Journal of Smooth Muscle Research最新文献

{"title":"Effects of EMD57033, an activator of actomyosin ATPase activity, on the relaxation process of cell membrane-permeabilized carotid artery and taenia cecum from guinea pigs.","authors":"Yasuyuki Naraki, Masaru Watanabe","doi":"10.1540/jsmr.61.1","DOIUrl":"10.1540/jsmr.61.1","url":null,"abstract":"<p><p>Smooth muscle relaxation after contraction is thought to reflect \"latch-like\" slow cycling bridge formation and deformation. However, how actin-myosin interaction contributes to the transfer from fast-cycling cross bridges to slow-cycling bridges is still unclear. The thiadiazinone compound EMD57033 is known to bind to an allosteric pocket in the myosin motor domain and to increase basal and actin-activated myosin ATPase activity and contractile force in striated muscles. Therefore, we investigated whether EMD57033 affected the relaxation process after Ca²⁺ removal by affecting slow cycling bridge formation and/or deformation in β-escin skinned (cell membrane-permeabilized) carotid artery and taenia cecum from guinea pigs. EMD57033 at ≥30 µM decreased the force decay during relaxation in both the skinned carotid artery and taenia cecum, irrespective of the presence of ATP. A kinetic analysis in the present study indicated that EMD57033 significantly prolonged τslow-detach, a time constant of detachment of the slow cycling bridge, in both the skinned carotid artery and taenia cecum, irrespective of the presence of nucleoside triphosphates (ATP or ITP). Further studies are necessary to elucidate how EMD57033 modulates the smooth muscle myosin (SMM) structure, SMM activity, and thick filament organization, affecting slow cycling bridge formation and deformation, although EMD57033 might change slow cycling bridge formation, resulting in both cycling rate modulation and an increase in the affinity of SMM to actin.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"61 ","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11840141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histamine-induced cytosolic calcium mobilization in human bronchial smooth muscle cells.","authors":"Kyung Jin Choi, Woo Young Jeon, Mee Young Lee, Se Hoon Kim, Hyung Seo Park","doi":"10.1540/jsmr.61.29","DOIUrl":"https://doi.org/10.1540/jsmr.61.29","url":null,"abstract":"<p><p>Histamine is a well-known mediator of bronchoconstriction. Despite the widespread use of histamine as a tool to study the bronchial smooth muscle function, the precise mechanism by which it causes calcium mobilization in bronchial smooth muscle cells remains unclear. Therefore, the current study aimed to investigate the mechanism of action of histamine in calcium mobilization in cultured human bronchial smooth muscle cells. A series of in vitro calcium imaging experiments have shown that histamine increases intracellular calcium levels in a concentration-dependent manner. The half maximum concentration of cytosolic Ca²⁺ peak was 3.00 ± 0.25 µM of histamine. Histamine was able to mobilize calcium from intracellular stores, even in the absence of extracellular calcium. These histamine-induced calcium elevations were completely blocked by the H₁ receptor antagonist chlorpheniramine (1 µM). Histamine-induced calcium elevation was also completely inhibited by the phospholipase C (PLC) inhibitor U73122 (1 µM) and inositol 1,4,5-trisphosphate (InsP₃) receptor inhibitor caffeine (20 mM). Cyanide p-(trifluoromethoxy)phenylhydrazone (1 µM) and oligomycin (1 µg/ml) effectively attenuated histamine-induced calcium release from intracellular stores. In the presence of histamine, cytosolic calcium elevation induced by reperfusion of 1.28 mM extracellular calcium after the depletion of stores was significantly inhibited by FCCP and oligomycin, unlike in the presence of thapsigargin. Based on the above results, we can conclude that histamine activates the intracellular PLC/InP₃ pathway through the H₁ receptor, which in turn activates the InP₃ receptor present in intracellular stores to mobilize calcium in human bronchial smooth muscle cells. In addition, the mitochondria appear to be involved in the release of calcium from intracellular stores. These results provide insights into the mechanisms underlying histamine-induced calcium mobilization for bronchoconstriction under pathophysiological conditions.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"61 ","pages":"29-42"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11996695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular and molecular mechanisms underlying aging-related gastric neuromuscular dysfunction.","authors":"Yuebo Zhang, Egan L Choi, Yujiro Hayashi","doi":"10.1540/jsmr.61.43","DOIUrl":"10.1540/jsmr.61.43","url":null,"abstract":"<p><p>Aging is linked to a gradual decline in the gastric motor function, contributing to reduced food intake, and its association with frailty and sarcopenia. A key cellular change in the gastric neuromuscular apparatus is the loss of interstitial cells of Cajal (ICC), pacemaker cells of the gut. The ICC function as pacemakers that generate electrical slow waves and mediate enteric neurotransmission, playing a critical role in gastric motility. Aging-related ICC depletion leads to impaired gastric compliance and reduced slow wave activity, which contributes to early satiety and reduced food intake. Recent studies have elucidated the molecular and epigenetic mechanisms underlying aging-related ICC decline, highlighting the roles of ICC stem/precursor cells (ICC-SCs), transformation-related protein 53 (TRP53), extracellular signal-regulated kinase (ERK), and insulin-like growth factor 1 (IGF1) pathways, and epigenetic regulation mediated by the histone methyltransferase enhancer of zeste 2 (EZH2). By synthesizing the current findings, this review aims to provide a comprehensive understanding of the mechanisms driving ICC decline and to explore potential therapeutic strategies for preserving gastric motility in aging populations. Future research should aim to translate these discoveries into clinical applications to improve the gastric motor function and overall health in the aging population. Identifying effective interventions targeting ICC maintenance may ultimately help to alleviate age-related gastric motor dysfunction and its associated health burdens, including frailty, malnutrition, and impaired quality of life.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"61 ","pages":"43-50"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11996696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gastric emptying after distal gastrectomy from physiologic viewpoint: accelerated or delayed?","authors":"Chikashi Shibata, Kentaro Sawada, Atsushi Mitamura, Toru Nakano","doi":"10.1540/jsmr.61.20","DOIUrl":"10.1540/jsmr.61.20","url":null,"abstract":"<p><p>Distal gastrectomy is the most frequently performed procedure for gastric cancer. Gastric emptying after distal gastrectomy is generally considered to be accelerated due to resection of the antrum, pylorus, and duodenal bulb. Food residue, however, is frequently observed in the gastric remnant in patients after distal gastrectomy at the time of endoscopy after routine overnight fasting. This observation suggests delayed gastric emptying and conflicts with the general understanding of accelerated gastric emptying after distal gastrectomy. We searched for reports that evaluated the separate gastric emptying of liquids and solids with scintigraphy after distal gastrectomy in humans and also addressed the physiologic changes in gastric emptying after distal gastrectomy. Most all reports showed that gastric emptying of liquids after distal gastrectomy was accelerated compared to healthy controls, especially immediately after feeding. In contrast, some gastric emptying of solids was accelerated early after the meal ingestion, but thereafter emptying of solids remaining in the stomach was delayed beginning about 60 min after the meal in patients after distal gastrectomy. This delayed solid gastric emptying after distal gastrectomy was considered associated with food residue in the remnant stomach. We conclude that gastric emptying after distal gastrectomy was accelerated for liquids and solids soon after the meal ingestion but delayed for solids later than 60 min after the meal ingestion.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"61 ","pages":"20-28"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11807776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of recent developments in the imaging of disorders of gut-brain interaction.","authors":"Noriaki Manabe, Masafumi Wada, Tsutomu Takeda, Emiko Bukeo, Hirotaka Tsuru, Mariko Hojo, Minoru Fujita, Eikichi Ihara, Akihito Nagahara, Takeshi Kamiya","doi":"10.1540/jsmr.61.11","DOIUrl":"10.1540/jsmr.61.11","url":null,"abstract":"<p><p>A number of factors have been recently associated with the development of disorders of gut-brain interaction (DGBI), including genetic predisposition, early-life environment, intestinal microbiota, infection, microinflammation, and increased mucosal permeability. In addition, impaired gastrointestinal motility is important not only as a cause of DGBI but also as a consequent final phenotype. Gastrointestinal motor measurements are the predominant method for the assessment of and therapeutic intervention into motor abnormalities. As such, these measurements should be considered for DGBI patients who do not respond to first-line approaches such as behavioral therapy, dietary modifications, and pharmacotherapy. This comprehensive review focuses on the functional changes in the upper gastrointestinal tract caused by DGBI and describes ongoing attempts to develop imaging modalities to assess these dysfunctions in the esophageal and gastric regions. Recent advances in imaging techniques could help elucidate the pathophysiology of DGBI, with exciting potential for research and clinical practice.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"61 ","pages":"11-19"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11807775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The critical role of muscularis macrophages in modulating the enteric nervous system function and gastrointestinal motility","authors":"Egan L. Choi, Negar Taheri, Yuebo Zhang, Kenjiro Matsumoto, Yujiro Hayashi","doi":"10.1540/jsmr.60.1","DOIUrl":"https://doi.org/10.1540/jsmr.60.1","url":null,"abstract":"Macrophages are the originators of inflammatory compounds, phagocytic purifiers in their local environment, and wound healing protectors in oxidative environments. They are molded by the tissue milieu they inhabit, with gastrointestinal (GI) muscularis macrophages (MMs) being a prime example. MMs are located in the muscular layer of the GI tract and contribute to muscle repair and maintenance of GI motility. MMs are often in close proximity to the enteric nervous system, specifically near the enteric neurons and interstitial cells of Cajal (ICCs). Consequently, the anti-inflammatory function of MMs corresponds to the development and maintenance of neural networks in the GI tract. The capacity of MMs to shift from anti-inflammatory to proinflammatory states may contribute to the inflammatory aspects of various GI diseases and disorders such as diabetic gastroparesis or postoperative ileus, functional disorders such as irritable bowel syndrome, and organic diseases such as inflammatory bowel disease. We reviewed the current knowledge of MMs and their influence on neighboring cells due to their important role in the GI tract.","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"54 13","pages":"1 - 9"},"PeriodicalIF":0.0,"publicationDate":"2024-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140077036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antispasmodic and antidiarrheal effects of Juniperus oxycedrus L. on the jejunum in rodents.","authors":"Ouafa Amrani, Ahmed Karim, Mohamed Marghich, Leila Beyi, Saliha Bouknana, Mohammed Aziz","doi":"10.1540/jsmr.60.10","DOIUrl":"10.1540/jsmr.60.10","url":null,"abstract":"<p><p>Functional bowel disorders (FBD) have a major potential to degrade the standards of public life. Juniperus oxycedrus L. (J. oxycedrus) (Cupressaceae) has been described as a plant used in traditional medicine as an antidiarrheal medication. The present study is the first to obtain information on the antispasmodic and antidiarrheic effects of J. oxycedrus aqueous extract through in vitro and in vivo studies. An aqueous extract of J. oxycedrus (AEJO) was extracted by decoctioning air-dried aerial sections of the plant. Antispasmodic activity was tested in an isolated jejunum segment of rats exposed to cumulative doses of drogue extract. The antidiarrheic activity was tested using diarrhea caused by castor oil, a transit study of the small intestine, and castor oil-induced enteropooling assays in mice. In the jejunum of rats, the AEJO (0.1, 0.3 and 1 mg/ml) diminished the maximum tone induced by low K⁺ (25 mM), while it exhibited a weak inhibitory effect on high K⁺ (75 mM) with an IC₅₀=0.49 ± 0.01 mg/ml and IC₅₀=2.65 ± 0.16 mg/ml, respectively. In the contractions induced by CCh (10^-6 M), AEJO diminished the maximum tone, similar to that induced by low K⁺ (25 mM). with an IC₅₀=0.45 ± 0.02 mg/ml. The inhibitory effect of AEJO on low K⁺ induced contractions was significantly diminished in the presence of glibenclamide (GB) (0.3 µM) and 4-aminopyrimidine (4-AP) (100 µM), with IC₅₀ values of 1.84 ± 0.09 mg/ml. and 1.63 ± 0.16 mg/ml, respectively). The demonstrated inhibitory effect was similar to that produced by a non-competitive antagonist acting on cholinergic receptors and calcium channels. In castor oil-induced diarrhea in mice, AEJO (100, 200, and 400 mg/kg) caused an extension of the latency time, a reduced defecation frequency, and a decrease in the amount of wet feces compared to the untreated group (distilled water). Moreover, it showed a significant anti-motility effect and reduced the amount of fluid accumulated in the intestinal lumen at all tested doses. These findings support the conventional use of Juniperus oxycedrus L. as a remedy for gastrointestinal diseases.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"60 ","pages":"10-22"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11109480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141082633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of detrusor underactivity with aging and metabolic syndrome: suggestions from animal models.","authors":"Shogo Shimizu","doi":"10.1540/jsmr.60.23","DOIUrl":"10.1540/jsmr.60.23","url":null,"abstract":"<p><p>Detrusor underactivity, a condition in which the bladder muscle does not contract strongly or long enough to empty the bladder completely or within the normal time frame, is a common cause of lower urinary tract symptoms in older individuals of both sexes. Although aging is a known risk factor for detrusor underactivity, its pathophysiological mechanisms are not fully understood. Therefore, establishing animal models that closely mimic the pathophysiology of detrusor underactivity in humans is necessary to elucidate these mechanisms. Metabolic syndrome is a cluster of several risk factors, including obesity, hyperlipidemia, hyperglycemia, and hypertension, which are associated with the development of diabetes, cardiovascular disease, and lower urinary tract dysfunction in both sexes. Notably, bladder dysfunction resulting from detrusor underactivity is observed at an earlier age in animal models with diabetes mellitus than in those without. Recently, detrusor underactivity-like phenotypes have been observed at a relatively early age in animal models with metabolic syndrome, involving obesity, hyperlipidemia, and hypertension, compared with those without. Therefore, this review introduces the association of detrusor underactivity with aging and metabolic syndrome, as well as possible pathophysiological mechanisms for detrusor underactivity from reports of various animal models. Notably, metabolic syndrome may accelerate the onset of age-related detrusor underactivity, and further analysis of old animal models with metabolic syndrome may help elucidate the pathogenesis of detrusor underactivity in humans.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"60 ","pages":"23-30"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11291108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naloxone selectively inhibits vasoconstriction caused by phenylephrine but not endogenous noradrenaline in the rat mesenteric vasculature.","authors":"Muneaki Hidaka, Takayuki Matsumoto, Takayuki Nagano, Ryuichi Yamamoto, Naoko Tanaka-Totoribe","doi":"10.1540/jsmr.60.54","DOIUrl":"10.1540/jsmr.60.54","url":null,"abstract":"<p><p>Although naloxone is an antagonist of the opioid µ receptor, its effect on the peripheral sympathetic nerve function in the blood vessels has not yet been definitively elucidated. Therefore, we examined the effects of naloxone on vasoconstriction of the vascular smooth muscle of rats. Isolated rat mesenteric vascular-intestinal loop preparations were treated with either endogenous or exogenous α₁ adrenoceptor agonists followed by prazosin, a selective antagonist of the α₁ adrenoceptor, or naloxone, and noradrenaline overflow was measured. Vasoconstriction caused by peri-arterial nerve stimulation (PNS) and phenylephrine, an exogenous agonist of the α₁ adrenoceptor, was abolished by prazosin. However, prazosin did not affect PNS-induced endogenous noradrenaline overflow. Naloxone did not affect either PNS-induced endogenous noradrenaline overflow or vasoconstriction. However, naloxone did inhibit phenylephrine-induced vasoconstriction. In addition, naloxone did not affect the angiotensin II-induced vasoconstriction. These results demonstrate that naloxone selectively inhibits vasoconstriction caused by phenylephrine, but not vasoconstriction caused by endogenous noradrenaline released from sympathetic nerve cells in the rat mesenteric vasculature.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"60 ","pages":"54-63"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antidiarrheal and antispasmodic effects of methanol fraction of Ammodaucus leucotrichus in gastrointestinal problems: an integrative medicine approach.","authors":"Ahmed Karim, Sanae Malek, Mohamed Marghich, Ouafa Amrani, Abdelhay Addous, Leila Beyi, Mohammed Aziz","doi":"10.1540/jsmr.60.39","DOIUrl":"10.1540/jsmr.60.39","url":null,"abstract":"<p><p>Diarrhea is the second leading cause of death in children under five years of age globally. Traditional medicinal practices often use plants to manage gastrointestinal issues. Ammodaucus leucotrichus is a medicinal plant that holds significant importance in Moroccan traditional medicine for treating gastrointestinal problems. This study aimed to validate the traditional use of A. leucotrichus by providing scientific evidence for its efficacy. We evaluated the effectiveness of the methanol fraction of A. leucotrichus in alleviating diarrhea and reducing smooth muscle contractions using comprehensive in vivo and in vitro models. In vitro experiments were performed using an isotonic transducer in the jejunum of rats and rabbits. In vivo antidiarrheal effects were evaluated in mice with castor oil-induced diarrhea. The methanol fraction of A. leucotrichus (MFAl) inhibited diarrhea in a dose-dependent manner. It also exhibited spasmolytic activity at doses ranging from 5.5 to 65 μg/ml, with IC₅₀ values of 43.43 ± 2.63 μg/ml for potassium chloride (KCl) and 28.91 ± 0.43 μg/ml for carbachol (CCh). The obtained spasmolytic activities were comparable to those of a non-competitive antagonist of calcium channels and muscarinic receptors by rightward and downward shifts in the concentration-response curves for calcium and carbachol. Our results demonstrate that, with the addition of nifedipine, the spasmolytic effect of MFAl decreased by 70.11%. This indicates that the spasmolytic effect of MFAl is possibly mediated by the inhibition of Ca²⁺ influx. In addition, the presence of hexamethonium significantly modified the relaxation effect of MFAl by 46.20%, indicating that MFAl also acts through nicotinic receptors. These findings support the traditional use of A. leucotrichus for gastrointestinal disorders and highlight the need for further research to develop new anti-diarrheal and anti-spasmodic treatments.</p>","PeriodicalId":39619,"journal":{"name":"Journal of Smooth Muscle Research","volume":"60 ","pages":"39-53"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}