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PubMed1978

The generation and conduction of activity in smooth muscle.

Smooth muscle, especially gastrointestinal smooth muscle, spontaneously generates oscillatory electrical activity that can control contractions in time and space by altering excitability. The origin and ionic mechanisms underlying these electrical control activities are still controversial, but they behave as coupled relaxation oscillators and they control muscle excitability. Normally, contractions are produced by the addition, during the depolarized phase of the oscillations, of further depolarization by acetylcholine or other means. Pharmacologists who wish to study drug actions on such muscles must be aware of the possibility that drug effects may be determined by these oscillations and may influence contractions by affecting these oscillations as well as by releasing, mimicking, or inhibiting the effects of nerve mediators or by affecting excitation-contraction coupling. Also the use of simplified organ bath preparations may eliminate or alter these control potentials so that results in vitro may not apply in vivo.

Animals↗
PubMed1975

Antiphosphodiesterase activity and nonspecific smooth muscle relaxation tested on intestinal smooth muscles.

Mitochondrial, microsomal and soluble fractions separated from the guinea pig taenia and from the dog longitudinal smooth muscle were used as phosphodiesterase preparation. Each preparation had low and high Km values, indicating the existence of at least two kinds of phosphodiesterase. Papaverine and Aspaminol (1, 1-diphenyl-3-piperidinobutanol hydrochloride), hydralazine, caffeine Na benzoate and aminophylline were used at test drugs. Aspaminol had little inhibitory effect on phosphodiesterase. Ki value of papaverine almost equalled the concentration (M) which was necessary to produce 50% relaxation. Relaxation of the guinea pig taenia by papaverine was preceded by an increase of intracellular cyclic AMP,. Therefore, the action of papaverine is likely to be mediated by an increase in cyclic AMP, which is caused by inhibition of the phosphodiesterase-catalyzed breakdown of cyclic AMP. There was little correlation between relaxing activities of the drugs used and their antiphosphodiesterase activities. Relaxation of the smooth muscle induced by the smooth muscle relaxants excepting papaverine is not due to inhibition of phosphodiesterase.

Animals↗
PubMed1979

Role of calcium and cyclic adenosine 3':5' monophosphate in regulating smooth muscle contraction. Mechanisms of excitation-contraction coupling in smooth muscle.

Caclium initiates smooth muscle contraction by activating an enzyme, myosin light chain kinase. This enzyme catalyzes the transfer of phosphate from adenosine triphosphate to the 20,000 dalton light chain of myosin. In its phosphorylated form myosin interacts with actin to produce muscle contraction. The mechanism by which calcium activates myosin kinase requires (1) the binding of calcium to a 16,500 dalton calcium-binding protein (calmodulin), and (2) the binding of calmodulin-calcium to a 125,000 dalton catalytic subunit. This two protein complex is the active form of myosin light chain kinase. Smooth muscle relaxation is mediated by cyclic adenosine 3':5' monophosphate (cyclic AMP). One nechanism by which the latter may exert a direct effect on actin-myosin interaction is through the activation of a cyclic AMP-dependent protein kinase that can phosphorylate the 125,000 dalton component of myosin light chain kinase. Phosphorylation of myosin light chain kinase decreases the activity of the enzyme, thus favoring the unphosphorylated form of myosin, which cannot interact with actin to produce smooth muscle contraction.

Actins↗
PubMed1979

Responsiveness to insulin of glucose metabolism in cultured rat and human arterial smooth muscle cells.

Smooth muscle cells growing in the primary culture derived from outgrowths of the intimal-medial explants of both rat and human arteries were used. The 72-hr sequential glucose uptake by the cells of both species in culture dishes was enhanced only slightly with time by the addition of insulin to culture medium, and this enhancement was statistically not significant. The glucose conversions to CO2 and lipids by the rat and human cells dissociated for tracer study were not affected significantly during the 2-hr incubation by the insulin addition in vitro. The smooth muscle cells of both species cultured for a week in medium enriched with insulin and then dissociated revealed the significantly increased glucose conversion to lipids, while the increase in the glucose coversion to CO2 was not significant in these cells. Thus, the smooth muscle cells of both rat and human seem to show significant metabolic response to chronic, but not acute, exposure to insulin. Therefore, it is likely that the persistent change in the insulin level may lead to abnormal metabolic state in the artery.

Animals↗
PubMed1979

Glycoprotein, elastin, and collagen secretion by rat smooth muscle cells.

Smooth muscle cells from rat heart secreted extracellular matrix components at high rates for many generations in culture. The matrix proteins remained anchored to the culture dish and were characterized after removal of cellular material with sodium dodecyl sulfate. Sequential enzyme digestion demonstrated the presence of at least three components, including glycoprotein(s), elastin, and collagen. Prolonged extraction of the matrix with detergent under reducing conditions solubilized a fucosylated glycoprotein having an apparent molecular weight of 250,000 and two other proteins with molecular weights of 72,000 and 45,000, respectively. Sublines derived from discrete colonies of smooth muscle cells synthesized all of the matrix components, and the proportion of collagen secreted by some sublines increased with time in culture. The biosynthesis of a mixed extracellular matrix and the relationships among the component proteins were therefore studied in one system producing milligram quantities of material.

Animals↗
PubMed1977

Distinction between smooth muscle, fibroblasts and endothelial cells in culture by the use of fluoresceinated antibodies against smooth muscle actin.

FITC-labelled antibodies against native actin from chicken gizzard smooth muscle (Gröschel-Stewart et al., 1976) have been used to stain cultures of guinea-pig vas deferens and taenia coli, rabbit thoracic aorta, rat ventricle and chick skeletal muscle. The I-band of myofibrils of cardiac muscle cells and skeletal muscle myotubes stains intensely. In isolated smooth muscle cells, the staining is located exclusively on long, straight, non-interrupted fibrils which almost fill the cell. Smooth muscle cells which have undergone morphological "dedifferentiation" to resemble fibroblasts with both phase-contrast microscopy and electronmicroscopy still stain intensely with the actin antibody. In those muscle cultures which contain some fibroblasts or endothelial cells, the non-muscle cells are not stained with the actin antibody even when the reactions are carried out at 37 degrees C for 1 h or after glycerination. Prefusion skeletal muscle myoblasts also do not stain with this antibody. It is concluded that the actin antibody described in this report is directed against a particular sequence of amino acids in muscle actin which is not homologous with non-muscle actin. The usefulness of this antibody in determining the origin of cells in certain pathological conditions such as atherosclerosis is discussed.

Actins↗
PubMed1975

Effect of insulin on the proliferation of cultured primate arterial smooth muscle cells.

Smooth muscle cells were grown from thoracic aortas of 1-year-old monkeys (Macaca nemistrina). The effect of insulin on the proliferation of these cells was studied by comparing the growth of cells in culture medium to which insulin had been added with that of cells in basal (1% monkey serum) medium and in growth-promoting 5% monkey serum. Insulin in concentrations of 10, 100, 1,000, and 10,000 muunits/ml resulted in successively greater stimulation of growth which was highly significant (P smaller than 0.001) by analysis of variance. There was a significant linear relationship between the logarithm of the insulin dose and cell growth. However, the highest concentration of insulin produced only 50% of the effect of 5% monkey serum. Serum from which insulin had been removed stimulated growth less well (P smaller than 0.05) than did untreated serum at the same concentration (5%) but had significant (P smaller than 0.05) stimulating properties compared with whole serum at a lower concentration. Cells that were older in culture life (eight or nine passages) did not show a growth response to insulin and had an attenuated response to 5% serum. The effect of insulin (100 muunits/ml) was inhibited by dibutyryl cyclic adenosine monophosphate (db-cAMP) (5 times 10-5 M), although there was a latent period of 3 days before inhibition occurred; db-cAMP had no effect on cell counts in the absence of insulin. The electron microscopic appearance of the cells was unaltered by insulin.

Analysis of Variance↗
PubMed1975

[Studies of in vitro cultivated cells from the smooth muscle organs. 3. Effectiveness of some drugs on pulsation frequency of isolated smooth muscle cells of the chicken amnion].

The effects of some drugs on the beating frequency of isolated cells of the chick amnion cultivated on cover slips were investigated. Cholinergic and adrenergic agonists and antagonists, serotonine, antispasmodics, coronary dilatants and local anesthetics influenced the beating frequency significantly. The isolated chick amnion cells equal in their pharmacological behaviour the intact chick amnion and smooth muscle cells of mammals but differ from isolated beating heart cells.

Adrenergic beta-Antagonists↗
PubMed2026

Structural and functional gastrointestinal abnormalities in ACTA2 R179H mice modeling multisystemic smooth muscle dysfunction syndrome.

Multisystemic smooth muscle dysfunction syndrome (MSMDS) is a rare disorder caused by ACTA2 mutations, including the R179H variant, which alters actin filament stability and dynamics and smooth muscle contractility. Cardiovascular complications dominate its clinical presentation, but gastrointestinal (GI) dysfunction significantly affects quality of life. To investigate the structural, functional, and cellular basis of gut dysmotility in MSMDS, we reviewed clinical data from 24 patients with MSMDS and studied the ACTA2 R179H mouse model. Patients exhibited severe gut dysmotility, with 75% requiring medication for chronic constipation. ACTA2 mutant mice displayed cecal and colonic dilatation, reduced intestinal length, and disrupted colonic migrating motor complexes. Delayed whole-gut transit and impaired contractile responses to electrical and pharmacological stimulation were observed. Transcriptomic analysis revealed significant actin cytoskeleton-related gene changes in smooth muscle cells, and immune profiling identified increased lymphocytic infiltration. Despite functional abnormalities, there were no obvious changes in the enteric nervous system. These findings establish ACTA2 mice as a robust model for studying GI pathology in MSMDS, elucidating the role of smooth muscle dysfunction in gut dysmotility. This model provides a foundation for developing targeted therapies aimed at restoring intestinal motility by directly addressing actin cytoskeletal disruptions in smooth muscle cells.

Animals↗
PubMed1979

Smooth muscle autoantibodies and autoantigens.

Smooth muscle autoantibody (SMA) was first found in the sera of patients with chronic active hepatitis and subsequently in the sera of patients with other autoimmune liver diseases, viral infections, certain cancers, heroin addicts and female infertility. SMA from patients with chronic active hepatitis reacts with many muscle and 'non-muscle' tissues while SMA from patients with other diseases usually reacts only with smooth muscle. These differences in immunofluorescent staining reactions suggest that SMA is a heterogeneous group of autoantibodies reactive with different smooth muscle autoantigens. As further evidence for this are findings that broad-reacting SMA can be absorbed out by actin, whereas autoantibodies reactive only with smooth muscle cannot, and that different SMAs give different immunofluorescent staining patterns using fibroblasts in tissue culture. Such staining patterns correspond to reactivity with either microfilaments, microtubules or intermediate filaments, ubiquitous cytoplasmic structures which make up the 'cytoskeleton'. Autoantibodies to actin-like microfilaments appear specific for chronic active hepatitis, autoantibodies to microtubules occur in infectious mononucleosis whereas autoantibodies to intermediate filaments occur in infectious hepatitis, chickenpox, measles and mumps. Predictably, future studies will show that presence of SMA with specificities for other proteins in the three types of cytoplasmic filaments, and given more information on antigenicity of the proteins and pathogenicity of the corresponding autoantibodies.

Actins↗
PubMed1975

Trophic influences of sympathetic nerves and cyclic AMP on differentiation and proliferation of isolated smooth muscle cells in culture.

Smooth muscle cells of the newborn guinea-pig vas deferens dispersed into single cells and grown in culture maintain their differentiation for approximately 5 days before undergoing dedifferentiation and mitosis. The presence of sympathetic nerve fibres in contact with the isolated cells delays this process by 3-7 days (Chamley et al., 1974). A similar delay in dedifferentiation of vas deferens smooth muscle cells in tissue culture in the presence of sympathetic ganglion extract is described in the present report, demonstrating that the trophic effect is elicited by a chemical substance. This effect is mimicked by the presence of either a confluent layer of RKA epithelial cells, dibutyryl cyclic AMP or theophylline. A similar, but considerably weaker, effect is also obtained with spinal cord and liver extracts and noradrenaline. Acetylcholine does not show an effect. It is suggested that a trophic substance (probably not noradrenaline) from sympathetic neurons activates the adenyl cyclase system of smooth muscle cells to increase the intracellular level of cyclic AMP which in turn promotes and maintains the differentiation of the cultured smooth muscle cells.

Acetylcholine↗
PubMed1979

Interaction of acetylcholine and cholecystokinin with dispersed smooth muscle cells.

Isolated gastric smooth muscle cells were prepared from the stomach of Bufo marinus by successive incubation in collagenase without added trypsin. Contraction was determined by image-splitting micrometry and expressed as the mean percentage decrease in cell length from control. Peak contractile response was attained within 30 s. Dose-response curves constructed from peak responses showed that the maximal responses to CCK-OP (37.2 +/- 3.8%), acetylcholine (35.3 +/- 2.5%), and Ca2+ (42.3 +/- 0.9%) were similar. The D50s for octapeptide of cholecystokinin (CCK-OP) and acetylcholine were around 10(-12) M and 10(-11) M, respectively. The response to a combination of submaximal concentrations of acetylcholine and CCK-OP exceeded the individual responses but did not exceed the maximal response to either agent alone. A low concentration of atropine (5 X 10(-10) M) inhibited specifically the maximal response to acetylcholine. A high concentration of atropine (5 X 10(-8) M) inhibited partially the maximal response to CCK-OP but had no effect on the maximal response to Ca2+. It was concluded that 1) dispersed gastric smooth muscle cells are highly sensitive to stimulation; 2) CCK-OP has a direct (myogenic) contractile effect on gastric smooth muscle; and 3) the effect of CCK-OP and acetylcholine are mediated by separate receptors.

Acetylcholine↗
PubMed1975

Synthesis of type I collagen by human smooth muscle cells in vitro.

Human vascular smooth muscle cells, derived from explants of medial smooth muscle of a fetal aorta, were grown in vitro and examined with phase and electron microscopy for characteristic morphologic features of smooth muscle cells and for the biosynthesis of connective tissue proteins. Their patterns of growth and ultrastructure were similar to those described for other species of cultured arterial smooth muscle cells. Most cells contained varying amounts of myofilaments interpersed with dense bodies, rough and smooth endoplasmic reticulum, mitochondria, various sized vesicles, lysosomes, and lipid droplets. Extracellularly, small amounts of electron-dense material and microfilaments were observed adjacent to or between the cells. The over-all morphology suggested that the smooth muscle cells were actively engaged in protein synthesis. Although we could not identify banded collagen fibrils in 10- to 14-day-old cultures by electron microscopy, the cells synthesized and secreted a collagen characterized as type I collagen. A hydroxyproline-containing protein composed of two alpha-1 and one alpha-2 chains was extracted from the cell layer. The triple helical precursor of type I collagen, procollagen, was secreted into the medium.

Aorta↗
PubMed1979

Temperature- and Mg-ATP-dependent regulation of Ca2+ sensitivity of smooth muscle actomyosin ATPase.

Many smooth muscles on metabolic depletion undergo a contraction that is insensitive to EGTA [ethylene glycol-bis (beta-aminoethylether)N,N-tetraacetic acid]. Chicken gizzard actomyosin shows a progressive loss of Ca sensitivity accompanied by activation of EGTA-Mg-ATPase at temperatures near 37 degrees C with decreasing ATP concentrations. Ca2+-dependent phosphorylation still occurs under these conditions when the ATPase is Ca insensitive. Activation of EGTA-Mg-ATPase at low ATP concentration is not due to a pseudo-ATPase, or due to denautration of the actomyosin at 37 degrees C. Magnesium concentrations above 1 mM are required for observing the enhanced EGTA-Mg-ATPase activity and the Ca sensitivity is very markedly influenced by the magnesium concentrations of medium at low ATP. When the Mg-to-ATP ratio (5:1) was kept constant for varying ATP concentrations, activation of EGTA-ATPase was not observed. This activation was not due to the characteristics of the ATP regenerating system (phosphoenolpyruvate and pyruvate kinase) because with phosphocreatine and creatine phosphokinase similar results were obtained. Thus the EGTA-insensitive rise in tension during metabolic depletion is due to activation of Mg-ATPase and loss of Ca sensitivity at 37 degrees C, a temperature at which mammalian smooth muscles normally function.

Actomyosin↗
PubMed1976

Lipoprotein uptake and degradation by cultured human arterial smooth muscle cells.

The multipotential smooth muscle cell (SMC) is the predominant cell in intima and media of large arteries, proliferating eraly in the development of atheroma to become the lipid-laden foam cell. Thomogeneous cultures of human SMA have now been successfully grown from explants of normal pieces of artery obtained during surgery. In contrast to previous results with rat SMC, human SMC preferentially bind and take up large, lipid-rich lipoproteins (I125 labeled low density and very low denstiy lipoproteins) (LDL and VLDL), in comparison to smaller, high density lipoproteins (HDL). This species selectivity appears to be related to differences both in cells and in lipoproteins. Specific binding of lipoproteins by SMC, analyzed by release of radioactive protein from the cell surfaces by trypsin, accounted for approximately hal of the protein radioactivity associated with the cell layer during the first few hours of incubation. Specific binding appears to be related to the presence of apoprotein B on the lipoproteins. Lipoproteins progressively accumulate within cells as a function of incubation time. Lipoprotein degradation, assessed by appearance of TCA soluble, non-iodide radioactivity in the incubation medium, increased rapidly after an initial delay of 2 to 4 hours. Cells grown under hypoxic (5% O2) conditions instead of the usual room air showed impaired degradation of lipoproteins. These results suggest that there are receptors on arterial SMC, highly specific for different lipoproteins (as shown for skin fibroblasts). This tissue culture system may be useful for assessment of the effects of a variety of hormones, metabolites, and drugs on the handling of lipoproteins by arterial smooth muscle cells.

Arteries↗