Effects of thapsigargin and ryanodine on vascular contractility: cross-talk between sacroplasmic reticulum and plasmalemma

Low, Amy; Darby, Peter J.; Kwan, Chiu‐Yin; Daniel, E. E.

doi:10.1016/0014-2999(93)90409-b

Cited by 48 publications

(23 citation statements)

References 34 publications

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“…Unlike rat aorta, in which SR may play a more prominent role as an intracellular Ca 2+ sink, in smaller arteries such as rat tail artery, the plasma membrane function may be relatively more prominent such that the accumulated cytosolic Ca 2+ in the presence of CPA may be more effectively removed via extrusion across the plasma membrane. 13 It is therefore possible that quantitative or qualitative changes in contractile responses may be present in different vasculatures, or under different experimental conditions, in which the relative contribution of plasmalemmal or SR activities in Ca 2+ handling may be differentially altered in hypertension. The present findings on vascular smooth muscle indeed underscore some functional alterations of vascular smooth muscle reported in SHR.…”

Section: Discussionmentioning

confidence: 99%

Effects of sarcoplasmic reticulum calcium pump inhibitors on vascular smooth muscle.

Kwan

Chaudhary²,

Zheng³

et al. 1994

Hypertension

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A dysfunctioning of Ca 2+ pump ATPase in the sarcoplasmic reticulum in vascular smooth muscle has been proposed as a contributing factor for the development of genetic hypertension. In this study, we determined whether in vitro inhibition of the sarcoplasmic reticulum Ca 2+ pump in vascular smooth muscle tissues and cultured cells isolated from aortas of spontaneously hypertensive rats (SHR) and WistarKyoto (WKY) rats would elicit the known alterations of contractile function and cell growth. We found the following common vascular effects of thapsigargin and cyclopiazonic acid, which are known to be selective inhibitors of sarcoplasmic reticulum Ca 2+ -ATPase in a number of tissues including smooth muscle: (1)

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Section: Discussionmentioning

confidence: 99%

Effects of sarcoplasmic reticulum calcium pump inhibitors on vascular smooth muscle.

Kwan

Chaudhary²,

Zheng³

et al. 1994

Hypertension

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“…Although numerous studies have shown that high K is ineffective in releasing intracellular Ca as well as in developing vas cular muscle contraction via intracellularly re leased Ca [12,14,35,36], a few reports argued that a high K could elicit a direct release of Ca from intracellular stores in cul tured rat aortic smooth muscle cells [37], Therefore, we further tested such a possibility by emptying the internal Ca stores with differ ent modulators of Ca mobilization across the sarcoplasmic reticulum (SR). These modula tors included norepinephrine (10-5 M ) or caf feine (10 mM), which deplete the SR Ca store [38][39][40][41], ryanodine (30 pM), which depletes SR by holding the Ca release channel in a sub- conductance state [42,43], or Ca ionophore A23187 (5 pA/), which releases Ca from all intracellular compartments [44]. Figure 3b shows that none of these drugs is effective in inhibiting the K-EDTA contraction.…”

Section: K-induced Contraction In Ca-free Solutionsmentioning

confidence: 99%

A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane

Kravtsov¹,

Kwan²

1995

Neurosignals

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Aortic rings of Sprague-Dawley rats developed reproducible contractions in Ca-free, nominally Mg-free (2 µM), Na-free, K solution, but not in Ca-free, nominally Mg-free, K-free, Na solution. Further reduction of the residual Mg by 0.5 µM EDTA in the above solutions potentiated this K-induced contraction and allowed the development of a relatively small contraction in Na-rich medium, respectively. The amplitude of EDTA-enhanced, K-induced contraction was almost the same as the amplitude of contraction induced in K-rich ([K] = 142 mM), Ca-containing (2.5 mM) solution. Such K-induced contraction was completely inhibited by 38 mM Na and by 3 mM of Mg (and Ni or Cd). Nifedipine (1 µM) also inhibited aortic smooth muscle contraction produced in K-EDTA, Ca-free solution. Modulators of Ca in sarcoplasmic reticulum (ryanodine, caffeine and norephinephrine), Ca-ionophore (A-23187) and protein kinase C inhibitor (Calphostin C) had no effect on EDTA-enhanced, K-induced contraction. It was suggested that K-induced contraction in rat aorta is not dependent on the increase in cytosolic Ca following membrane depolarization, is not a result of the release of Ca from intracellular stores, and is not due to change of Ca sensitivity upon the activation of protein kinase C. We propose that the competition of K for Mg and Na at external binding sites on the plasma membranes of the smooth muscle cells is primarily responsible for the development of vascular contraction.

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“…CPA is a highly selective Ca 2+ -pump inhibitor of ER/SR, and could deplete intracellular Ca 2+ stores and induce Ca 2+ -release activated Ca 2+ influx (CRAC) [11, 12]. However, in the Ca 2+ -free medium, Ach and CPA increased the [Ca 2+ ] i of the smooth muscle cells of the colon only by the release of intracellular Ca 2+ .…”

Section: Discussionmentioning

confidence: 99%

Effects of Berberine on Intracellular Free Calcium in Smooth Muscle Cells of Guinea Pig Colon

Cao

Luo²,

Yu³

et al. 2001

Digestion

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Aim: To investigate the effects and mechanism of berberine (Ber) on the intracellular free calcium concentration ([Ca²⁺]_i) in the smooth muscle cells of guinea pig colon. Methods: The changes of [Ca²⁺]_i were assayed by the biwavelength spectrophotometry with Fura 2-AM in the cell suspension of the smooth muscle cells, which were freshly isolated from guinea pig colon. Results: In the resting state, [Ca²⁺]_i in the HEPES-Ringer solution (CaCl₂ 1.5 mmol·l^–1) was (108 ± 9.4) nmol·l^–1 (n = 7). Ber had no significant effects on the resting [Ca²⁺]_i, but markedly inhibited the increase in [Ca²⁺]_iinduced by 60 mmol·l^–1 KCl in a concentration-dependent manner. The value of IC₅₀was 34.09 µmol·l^–1. 30 and 100 µmol·l^–1 Ber also inhibited the elevation of [Ca²⁺]_i evoked by 10 µmol·l^–1 Ach in a dose-dependent fashion in the presence or absence of extracellular Ca²⁺. In addition, Ber inhibited the elevation of [Ca²⁺]_i stimulated by cyclopiazonic acid (CPA) in a dose-dependent manner. This effect was more potent in the HEPES-Ringer solution (IC₅₀ = 37.79 µmol·l^–1) than Ca²⁺-free medium (IC₅₀ = 49.70 µmol·l^–1). Conclusions: Ber possessed an inhibitory effect on the influx of extracellular Ca²⁺ and Ca²⁺-release from intracellular stores in the smooth muscle cells of colon. That is to say Ber may be a blocker of Ca²⁺ channels.

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Effects of thapsigargin and ryanodine on vascular contractility: cross-talk between sacroplasmic reticulum and plasmalemma

Cited by 48 publications

References 34 publications

Effects of sarcoplasmic reticulum calcium pump inhibitors on vascular smooth muscle.

Effects of sarcoplasmic reticulum calcium pump inhibitors on vascular smooth muscle.

A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane

Effects of Berberine on Intracellular Free Calcium in Smooth Muscle Cells of Guinea Pig Colon

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