Different Inhibitory Effects of Volatile Anesthetics on T- and L-type Voltage-dependent Ca2+Channels in Porcine Tracheal and Bronchial Smooth Muscles

2001 ◽  
Vol 94 (4) ◽  
pp. 683-693 ◽  
Author(s):  
Michiaki Yamakage ◽  
Xiangdong Chen ◽  
Naoki Tsujiguchi ◽  
Yasuhiro Kamada ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Tension ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Volatile Anesthetics ◽  
Smooth Muscle Contraction ◽  
Inhibitory Effects ◽  
Bronchial Smooth Muscle ◽  
Voltage Dependent

Background The distal airway is more important in the regulation of airflow resistance than is the proximal airway, and volatile anesthetics have a greater inhibitory effect on distal airway muscle tone. The authors investigated the different reactivities of airway smooth muscles to volatile anesthetics by measuring porcine tracheal or bronchial (third to fifth generation) smooth muscle tension and intracellular concentration of free Ca2+ ([Ca2+]i) and by measuring inward Ca2+ currents (ICa) through voltage-dependent Ca2+ channels (VDCs). Methods Intracellular concentration of free Ca2+ was monitored by the 500-nm light emission ratio of Ca2+ indicator fura-2. Isometric tension was measured simultaneously. Whole-cell patch clamp recording techniques were used to investigate the effects of volatile anesthetics on ICa in dispersed smooth muscle cells. Isoflurane (0-1.5 minimum alveolar concentration) or sevoflurane (0-1.5 minimum alveolar concentration) was introduced into a bath solution. Results The volatile anesthetics tested had greater inhibitory effects on carbachol-induced bronchial smooth muscle contraction than on tracheal smooth muscle contraction. These inhibitory effects by the anesthetics on muscle tension were parallel to the inhibitory effects on [Ca2+]i. Although tracheal smooth muscle cells had only L-type VDCs, some bronchial smooth muscle cells (approximately 30%) included T-type VDC. Each of the two anesthetics significantly inhibited the activities of both types of VDCs in a dose-dependent manner; however, the anesthetics had greater inhibitory effects on T-type VDC activity in bronchial smooth muscle. Conclusions The existence of the T-type VDC in bronchial smooth muscle and the high sensitivity of this channel to volatile anesthetics seem to be, at least in part, responsible for the different reactivities to the anesthetics in tracheal and bronchial smooth muscles.

Inhibitory Effects of Volatile Anesthetics on K+and Cl−Channel Currents in Porcine Tracheal and Bronchial Smooth Muscle

2002 ◽  
Vol 96 (2) ◽  
pp. 458-466 ◽  
Author(s):  
Xiangdong Chen ◽  
Michiaki Yamakage ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Volatile Anesthetics ◽  
Delayed Rectifier ◽  
Inhibitory Effects ◽  
Bronchial Smooth Muscle ◽  
K Channels ◽  
Channel Currents ◽  
K Currents

Background K+ and Ca2+-activated Cl- (ClCa) channel currents have been shown to contribute to the alteration of membrane electrical activity in airway smooth muscle. This study was conducted to investigate the effects of volatile anesthetics, which are potent bronchodilators, on the activities of these channels in porcine tracheal and bronchial smooth muscles. Methods Whole-cell patch clamp recording techniques were used to investigate the effects of superfused isoflurane (0-1.5 minimum alveolar concentration) or sevoflurane (0-1.5 minimum alveolar concentration) on K+ and ClCa channel currents in dispersed smooth muscle cells. Results Isoflurane and sevoflurane inhibited whole-cell K+ currents to a greater degree in tracheal versus bronchial smooth muscle cells. More than 60% of the total K+ currents in tracheal smooth muscle appeared to be mediated through delayed rectifier K+ channels compared with less than 40% in bronchial smooth muscle. The inhibitory effects of the anesthetics were greater on the delayed rectifier K+ channels than on the remaining K+ channels. Cl- currents through ClCa channels were significantly inhibited by the anesthetics. The inhibitory potencies of the anesthetics on the ClCa channels were not different in tracheal and bronchial smooth muscle cells. Conclusions Volatile anesthetics isoflurane and sevoflurane significantly inhibited Cl- currents through ClCa channels, and the inhibitory effect is consistent with the relaxant effect of volatile anesthetics in airway smooth muscle. Different distributions and different anesthetic sensitivities of K+ channel subtypes could play a role in the different inhibitory effects of the anesthetics on tracheal and bronchial smooth muscle contractions.

Inhibitory Effects of Thiopental, Ketamine, and Propofol on Voltage-dependent Calcium sup 2+ Channels in Porcine Tracheal Smooth Muscle Cells

1995 ◽  
Vol 83 (6) ◽  
pp. 1274-1282 ◽  
Author(s):  
Michiaki Yamakage ◽  
Carol A. Hirshman ◽  
Thomas L. Croxton
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ion Channel ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Inhibitory Effects ◽  
Intravenous Anesthetics ◽  
Anesthetic Agents ◽  
Voltage Dependent

Abstract Background Intravenously administered anesthetics directly inhibit airway smooth muscle contraction. Because many anesthetic agents affect membrane ion channel function and sustained contraction of airway smooth muscle requires the influx of Calcium2+ through voltage-dependent Calcium2+ channels, it was hypothesized that intravenous anesthetics inhibit airway smooth muscle voltage-dependent Calcium2+ channels.

Low-temperature Modification of the Inhibitory Effects of Volatile Anesthetics on Airway Smooth Muscle Contraction in Dogs

2000 ◽  
Vol 93 (1) ◽  
pp. 179-188 ◽  
Author(s):  
Michiaki Yamakage ◽  
Naoki Tsujiguchi ◽  
Jun-ichi Hattori ◽  
Yasuhiro Kamada ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Low Temperature ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Volatile Anesthetics ◽  
Smooth Muscle Contraction ◽  
Channel Activity ◽  
Inhibitory Effects ◽  
High K ◽  
Voltage Dependent

Background Because exposure to low temperature can modify the effect of volatile anesthetics on airway smooth muscle contraction, this study was conducted to investigate low-temperature modifications of the inhibitory effects of isoflurane and sevoflurane on canine tracheal smooth muscle tone by simultaneously measuring the muscle tension and intracellular concentration of Ca2+ ([Ca2+]i) and by measuring voltage-dependent Ca2+ channel activity. Methods [Ca2+]i was monitored by the 500-nm light emission ratio of preloaded fura-2, a Ca2+ indicator. Isometric tension was measured simultaneously. Whole cell patch clamp recording techniques were used to observe voltage-dependent Ca2+ channel activity in dispersed muscle cells. Isoflurane (0-3.0%) or sevoflurane (0-3%) was introduced to a bath solution at various temperatures (37, 34, or 31 degrees C). Results Low temperature (34 or 31 degrees C) reduced high-K+-induced (72.7 mm) muscle contraction and increased [Ca2+]i, but it enhanced carbachol-induced (1 microm) muscle contraction with a decrease in [Ca2+]i. The volatile anesthetics tested showed significant inhibition of both high-K+-induced and carbachol-induced airway smooth muscle contraction, with a concomitant decrease in [Ca2+]i. The inhibition of the carbachol-induced muscle contraction by volatile anesthetics was abolished partially by exposure to low temperature. Volatile anesthetics and low-temperature exposure significantly inhibited voltage-dependent Ca2+ channel activity of the smooth muscle. Conclusions Exposure of airway smooth muscle to low temperature leads to an increase in agonist-induced muscle contractility, with a decrease in [Ca2+]i. The inhibition of voltage-dependent Ca2+ channel activity by exposure to low temperature and by volatile anesthetics cam be attributed, at least in part, to the decrease in [Ca2+]i.

The Repolarizing Effects of Volatile Anesthetics on Porcine Tracheal and Bronchial Smooth Muscle Cells

2002 ◽  
Vol 94 (1) ◽  
pp. 84-88
Author(s):  
Michiaki Yamakage ◽  
Xiangdong Chen ◽  
Akira Kimura ◽  
Sohshi Iwasaki ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Volatile Anesthetics ◽  
Bronchial Smooth Muscle ◽  
Bronchial Smooth Muscle Cells

Inhibitory Effects of Diazepam and Midazolam on Ca2+and K+Channels in Canine Tracheal Smooth Muscle Cells 

1999 ◽  
Vol 90 (1) ◽  
pp. 197-207 ◽  
Author(s):  
Michiaki Yamakage ◽  
Takashi Matsuzaki ◽  
Naoki Tsujiguchi ◽  
Yasuyuki Honma ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Relaxation ◽  
Muscle Cells ◽  
Tracheal Smooth Muscle ◽  
Inhibitory Effects ◽  
K Channels ◽  
Voltage Dependent ◽  
Channel Currents

Background Benzodiazepines have a direct bronchodilator action in airway smooth muscle, but the mechanisms by which these agents produce muscle relaxation are not fully understood. The current study was performed to identify the effects of the benzodiazepines diazepam and midazolam on Ca2+ and K+ channels in canine tracheal smooth muscle cells. Methods Whole-cell patch-clamp recording techniques were used to evaluate the effects of the benzodiazepines diazepam (10(-8) to 10(-3) M) and midazolam (10(-8) to 10(-3) M) on inward Ca2+ and outward K+ channel currents in dispersed canine tracheal smooth muscle cells. The effects of the antagonists flumazenil (10(-5) M) and PK11195 (10(-5) M) on these channels were also studied. Results Each benzodiazepine tested significantly inhibited Ca2+ currents in a dose-dependent manner, with 10(-6) M diazepam and 10(-5) M midazolam each causing approximately 50% depression of peak voltage-dependent Ca2+ currents. Both benzodiazepines promoted the inactivated state of the channel at more-negative potentials. The Ca2+-activated and voltage-dependent K+ currents were inhibited by diazepam and midazolam (> 10(-5) M and > 10(-4) M, respectively). Flumazenil and PK11195 had no effect on these channel currents or on the inhibitory effects of the benzodiazepines. Conclusions Diazepam and midazolam had inhibitory effects on voltage-dependent Ca2+ channels, which lead to muscle relaxation. However, high concentrations of these agents were necessary to inhibit the K+ channels. The lack of antagonized effects of their antagonists is related to the non-gamma-aminobutyric acid-mediated electrophysiologic effects of benzodiazepines on airway smooth muscle contractility.

The Repolarizing Effects of Volatile Anesthetics on Porcine Tracheal and Bronchial Smooth Muscle Cells

2002 ◽  
Vol 96 (Sup 2) ◽  
pp. A1307
Author(s):  
Michiaki Yamakage ◽  
Xiangdong Chen ◽  
Akira Kimura ◽  
Sohshi Iwasaki ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Volatile Anesthetics ◽  
Bronchial Smooth Muscle ◽  
Bronchial Smooth Muscle Cells

scholarly journals Calsequestrin is a component of smooth muscles: the skeletal- and cardiac-muscle isoforms are both present, although in highly variable amounts and ratios

1994 ◽  
Vol 301 (2) ◽  
pp. 465-469 ◽  
Author(s):  
P Volpe ◽  
A Martini ◽  
S Furlan ◽  
J Meldolesi
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vas Deferens ◽  
Striated Muscle ◽  
Smooth Muscles ◽  
High Capacity ◽  
Muscle Cells ◽  
Smooth Muscle Contraction ◽  
Similar Amount

Expression by smooth-muscle cells of calsequestrin (CS), the low-affinity/high-capacity Ca(2+)-binding protein of striated-muscle sarcoplasmic reticulum (SR), has been investigated in recent years with conflicting results. Here we report the purification and characterization from rat vas deferens of two CS isoforms, the first deemed skeletal muscle, the second cardiac type, on account of their N-terminal amino acids and other relevant biochemical and molecular properties. Compared with vas deferens, the smooth muscles from aorta and stomach, in that order, were found to express lower amounts of CS, whereas in the uterus and bladder the protein was not detectable. The ratio between the two CS isoforms was also variable, with the stomach and aorta predominantly expressing the skeletal-muscle type and the vas deferens expressing the two CSs in roughly similar amount. Because of the property of CSs to localize within the skeletal-muscle SR lumen not uniformly, but according to the distribution of their anchorage membrane proteins, the expression of the protein suggests the existence in smooth-muscle cells of discrete endoplasmic-reticulum areas specialized in the rapidly exchanging Ca2+ storage and release, and thus in the control of a variety of functions, including smooth-muscle contraction.

The Repolarizing Effects of Volatile Anesthetics on Porcine Tracheal and Bronchial Smooth Muscle Cells

2002 ◽  
Vol 94 (1) ◽  
pp. 84-88 ◽  
Author(s):  
Michiaki Yamakage ◽  
Xiangdong Chen ◽  
Akira Kimura ◽  
Sohshi Iwasaki ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Volatile Anesthetics ◽  
Bronchial Smooth Muscle ◽  
Bronchial Smooth Muscle Cells
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