Regular Article
Activation of Calcium Sparks by Angiotensin II in Vascular Myocytes

https://doi.org/10.1006/bbrc.1996.0808Get rights and content

Abstract

Contraction in smooth muscle is triggered by an increase in cytoplasmic free calcium ([Ca2+]i) which depends on both Ca2+influx through L-type Ca2+channels and Ca2+release from the sarcoplasmic reticulum (SR). Two mechanisms have been shown to be involved in SR Ca2+release. one is stimulated by Ca2+and involved ryanodine-sensitive Ca2+-release channels; the other is stimulated by an increase in inositol 1,4,5-trisphosphate (InsP3) generation induced by various mediators and involved InsP3-sensitive Ca2+release channels. Here, we examined the effects of angiotensin II on [Ca2+]iin single rat portal vein myocytes using both the whole cell patch-clamp method and a laser scanning confocal microscope. Elementary Ca2+release events (Ca2+sparks) were obtained spontaneously or in response to L-type Ca2+channel current activation, and resulted from activation of ryanodine-sensitive Ca2+-release channels in the SR. We show that angiotensin AT1receptors stimulate Ca2+sparks through activation of L-type Ca2+channels without involving InsP3-induced Ca2+release. This novel transduction pathway may be a common mechanism for vasoconstrictors which do not stimulate generation of chemical second messengers.

References (0)

Cited by (56)

  • Presenilin 1 mutation decreases both calcium and contractile responses in cerebral arteries

    2017, Neurobiology of Aging
    Citation 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 Neurobiology
    Citation 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 Calcium
    Citation 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.

  • [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 Communications
    Citation 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.

View all citing articles on Scopus
1

Corresponding author. Fax: (33)57 57 12 26.

View full text