• Journal of Chest Surgery
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• v.27 no.1
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• pp.9-14
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• 1994

Substance P[SP] has been known to be a peptide which may be plays a role as a neurotransmitter in central nervous system as well as peripheral autonomic nervous system. It has been reported that SP was widely distributed in the nerve of the tracheal smooth muscle and induced the muscle contraction. However, definite action mechanism of SP in the tracheal smooth muscle was not clear, yet. Thus, present experiment was performed to elucidate an effect of substance P and an action mechanism on contraction of the smooth muscle in rabbits. In order to find a neural mechanism to the effect of SP on the tracheal smooth muscle contraction, atropine sulfate, tetrodotoxin, propranol and phentolamine were administered at 10 min before the addition of SP. Otherwise,to find effect of SP antagonists on the action of SP, [D-Pro2, D-Try7,9]SP, [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP and [D-Pro4, D-Trp7,9]SP were administered as a same fashion. These following results were obtained. 1] SP induced contraction of the tracheal smooth muscle under resting condition and the contraction was increased dose-dependently. 2] Cholinergic blocker[atropine], neural blocker[tetrodotoxin] and adrenergic blocker[propranol and phentolamine] didn`t have an effect on the contractile response. 3] Three SP antagonists inhibited the contractile response. 4] Isoproterenol relaxed the contraction induced by SP. The above results suggested that SP induced contraction of the tracheal smooth muscle directly act to the smooth muscle in rabbits. The autonomic nervous system did not seem to participate in the SP action.

• The Journal of Korean Physical Therapy
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• v.19 no.5
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• pp.65-76
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• 2007

Purpose: It is generally accepted that smooth muscle contraction is triggered by intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) released from intracellular $Ca^{2+}$ stores such as sarcoplasmic teticulum (SR) and from the extracellular space. The increased $[Ca^{2+}]^i$ can phosphorylate the 20,000 dalton myosin light chain $(MLC_{20})$ by activating MLC kinase (MLCK), and this initiates smooth muscle contraction. In addition to the $[Ca^{2+}]_i$MACK-tension pathway, a number of intracellular signal molecules, including mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and others, play important roles in the regulation of smooth muscle contraction. However, the mechanisms regulating contraction of depletion of SR $Ca^{2+}$ in mouse gastric smooth muscle strips is not still clear. Methods: To investigate the rotes of $Ca^{2+}$ influx and SR $Ca^{2+}$ release channel on gastric motility, isometric contraction and $[Ca^{2+}]_i$ were examined in mouse gastric smooth muscle strips. Results: High KCl, ryanodine, an activator of $Ca^{2+-}$induced $Ca^{2+}$ release channel, and cyclopiazonic acid (CPA), an inhibitor of SR $Ca^{2+-}$ATPase evoked a sustained increase in muscle contraction and $[Ca^{2+}]_i$. These increases induced by high KCl, ryanodine, and CPA were partially blocked by application of verapamil ($10{\mu}M$), a L-type $Ca^{2+}$ channel inhibitor. Additionally, in $Ca^{2+-}$free solution (1 mM EGTA), ryanodine and CPA had no effect contraction and $[Ca^{2+}]_i$ in fundic muscle strips. Conclusion: These results that extracellular $Ca^{2+}$ influx and depletion of SR trigger $Ca^{2+}$ influx through verapamil-sensitive $Ca^{2+}$ channel, and extracellular and SR $Ca^{2+}$ store may functionally involve in the subcellular $Ca^{2+}$ mobilization in mouse gastric muscle.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.3
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• pp.211-217
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• 2000

Paxillin is a regulatory component of the complex of cytoskeletal proteins that link the actin cytoskeleton to the plasma membrane. However, the role of paxillin during smooth muscle contraction is unclear. We investigated a possible role for the membrane-associated dense plaque protein paxillin in the regulation of contraction in rat aortic vascular smooth muscle. The tyrosine phosphorylation of paxillin, which was increased by norepinephrine, reached a peak level after 1 min stimulation and then decreased with time. However, norepinephrine induced a sustained contraction that reached a steady state 30 min after application. Pretreatment with tyrphostin, an inhibitor of tyrosine kinase, inhibited the tyrosine phosphorylation of paxillin and also the contraction stimulated by norepinephrine. Both inhibitions were concentration-dependent, and the degree of correlation between them was high. These results show that, in rat aortic smooth muscle, tyrosine kinase(s) activated by norepinephrine may phosphorylate the tyrosine residues of paxillin, thereby providing a source of regulation during vascular smooth muscle contraction.

• Korean Journal of Veterinary Research
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• v.34 no.3
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• pp.471-478
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• 1994

Effects of histamine on the ruminal smooth muscle motility of cattle were investigated in the longitudinal and circular smooth muscle strips. In order to these experiments, specimens were obtained from 35 korean native cattles, 3-4 years old, in Kwang-ju area slaughterhouse. Smooth muscle strips of rumen were made from sample, and then measured the isometric contraction with physiograph in $37{^{\circ}C}$ organ bath. The results were as follows : 1. Histamine caused two different types of response(a contraction or a relaxation) on the smooth muscle of cattle rumen. These responses increased in dose dependant manner. 2. Pyrilamine($H_1$-receptor antagonist) completely blocked contraction in all the preparation and converted the response into relaxation. 3. Cimetidine($H_2$-receptor antagonist) completely blocked relaxation in all the preparation and converted the response into contraction. 4. The contraction induced by histamine($10^{-3}M$) was not Mocked by cholinergic, adrenergic blocker or hexamethonium. 5. The contraction induced by histamine($10^{-3}M$) was markedly inhibited in the $Ca^{2+}$ free(or EDTA 2Na) Kreb's solution and by verapamil.

• Journal of Korean Physical Therapy Science
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• v.11 no.1
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• pp.20-27
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• 2004

It is widely accepted that smooth muscle contraction is triggered by intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) released from intracellular $Ca^{2+}$ stores such as sarcoplasmic reticulum (SR) and from the extracellular space, The increased $[Ca^{2+}]_i$ can phosphorylate the 20-kDa myosin light chain ($MLC_{20}$) by activating MLC kinase (MLCK), and this initiates smooth muscle contraction. In addition to the $[Ca^{2+}]_i$-MLCK-tension pathway, a number of intracellular signal molecules, including mitogen-activated protein kinase (MAPK), protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), and Rho-associated coiled coil-forming protein kinase (ROCK), play important roles in the regulation of smooth muscle contraction. However, the mechanisms regulating contraction of caldesmon (CaD), actin-binding protein, are not entirely elucidated in the presence of $Ca^{2+}$. It is known that CaD tightly interacts with actin and inhibits actomyosin ATPase activity. Therefore, the purpose of the present study was to investigate the roles of $Ca^{2+}$-dependent CaD in smooth muscle contraction. Endothelin-1 (ET-1), G-protein coupled receptor agonist and vasoconstrictor, increased both vascular smooth contraction and phosphorylation of CaD in the presence of $Ca^{2+}$. These results suggest that ET-1 induces contraction and phosphorylation of CaD in rat aortic smooth muscle, which may he mediated by the increase of $[Ca^{2+}]_i$.

• Archives of Pharmacal Research
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• v.21 no.3
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• pp.315-319
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• 1998

Gastric smooth muscle of cats was used to investigate the involvement of protein kinase in vanadate-induced contraction. Vanadate caused a contraction of cat gastric smooth muscle in a dose-dependent manner. Vanadate-induced contraction was totally inhibited by 2 mM EGTA and 1.5 mM $LACI_3$ and significantly inhibited by $10\mu$M verapamil and $1\mu$M nifedipine, suggesting that vanadate-induced contraction is dependent on the extracellular $Ca^{2+}$ concentration, and the influx of extracellular $Ca^{2+}$ was mediated through voltage-dependent $Ca^{2+}$ channel. Both protein kinase C inhibitor and tyrosine kinase inhibitor significantly inhibited the vanadate-induced contraction and the combined inhibitory effect of two protein kinase inhibitors was greater than that of each one. But calmodulin antagonists did not have any influence on the vanadate-induced contraction. On the other hand, both forskolin ($1\mu$M) and sodium nitroprusside ($1\mu$M) significantly inhibited vanadate-induced contraction. Therefore, these results suggest that both protein kinase C and tyrosino kinase are involved in the vanadate-induced contraction which required the influx of extracellular $Ca^{2+}$ in cat gastric smooth muscle, and that the contractile mechanism of vanadate may be different from that of agonist binding to its specific receptor.

• The Journal of Internal Korean Medicine
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• v.13 no.1
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• pp.124-134
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• 1992

Effects of Haenginbanhatang Extract on the Contraction of Isolated Guinea Pig Trachea Smooth Muscle. This study was carried out to investigate the effect of Haenginbanhatang extract on the contractile force of the isolated guinea pig trachea smooth muscle and elucidate its mechanism. The results were obtained as follows: 1. The contratile response of the trachea smooth muscle of the guinea pig to histamine was significantly inhibited by Haenginbanhatang. 2. Effects of Haenginbanhatang extract on the contractile response of the isolated guinea pig smooth muscle pretreated propranolol was not significant. 3. The contractile response of isolated guinea pig smooth muscle pretreated methylene blue was significantly inhibited by Haenginbanhatang, 4. The contractile response of the trachea smooth muscle of the guinea pig to prostaglandin F2a was significantly inhibited by Haenginbanhatang. 5. Effect of prostaglandin F2a on the contractile response of guinea pig smooth muscle pretreated Haenginbanhatang was not significant. According to the above results, it was suggested that the contractile response mechanism of the guinea pig smooth muscle to Haenginbanhatang was related to cyclic GMP.

• Biomolecules & Therapeutics
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• v.27 no.1
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• pp.101-106
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• 2019

Most diabetic patients experience diabetic mellitus (DM) urinary bladder dysfunction. A number of studies evaluate bladder smooth muscle contraction in DM. In this study, we evaluated the change of bladder smooth muscle contraction between normal rats and DM rats. Furthermore, we used pharmacological inhibitors to determine the differences in the signaling pathways between normal and DM rats. Rats in the DM group received an intraperitoneal injection of 65 mg/kg streptozotocin and measured blood glucose level after 14 days to confirm DM. Bladder smooth muscle contraction was induced using acetylcholine (ACh, $10^{-4}M$). The materials such as, atropine (a muscarinic receptor antagonist), U73122 (a phospholipase C inhibitor), DPCPX (an adenosine $A_1$ receptor antagonist), udenafil (a PDE5 inhibitor), prazosin (an ${\alpha}_1$-receptor antagonist), papaverine (a smooth muscle relaxant), verapamil (a calcium channel blocker), and chelerythrine (a protein kinase C inhibitor) were pre-treated in bladder smooth muscle. We found that the DM rats had lower bladder smooth muscle contractility than normal rats. When prazosin, udenafil, verapamil, and U73122 were pre-treated, there were significant differences between normal and DM rats. Taken together, it was concluded that the change of intracellular $Ca^{2+}$ release mediated by PLC/IP3 and PDE5 activity were responsible for decreased bladder smooth muscle contractility in DM rats.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.248.1-248.1
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• 2002

It has been shown that C2-ceramide (C2), short chain ceramide, plays a role in mediating contraction of cat esophageal smooth muscle cells. We examined the effect of newly synthesized ceramide analogues on the C2-ceramide induced contraction in esophageal smooth muscle cells isolated with collagenase. C2-ceramide produced contraction of smooth muscle cells in a dose dependent manner. (omitted)

• The Journal of Internal Korean Medicine
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• v.19 no.1
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• pp.385-408
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• 1998

Pyeongpaesan (平肺散) has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Pyeongpaesan (平肺散) on tracheal smooth muscle is not known. The purpose of the present study is to determine the effect of Pyeongpaesan (平肺散) on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig (500 g, male) and Sprague Dawley rats (200 g, male) were killed by $CO_2$ exposure and a segment (8-10 mm) of the thoracic trachea from each rat and guinea pig was cut into equal segments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force displacement transducers under 0.5 g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response ($ED_{50}$) was obtained from cumulative dose response curves for histamine and acetylcholine $(10^{-7}{\sim}10^{-4}M)$. Contractions evoked by His $(ED_{50})$ and Ach $(ED_{50})$ were inhibited significantly by Pyeongpaesan (平肺散). In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was 13.5% (p<0.05) after $10{\mu}l/ml$ Pyeongpaesan (平肺散), $64.6\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散), and $92.8\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $60.9\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散), and $91.2\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $104.8\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散) and $142.3\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $63.7\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散), and $107.5\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). Propranolol $(10^{-7}M)$ slightly but significantly attenuated the inhibitory effects of Pyeongpaesan (平肺散). Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$ Pyeongpaesan (平肺散) fell to 15.7% (p<0.05) in guinea pig induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Pyeongpaesan (平肺散) fell to 22.3% (p<0.05) in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Pyeongpaesan (平肺散) fell to 28.7% (p<0.01) in rat induced by histamine contraction. Indomethacin and methylene blue $(10^{-7}\;M)$ did not significantly alter the inhibitory effect of Pyeongpaesan (平肺散). Also, I could find the effects of Pyeongpaesan (平肺散) and Pyeongpaesanga (平肺散加) morphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Pyeongpaesan. (平肺散) can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects and the release of cyclooxygenase products.