmin/Rmax − R was 0.26 ± 0.08 in control arteries and 0.24 ± 0.16 in arteries treated with asTRPP2, p = 0.88, n = 6 arteries in each condition.
Local Regulation of Microvascular Perfusion
2008, Microcirculation[Ca<sup>2+</sup>]<inf>i</inf> and PKC-α are involved in the inhibitory effects of Ib, a novel nonpeptide AngiotensinII subtype AT<inf>1</inf> receptor antagonist, on AngiotensinII-induced vascular contraction in vitro
2007, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Intracellular Ca2+ mobilization by AngII has been reported to be mediated by IP3 receptors [24], therefore, IP3 receptors are needed to verify the effect of Ib on intracellular Ca2+ mobilization. In addition, exact mechanisms whereby AngII stimulates Ca2+ influx are unclear but may involve voltage-dependent calcium channels, which are directly or indirectly activated by AngII, nonspecific dihydropyridine-insensitive cation channels, receptor-gated Ca2+ channels, Ca2+-activated Ca2+ release channels, and activation of the Na+/Ca2+ exchanger [25]. In our future work, further studies are needed to done to clarify the detailed mechanisms of Ib to attenuate AngII-induced elevation of [Ca2+]i.
Involvement of Ca<sup>2+</sup> in the inhibition by crocetin of angiotensin II-induced ERK1/2 activation in vascular smooth muscle cells
2007, European Journal of Pharmacology
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