An isometric method to study respiratory smooth muscle responses in mice

Garssen, Johan; Loveren, Henk Van; Vliet, H. van der; Nijkamp, Frans P.

doi:10.1016/0160-5402(90)90031-f

Cited by 52 publications

(26 citation statements)

References 9 publications

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“…Each bronchial ring was mounted horizontally on two tungsten triangles (diameter of tungsten wire, ϳ100 m) and submerged in Krebs buffer in a thermostatted organ bath constantly bubbled with a pre-mixed gas consisting of 20% O 2 , 5% CO 2 and balance N 2 (44). The temperature in the organ bath was maintained at 37°C.…”

Section: Rt-pcr Analyses Of Ryr Isoforms In Mousementioning

confidence: 99%

Ryanodine Receptors in Muscarinic Receptor-mediated Bronchoconstriction

Stiber

Rosenberg

et al. 2005

Journal of Biological Chemistry

130

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Ryanodine receptors (RyRs), intracellular calcium release channels essential for skeletal and cardiac muscle contraction, are also expressed in various types of smooth muscle cells. In particular, recent studies have suggested that in airway smooth muscle cells (ASMCs) provoked by spasmogens, stored calcium release by the cardiac isoform of RyR (RyR2) contributes to the calcium response that leads to airway constriction (bronchoconstriction). Here we report that mouse ASMCs also express the skeletal muscle and brain isoforms of RyRs (RyR1 and RyR3, respectively). In these cells, RyR1 is localized to the periphery near the cell membrane, whereas RyR3 is more centrally localized. Moreover, RyR1 and/or RyR3 in mouse airway smooth muscle also appear to mediate bronchoconstriction caused by the muscarinic receptor agonist carbachol. Inhibiting all RyR isoforms with >200 M ryanodine attenuated the graded carbachol-induced contractile responses of mouse bronchial rings and calcium responses of ASMCs throughout the range of carbachol used (50 nM to >3 M). In contrast, inhibiting only RyR1 and RyR3 with 25 M dantrolene attenuated these responses caused by high (>500 nM) but not by low concentrations of carbachol. These data suggest that, as the stimulation of muscarinic receptor in the airway smooth muscle increases, RyR1 and/or RyR3 also mediate the calcium response and thus bronchoconstriction. Our findings provide new insights into the complex calcium signaling in ASMCs and suggest that RyRs are potential therapeutic targets in bronchospastic disorders such as asthma.

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Section: Rt-pcr Analyses Of Ryr Isoforms In Mousementioning

confidence: 99%

Ryanodine Receptors in Muscarinic Receptor-mediated Bronchoconstriction

Stiber

Rosenberg

et al. 2005

Journal of Biological Chemistry

130

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“…In order to measure airway responsiveness in vitro, tracheae were isolated and the responsiveness to methacholine was measured in an organ bath as originally described by Garssen et al (1990). In previous experiments it was established that the optimal time-point to measure tracheal hyperresponsiveness to methacholine in vitro was at 3 h after the last challenge (Hessel et al, 1994).…”

Section: Airway Responsiveness In Vitromentioning

confidence: 99%

Effect of dexamethasone and endogenous corticosterone on airway hyperresponsiveness and eosinophilia in the mouse

Bie

Hessel

Ark

et al. 1996

British J Pharmacology

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1 Mice were sensitized by 7 intraperitoneal injections of ovalbumin without adjuvant (10 /tg in 0.5 ml of sterile saline) on alternate days and after 3 weeks exposed to either ovalbumin (2 mg ml1-in sterile saline) or saline aerosol for 5 min on 8 consecutive days. One day before the first challenge, animals were injected intraperitoneally on a daily basis with vehicle (0.25 ml sterile saline), dexamethasone (0.5 mg kg'-) or metyrapone (30 mg kg'-). 2 In vehicle-treated ovalbumin-sensitized animals ovalbumin challenge induced a significant increase of airway responsiveness to metacholine both in vitro (27%, P<0.05) and in vivo (40%, P<0.05) compared to saline-challenged mice. Virtually no eosinophils could be detected after saline challenge, whereas the numbers of eosinophils were significantly increased (P<0.01) at both 3 and 24 h after the last ovalbumin challenge (5.48 + 3.8 x I03 and 9.13 + 1.7 x 103 cells, respectively). Furthermore, a significant increase in ovalbumin-specific immunoglobulin E level (583+103 units ml-', P<0.05) was observed after ovalbumin challenge compared to saline challenge (201 + 38 units ml-1). 4 From these data it can be concluded that exogenously applied corticosteroids can inhibit eosinophil infiltration as well as airway hyperresponsiveness. Vise versa, endogenously produced corticosteroids play a down-regulating role on the induction of both eosinophil infiltration and airway hyperresponsiveness.

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“…Isometric measurement of tracheal reactivity Tracheal reactivity was measured by the method of Garssen et al (1990). Mice were killed by an overdose of sodium pentobarbitone (0.3 ml; 60 mg kg-' i.p.).…”

Section: Animalsmentioning

confidence: 99%

The involvement of sensory neuropeptides in toluene diisocyanate‐induced tracheal hyperreactivity in the mouse airways

Scheerens

Buckley

Muis

et al. 1996

British J Pharmacology

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1 Recently, we developed a murine model to investigate toluene diisocyanate (TDI)-induced occupational asthma. After skin-sensitization and intranasal challenge with TDI (1%) mice exhibited tracheal hyperreactivity 24 h after the challenge. 2 The aim of the present study was to investigate the possible role for sensory neuropeptides in the development of this tracheal hyperreactivity. 3 First, we demonstrated that direct application of TDI in vitro induced the release of tachykinins from the sensory nerves in the mouse isolated trachea. Second, capsaicin pretreatment, resulting in the depletion of sensory neuropeptides, completely abolished the TDI-induced tracheal hyperreactivity 24 h after the challenge. Third, the selective neurokinin, (NK1)-receptor antagonist RP 67580 (0.2 Mumol kg-') also inhibited tracheal hyperreactivity when it was administered before the challenge. However, administration of RP 67580 during the sensitization phase did not result in a suppression of the TDIinduced tracheal hyperreactivity 24 after the challenge. 4 When TDI-sensitized mice were topically challenged with TDI a marked ear swelling response was observed. The cutaneous response after TDI application was not affected by capsaicin pretreatment or RP 67580 administration. 5 These results clearly show that sensory neuropeptides, particularly tachykinins, are essential for the development of TDI-induced tracheal hyperreactivity during the effector phase. The differences between the airways and skin with respect to the sensory neuropeptides is intriguing and could suggest a local action for the tachykinins in the airways.

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An isometric method to study respiratory smooth muscle responses in mice

Cited by 52 publications

References 9 publications

Ryanodine Receptors in Muscarinic Receptor-mediated Bronchoconstriction

Ryanodine Receptors in Muscarinic Receptor-mediated Bronchoconstriction

Effect of dexamethasone and endogenous corticosterone on airway hyperresponsiveness and eosinophilia in the mouse

The involvement of sensory neuropeptides in toluene diisocyanate‐induced tracheal hyperreactivity in the mouse airways

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