Different Inhibitory Effects of Sevoflurane on Hyperreactive Airway Smooth Muscle Contractility in Ovalbumin-sensitized and Chronic Cigarette-smoking Guinea Pig Models

2006 ◽  
Vol 105 (4) ◽  
pp. 753-763 ◽  
Author(s):  
Soshi Iwasaki ◽  
Michiaki Yamakage ◽  
Jun-Ichi Satoh ◽  
Akiyoshi Namiki
Keyword(s):  
Smooth Muscle ◽  
Cigarette Smoking ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Inhibitory Effect ◽  
Ca Channel ◽  
Channel Activity ◽  
Inhibitory Effects ◽  
Smooth Muscle Contractility ◽  
Voltage Dependent

Background The authors hypothesized that sevoflurane had different inhibitory effects on hyperreactive airway smooth muscle contractility in different types of hyperreactive airway models. Methods The effects of sevoflurane on hyperreactive airways in ovalbumin-sensitized and chronic cigarette-smoking guinea pig models were investigated by measuring (1) total lung resistance, (2) smooth muscle tension and intracellular concentration of free Ca, (3) voltage-dependent Ca channel activity, and (4) cyclic adenosine monophosphate levels. Results Ovalbumin and muscarinic airway hyperreactivity was seen in ovalbumin-sensitized animals. Enlarged alveolar ducts/alveoli and lesser muscarinic hyperreactivity were observed in chronic cigarette-smoke animals. Although sevoflurane inhibited the acetylcholine-induced increase in total lung resistance in the control and ovalbumin-sensitized models, the anesthetic had a smaller effect in the chronic cigarette-smoking model. Similarly, in the chronic cigarette-smoking model, sevoflurane had a smaller inhibitory effect on carbachol-induced muscle contraction and increase in intracellular concentration of free Ca. Sevoflurane also had a smaller inhibitory effect on voltage-dependent Ca channel activity in the chronic cigarette-smoking group than in the other two groups. The sevoflurane-induced increase in cyclic adenosine monophosphate that was seen in the control and ovalbumin-sensitized groups was significantly suppressed in the chronic cigarette-smoking group. Conclusions Although sevoflurane potently inhibited airway contractility in control and ovalbumin-sensitized models, the anesthetic had a smaller effect in a chronic cigarette-smoking model. The different inhibitory effects of sevoflurane on airway contractility depend, at least in part, on different effects on voltage-dependent Ca channel activity and cyclic adenosine monophosphate level.

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.

Effect of dopamine on adenylate cyclase activity, polyphosphoinositide metabolism and cytosolic calcium concentrations in frog pituitary melanotrophs

1993 ◽  
Vol 136 (3) ◽  
pp. 421-429 ◽  
Author(s):  
L. Desrues ◽  
M. Lamacz ◽  
B. G. Jenks ◽  
H. Vaudry ◽  
M. C. Tonon
Keyword(s):  
Calcium Channels ◽  
Inositol Trisphosphate ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Cytosolic Calcium ◽  
Inhibitory Effect ◽  
Intermediate Lobe ◽  
Camp Production ◽  
Membrane Phospholipids ◽  
Voltage Dependent

ABSTRACT It has previously been shown that dopamine plays a pivotal role in the regulation of α-melanocyte-stimulating hormone (α-MSH) secretion from the intermediate lobe of the pituitary. In the present study, we have investigated the various intracellular mechanisms that are associated with the action of dopamine on frog pituitary melanotrophs. Dopamine reduced forskolin-stimulated cyclic adenosine monophosphate (cAMP) production and the inhibitory effect of dopamine was blocked by the dopaminergic D2 receptor antagonist sulpiride. The D2 receptor agonist apomorphine inhibited incorporation of [3H]inositol into membrane phospholipids. Dopamine also inhibited the formation of inositol trisphosphate and provoked accumulation of phosphatidylinositol bisphosphate. The inhibitory effect of dopamine on inositol trisphosphate production was mimicked by D2 receptor agonists and blocked by sulpiride. Using a double-wavelength microfluorimetric approach, we found that dopamine caused a rapid and transient decrease in K+-evoked stimulation of intracellular calcium concentration. The timecourses of the responses of the various intracellular messengers indicate that blockage of voltagedependent calcium channels is the primary event associated with activation of dopamine D2 receptors, while inhibition of polyphosphoinositide breakdown, related to blockage of voltage-dependent calcium channels, and reduction of cAMP production are secondary events which may contribute to the sustained inhibitory effect of dopamine on α-MSH release. Journal of Endocrinology (1993) 136, 421–429

U46619, a thromboxane A2 agonist, inhibits KCa channel activity from pig coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. C708-C713 ◽  
Author(s):  
F. S. Scornik ◽  
L. Toro
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Lipid Bilayers ◽  
Thromboxane A2 ◽  
Inhibitory Effect ◽  
Channel Activity ◽  
Open Probability ◽  
Control Value ◽  
Kca Channels ◽  
Internal Side

Thromboxane A2 (TxA2) is a potent vasoconstrictor derived from the metabolism of arachidonic acid. Because potassium channels are involved in the contraction of vascular smooth muscle, their blockade could contribute to the TxA2-induced contraction. To test this possibility, we studied the effect of the TxA2 stable analogue U46619 on calcium-activated potassium (KCa) channels from coronary artery reconstituted into lipid bilayers. Addition of U46619 (50-150 nM) to the external but not to the internal side of the channel decreased the channel open probability (Po) between 15 and 80% of the control value. The inhibitory effect of U46619 affected both the open and closed states of the channel and could be reversed by internal calcium. Thromboxane B2, the inactive hydrolysis derivative of TxA2, did not affect channel activity. SQ 29548, a TxA2 receptor antagonist, was able to prevent the inhibition by U46619. Furthermore, SQ 29548 added after U46619 could restore channel activity to near control values. These results suggest that TxA2 could be a regulatory factor of KCa channels from coronary smooth muscle and that this regulation could be related to its action as a vasoconstrictor.

Phosphodiesterase 4 Inhibitor Roflumilast Improves the Bronchodilative Effect of Sevoflurane in Sensitized Airways

2014 ◽  
Vol 120 (5) ◽  
pp. 1152-1159 ◽  
Author(s):  
Jing Zhou ◽  
Sohshi Iwasaki ◽  
Michiaki Yamakage
Keyword(s):  
Smooth Muscle ◽  
Volatile Anesthetic ◽  
Cyclic Adenosine Monophosphate ◽  
Relaxation Effect ◽  
Adenosine Monophosphate ◽  
Bronchodilator Effect ◽  
Phosphodiesterase 4 ◽  
Phosphodiesterase 4 Inhibitors ◽  
Lung Resistance ◽  
Total Lung Resistance

Abstract Background: Although phosphodiesterase 4 inhibitors and the volatile anesthetic sevoflurane are known to have independent bronchodilator properties, the combined administration of these two agents may have the potential to exert an additive or synergistic bronchodilator effect. The authors tested this hypothesis and investigated the common site of this combined relaxation effect in a model of airway hyperresponsiveness with ovalbumin-sensitized guinea pigs. Methods: Ovalbumin-sensitized animals (n = 138) were randomized into six groups: sensitized, sevoflurane, rolipram1.0, roflumilast1.0, sevoflurane/rolipram1.0, and sevoflurane/roflumilast1.0. Total lung resistance in vivo, airway smooth muscle tension in vitro, and intracellular cyclic adenosine monophosphate levels were measured to evaluate the relaxation effect. Results: Among the six sensitized groups, total lung resistance was higher in the order of sensitized > sevoflurane > rolipram 1.0 > roflumilast1.0 > sevoflurane/rolipram1.0 > sevoflurane/roflumilast1.0, with an increase in acetylcholine concentration. Compared with the other five groups, the muscle tensions in the sevoflurane/roflumilast1.0 group were significantly lower at carbacholine doses of 10−7, 10−6, and 10−5 M; the cyclic adenosine monophosphate concentrations (means ± SD) in the sevoflurane/rolipram1.0 (1.61 ± 0.34) and sevoflurane/roflumilast1.0 (1.50 ± 0.20) groups were higher than that in the sensitized (0.52 ± 0.15) and sevoflurane (1.12 ± 0.32) groups. Conclusions: The combined use of phosphodiesterase 4 inhibitors with the volatile anesthetic sevoflurane had an additive bronchodilator effect in ovalbumin-sensitized guinea pigs. The concurrent increase in cyclic adenosine monophosphate levels in sensitized airway smooth muscle might be a mechanism of this combined relaxation effect.

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