The initial inositol 1,4,5-trisphosphate response induced by histamine is strongly amplified by Ca2+ release from internal stores in smooth muscle

Rueda, Angélica; Garcı́a, Lucı́a; Soria-Jasso, Luis-Enrique; Arias‐Montaño, José‐Antonio; Guerrero‐Hernández, Agustín

doi:10.1054/ceca.2002.0270

Cited by 16 publications

(15 citation statements)

References 49 publications

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“…[Ca 2+ ] i (in nmol/L) was calculated from the ratio of 340/380 nm after correcting for background. Fluorescence emission ratios were converted to [Ca 2+ ] i according to the Grynkiewicz equation [48], using a dissociation constant for fura-2 of 239 nM. Values of 0.32, 5.7, and 10.3 obtained from fura-2 in situ calibration were used for Rmin, Rmax, and β, respectively.…”

Section: Methodsmentioning

confidence: 99%

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Abnormal Ca2+ Spark/STOC Coupling in Cerebral Artery Smooth Muscle Cells of Obese Type 2 Diabetic Mice

et al. 2013

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Diabetes is a major risk factor for stroke. However, the molecular mechanisms involved in cerebral artery dysfunction found in the diabetic patients are not completely elucidated. In cerebral artery smooth muscle cells (CASMCs), spontaneous and local increases of intracellular Ca2+ due to the opening of ryanodine receptors (Ca2+ sparks) activate large conductance Ca2+-activated K+ (BK) channels that generate spontaneous transient outward currents (STOCs). STOCs have a key participation in the control of vascular myogenic tone and blood pressure. Our goal was to investigate whether alterations in Ca2+ spark and STOC activities, measured by confocal microscopy and patch-clamp technique, respectively, occur in isolated CASMCs of an experimental model of type-2 diabetes (db/db mouse). We found that mean Ca2+ spark amplitude, duration, size and rate-of-rise were significantly smaller in Fluo-3 loaded db/db compared to control CASMCs, with a subsequent decrease in the total amount of Ca2+ released through Ca2+ sparks in db/db CASMCs, though Ca2+ spark frequency remained. Interestingly, the frequency of large-amplitude Ca2+ sparks was also significantly reduced in db/db cells. In addition, the frequency and amplitude of STOCs were markedly reduced at all voltages tested (from −50 to 0 mV) in db/db CASMCs. The latter correlates with decreased BK channel β1/α subunit ratio found in db/db vascular tissues. Taken together, Ca2+ spark alterations lead to inappropriate BK channels activation in CASMCs of db/db mice and this condition is aggravated by the decrease in the BK β1 subunit/α subunit ratio which underlies the significant reduction of Ca2+ spark/STOC coupling in CASMCs of diabetic animals.

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Section: Methodsmentioning

confidence: 99%

“…STOCs were recorded in the whole cell configuration of the patch clamp technique using solutions and protocol previously described [48]. The pipette solution (in mmol/L): 80 Kglutamate, 5 NaCl, 40 KCl, 1 MgCl 2 , 3 MgATP, 0.1 NaGTP, 0.05 KEGTA, 20 HEPES, pH 7.2 with KOH.…”

Section: Methodsmentioning

confidence: 99%

Abnormal Ca2+ Spark/STOC Coupling in Cerebral Artery Smooth Muscle Cells of Obese Type 2 Diabetic Mice

et al. 2013

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“…It has been shown that histamine increases phosphoinositide metabolism (Hill, 1990) and IP 3 levels (Chilvers et al, 1994) via activation of phospholipase C by a pertussis toxin-insensitive G protein (Leurs et al, 1994). Rueda et al (2002) studied the Ca 2ϩ -dependence and wortmannin-sensitivity of the initial IP 3 response induced by activation of H 1 receptors in smooth muscle 598 ANDERSSON AND WEIN from guinea pig urinary bladder. They suggested that the histamine-induced increase in IP 3 was more the consequence of Ca 2ϩ release from internal stores than a direct activation of phospholipase C by H 1 receptors.…”

Section: Peripheral Targetsmentioning

confidence: 99%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

454

364

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“…Conversely, partial depletion of SR Ca 2ϩ stores appears to participate in the termination of Ca 2ϩ release (9,60). Actually, in smooth muscle cells, a small reduction in luminal SR Ca 2ϩ level, far from complete depletion, totally inhibits the spontaneous activity of RyRs as revealed by a complete disappearance of STOCs (30,42,59). However, despite these data showing the importance of luminal SR Ca 2ϩ level in the modulation of Ca 2ϩ release channel activity, our data cannot be fully explained by changes in luminal SR Ca 2ϩ level.…”

Section: Serca Pump Facilitates Sr Ca 2ϩ Release In Smooth Muscle Cellsmentioning

confidence: 59%

Inhibition of SERCA pumps induces desynchronized RyR activation in overloaded internal Ca²⁺ stores in smooth muscle cells

Gómez-Viquez

Guerrero-Serna²,

Arvizu³

et al. 2010

American Journal of Physiology-Cell Physiology

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We have previously shown that rapid inhibition of sarcoplasmic reticulum (SR) ATPase (SERCA pumps) decreases the amplitude and rate of rise (synchronization) of caffeine induced-Ca(2+) release without producing a reduction of free luminal SR Ca(2+) level in smooth muscle cells (Gómez-Viquez L, Guerrero-Serna G, García U, Guerrero-Hernández A. Biophys J 85: 370-380, 2003). Our aim was to investigate the role of luminal SR Ca(2+) content in the communication between ryanodine receptors (RyRs) and SERCA pumps. To this end, we studied the effect of SERCA pump inhibition on RyR-mediated Ca(2+) release in smooth muscle cells with overloaded SR Ca(2+) stores. Under this condition, the amplitude of RyR-mediated Ca(2+) release was not affected but the rate of rise was still decreased. In addition, the caffeine-induced Ca(2+)-dependent K(+) outward currents revealed individual events, suggesting that SERCA pump inhibition reduces the coordinated activation of RyRs. Collectively, our results indicate that SERCA pumps facilitate the activation of RyRs by a mechanism that does not involve the regulation of SR Ca(2+) content. Importantly, SERCA pumps and RyRs colocalize in smooth muscle cells, suggesting a possible local communication between these two proteins.

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The initial inositol 1,4,5-trisphosphate response induced by histamine is strongly amplified by Ca2+ release from internal stores in smooth muscle

Cited by 16 publications

References 49 publications

Abnormal Ca2+ Spark/STOC Coupling in Cerebral Artery Smooth Muscle Cells of Obese Type 2 Diabetic Mice

Abnormal Ca2+ Spark/STOC Coupling in Cerebral Artery Smooth Muscle Cells of Obese Type 2 Diabetic Mice

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Inhibition of SERCA pumps induces desynchronized RyR activation in overloaded internal Ca²⁺ stores in smooth muscle cells

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The initial inositol 1,4,5-trisphosphate response induced by histamine is strongly amplified by Ca2+ release from internal stores in smooth muscle

Cited by 16 publications

References 49 publications

Abnormal Ca2+ Spark/STOC Coupling in Cerebral Artery Smooth Muscle Cells of Obese Type 2 Diabetic Mice

Abnormal Ca2+ Spark/STOC Coupling in Cerebral Artery Smooth Muscle Cells of Obese Type 2 Diabetic Mice

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Inhibition of SERCA pumps induces desynchronized RyR activation in overloaded internal Ca2+ stores in smooth muscle cells

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Inhibition of SERCA pumps induces desynchronized RyR activation in overloaded internal Ca²⁺ stores in smooth muscle cells