Effects of hemoglobin on smooth muscle.
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Animals↗
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Studies on isolated smooth muscle cells: The contractile apparatus.
Smooth muscle cells may be isolated from the taenia coli muscle of the guinea pig which, when made permeable by treatment with Triton X-100 (0-05%) show a sensitivity to Ca for contraction with MgATP. The rate of contraction, about 10 micron s-1, corresponds closely to the maximum velocity of shortening of the intact muscle. Electron microscopy of such partially demembranated muscle cells shows that myosin filaments of about 16-nm diameter are present in both the rigor and the relaxes states. In addition, the actin and myosin filaments are commonly seen to be associated in groups corresponding approximately in size to the fibrils recognizable in cells in rigor in the light microscope. The dense bodies and the 10-nm filaments are found located between the actin-myosin filament groups. The thick myosin filaments may be isolated by fragmentation of the cells under relaxing conditions. These native filaments range up to about 8 micron in length and show the same structural organization as filaments aseembled from purified smooth muscle myosin: there is no central bare zone and bare edges, about 0-2 micrin long, occur at the filament ends. The lack of bipolarity of the native smooth muscle muosin filaments and the absence, in the contractile apparatus, of actin-associated structures equivalent to Z-lines suggests that the amount of shearing that can occur between the actin and myosin filaments is considerably greater than in skeletal muscle.
Animals↗
Studies on the composition of phospholipids in rat small intestinal smooth muscle.
The phospholipid composition of rat small intestinal smooth muscle was investigated in comparison with those of the mucosa and liver. Phospholipid content per g of the wet smooth muscle was almost identical with that of the mucosa and was about 1/4 of that in the liver. The phospholipid/protein ratio of the smooth muscle was about 1/2 of the value in the liver. Sphingomyelin content was significantly high and amounted to 18% of total phospholipids. This value was about twice that in the mucosa and 4 times higher than that in the liver. On the other hand, the percent distribution of phosphatidylcholine was lowest in the smooth muscle. Distribution patterns of phosphatidylserine and phosphatidylinositol in the smooth muscle as well as in the mucosa were different from those in the liver. The occurrence of vinyl-ether and ether phospholipids was clearly demonstrated in the smooth muscle as well as in the mucosa. A major part of the ether lipids was detected in the phosphatidylethanolamine fraction, in which they amounted to about 50%; 40% as alkenyl-acyl type and 12% as alkyl-acyl type. A high content of ether lipids was also observed in the phosphatidylethanolamine fraction from mucosa, but the distribution was reversed, that is, 14% alkenyl-acyl type and 28% alkyl-acyl type. Fatty aldehydes, fatty alcohols, and fatty acids were also determined by gas-liquid chromatography. The compositions of fatty aldehydes in the phosphatidylethanolamine fraction from smooth muscle and from mucosa were similar, whereas the compositions of long chain fatty alcohol and fatty acids were clearly different. The compositions of fatty alcohols and fatty acids of the phosphatidylcholine fraction from smooth muscle showed significantly different patterns from those of the phosphatidylethanolamine fraction and from those of the same phospholipid fraction in the mucosa.
Aldehydes↗
The effect of lysolecithin on contractile force of isolated gastric smooth muscle.
Mechanical activity of smooth muscle preparations was recorded in circular strips of antrum, corpus, and fundus from guinea-pig stomach. Whereas acetylcholine stimulated both rhythmic and tonic (shift of the base line) activity of the tested muscles, lysolecithin induced tonic contractions, but had no influence on the rhythmic activity. Lysolecithin was ineffective in the absence of external calcium. The tonic activations of corpus and fundus preparations induced by lysolecithin were suppressed by sodium nitroprusside. D 600 (methoxy-verapamil) did not counteract the lysolecithin effect.
Animals↗
p-Chlorophenoxyisobutyrate enhanced retention of homologous lipoproteins by human aortic smooth muscle cells.
Human aortic smooth muscle cells (SMC) specifically bind and take up indiscriminately both the lipid and protein moieties of homologous 25I-very low density lipoproteins (VLDL) and 125I-low density lipoproteins LDL). Sixty-five to 80% of absorbed lipids are incorporated into the cell lipids, preferentially into the phospholipid fraction. Twenty to 35% of the lipid bound and the protein moiety are eliminated from the cells. Half of the eliminated protein label is recovered as TCA soluble products. Five mM of p-chlorophenoxyisobutyrate (CPIB) raise the level of intracellular radioactivity derived from the lipid moieties of VLDL and LDL by about 40% via a reduced elimination. The processing of the protein moiety and lipoprotein binding to the cell surface are not affected by 5.0 mM of CPIB. CPIB lowers the incorporation of 14C-acetate, 14C-pyruvate, and 32phosphate radioactivity into fatty acids and phospholipids of aortic SMC. Five mM of CPIB reduce the overall palmitic acid synthesis by shifting from de novo synthesis to the mechanism of chain elongation, although the further elongation to saturated C18-C24 fatty acids is also depressed. The CPIB-enhanced retention of the lipid-derived lipoprotein radio-activity is interpreted as a compensatory mechanism providing cellular fatty acids which are deficient as a result of the CPIB inhibited synthetic processes.
Aorta, Thoracic↗
Studies on the properties of triphosphoinositide phosphomonoesterase and phosphodiesterase of rabbit iris smooth muscle.
The rabbit iris smooth muscle has been shown to contain triphosphoinositide phosphomonoesterase (phosphatidyl-myo-inositol-4,5-bisphosphate phosphohydrolase, EC 3.1.3.36) and phosphodiesterase (triphosphoinositide inositoltrisphosphohydrolase, EC 3.1.4.11) activities. Under our experimental conditions about 77% of the phosphomonoesterase and 61% of the phosphodiesterase activities were localized in the particulate fraction. The kinetic properties of the enzymes in the microsomal fraction were examined. The enzyme preparation was specific to polyphosphoinositides; it did not attack phosphatidylinositol under the present assay condition. The effects of Ca2+ and Mg2+ were also studied. Although the microsomal enzymes did not require added divalent cations for their activities, both the phosphomonoesterase and phosphodiesterase were appreciably inhibited by 1 mM EDTA. Phosphodiesterase and phosphomonoesterase were stimulated by Ca2+ and Mg2+, respectively. The demonstration of triphosphoinositide phosphodiesterase in the iris muscle, coupled with the findings that this enzyme is activated by Ca2+ and is not influenced by acetylcholine add further support to our previous conclusion (J. Pharmacol. Exp. Ther. (1978) 204, 655--668; J. Neurochem. (1978) 30, 517--525) that an increased Ca2+ influx, following the interaction between the neurotransmitter and its receptor, could act to stimulate the phosphodiesterase, thus leading to increased triphosphoinositide breakdown and increased phosphatidic acid via increased diacylglycerol.
Animals↗
Mechanism of isoproterenol-induced desensitization of tracheal smooth muscle.
Isolated rat tracheal smooth muscle became considerably less sensitive to the relaxing action of isoproterenol after being incubated with 5 x 10(-6) M isoproterenol for 30 minutes. Pretreatment of the tissue with propranolol, but not with methylprednisolone, clearly reduced the isoproterenol-induced desensitization. This suggested that propranolol by occupying the beta adrenergic receptor prevented isoproterenol from binding to this receptor, thereby preventing the isoproterenol-induced desensitization. Furthermore, an isoproterenol-desensitized tracheal preparation exhibited a diminished sensitivity to other beta agonists, but not to the spasmolytic actions of D600, hydralazine, sodium nitrite and aminophylline. These results suggested that the beta receptor is specifically involved in the desensitization induced by isoproterenol. A highly desensitized tissue could always be made to undergo complete relaxation by exposing it to sufficiently high concentrations of isoproterenol. Thus, there appeared to be no positive indication of a very large change in the apparent intrinsic activity of the isoproterenol in the desensitized tissue. However, the dissociation constant for the propranolol-beta receptor complex in the desensitized tissue was shown to be 180-fold larger than that in the normal tissue. These findings provide strong evidence that one demonstrable cellular change that occurs in the desensitized tissue is a pronounced reduction in the affinity of the beta receptors for isoproterenol.
Adrenergic beta-Agonists↗
A new electrode for electromyographic study of bronchial smooth muscle.
The contribution of the bronchial smooth muscles to asthmatic attack has been supposed by many studies such as measurement of the intrabronchial pressure and bronchographical studies, but electromyographical evidence has not been established yet. A new bipolar platinum-ring electrode fixed on polyethylene catheter was invented in order to record action potentials from the bronchial smooth muscle through the intrabronchial lead. Action potentials obtained by this electrode were compared with those obtained by the direct peribronchial needle electrode during either artificial or spontaneous respiration in dogs and a monkey. Electrophotographical analysis confirmed that action potentials obtained by our new electrode were similar in discharge pattern to those by the direct peribronchial needle electrode. The active contribution of the bronchial smooth muscle to the maintenance of the bronchial caliber during spontaneous respiration was observed by our new electrode. Accordingly, this electrode is applicable to electromyographical studies of the bronchial smooth muscle.
Action Potentials↗
Ca2+ regulation in vascular smooth muscle.
Regulation of aorta smooth muscle contraction by Ca ion requires the collaboration of the 80,000 dalton factor and tropomyosin. A method for preparing pure actin from aorta smooth muscle is described.
Actins↗
Studies on the function and composition of the 10-NM(100-A) filaments of vertebrate smooth muscle.
The extraction of isolated vertebrate smooth muscle cells at high and low ionic strength yields cell ghosts which are seen in the electron microscope to be composed of a complex network of 10-nm filaments, together with residual actin. After SDS-gel electrophoresis of the cell ghosts only 2 bands may be recognized, one corresponding to actin and the other migrating at about 55 000 mol. wt that arises from the 10-nm filaments. The 10-nm filaments are extremely sensitive to proteolysis and are absent from cells exposed to crude collagenase in the presence of Triton X-100. Such cells, lacking 10-nm filaments, still contract in response to ATP. The data indicate that the 10-nm filaments are not essential for contraction, but rather form a specialized intracellular cytoskeleton. While completely insoluble in concentrated salt solutions the 55 000 mol. wt protein is readily extracted with acetic acid from homogenized and salt-extracted smooth muscle residue. The extracted protein reassembles, on dialysis, into filaments of about 10-nm diameter and has an amino acid composition almost identical to that deduced for vertebrate neurofilaments. From the cytoskeletal role that the 10-nm filaments play in smooth muscle and, as appears likely, in other cell types the filament protein has been tentatively termed 'skeletin'. Results relating to the proportion of skeletin in smooth muscle and the structure of the 10-nm filaments are described and discussed.
Amino Acids↗
Multi-omics analysis of glucocorticoid receptor crosstalk with Type I and Type II inflammatory signaling in human airway smooth muscle cells.
Airway smooth muscle (ASM) dysfunction in obstructive airway disease is treated with glucocorticoids. Through RNA-seq analysis of cultured human ASM, we identified repressive effects of dexamethasone, a glucocorticoid, on the baseline expression of a subset of genes that are induced by either IL1B or IL13, which model Type I and Type II inflammation, respectively. ChIP-seq analysis of glucocorticoid receptor (GR) and the p65 subunit of NFkB occupancy indicated canonical motifs for both factors occur at sites of p65 occupancy but did not provide biochemical support for significant repressive tethering between GR and p65. Instead, ATAC-seq revealed significant chromatin remodeling and increased accessibility at binding motifs for the NFkB complex in association with dex + IL1B co-treatment in comparison to IL1B treatment alone. Our data support a competition-based primary repressive effect of glucocorticoids on both IL1B and IL13 signaling and provide evidence for transcriptional cooperation between GR and NFkB on a genome-wide basis in ASM, including at regulatory elements that control expression of anti-inflammatorygenes.
chromatin↗
[18 O-exchange reactions catalyzed by myosin of calf intestine smooth muscle].
18O-exchange reactions of smooth muscle myosin of calf intestine were studied. Smooth muscle myosin, similar to skeletal myosin, catalyses two types of 18O-exchange reactions--intermediate and direct. Only quantitative differences of the exchange intensity are observed. 18O-exchange dependence on bivalent cation and nucleotide nature is found. The comparison of 18O-exchange characteristics for myosins of smooth and skeletal muscles confirms the hypothesis on the similarity of molecular mechanisms of ATP hydrolysis by myosin from different muscle types.
Adenosine Triphosphate↗
Adenosine as a natural prostaglandin antagonist in vascular smooth muscle.
Adenosine has actions on smooth muscle similar to those of prostaglandin (PG) antagonists. Like some PG antagonists it is a phosphodiesterase inhibitor and seems to interfere with calcium effects. It has agonist/antagonist interactions with theophylline, a PG antagonist. In rat mesenteric vascular smooth muscle adenosine blocked responses to noradrenaline which depend on release of intracellular calcium but not those to potassium ions which depend on calcium entry from extracellular fluid. Partial inhibition of endogenous PG synthesis by indomethacin enhanced the adenosine effect. In preparations in which vascular reactivity had been abolished by indomethacin and then partly restored by 1 or 5 ng/ml PG2, adenosine also inhibited responses to noradrenaline: the curve for the 5 ng/ml PG2 concentration was to the right of and parallel to the 1 ng/ml curve consistent with a competitive interaction between adenosine and PG2. Similar interactions between adenosine and PG2 were shown in human lymphocytes in which activation also depends on calcium release. These findings suggest how calcium-dependent metabolic responses may be controlled and indicate further reasons for caution in the interpretation of cyclic AMP experiments.
Adenosine↗
Characteristics of histamine tachyphylaxis in canine tracheal smooth muscle.
In isolated canine tracheal smooth muscle, repeated administrations of histamine result in a rapid reduction in contractile response to about 15% of the initial contraction (tachyphylaxis). Development of this tachyphylaxis is specific inasmuch as: 1) it does not develop to acetylcholine (10(-6) M or 10(-4) M), or serotonin (10(-5) M; and 2) maximally developed histamine tachyphylaxis is not associated with a parallel reduction in response to acetylcholine. Pretreatment with propranolol (10(-5) M) or phentolamine (10(-4) M) does not prevent tachyphylaxis: however, pretreatment with atropine (10(-4) M) does prevent tachyphylaxis in about 50% of the animals tested. Tachyphylaxis to histamine can be reversed in a dose- and time-dependent fashion with prostaglandin synthesis inhibiting agents. The order of potency obtained with such compounds (indomethacin greater than mefenamic acid greater than oxyphenbutazone greater than acetylsalicylic acid) is consistent with potencies for inhibition of prostaglandin synthesis found in the literature. Also, in indomethacin pretreated strips in which tachyphylaxis to histamine was prevented, exogenous addition of PGE2 (1.42 x 10(1-) M to 2.84 x 10(-9) M) and PGA2 in a high concentration (2.9 x 10(-9) M) are capable of selectively reducing the response to histamine without an effect on acetylcholine-induced contractions. These data suggest that the mechanism of histamine tachyphylaxis in the canine tracheal smooth muscle preparation involves prostaglandin synthesis.
Acetylcholine↗
Action potential generation in reaggregates of rat aortic smooth muscle cells in primary culture.
Cultured vascular smooth muscle cells were prepared from adult rat aortas. The cells were dispersed by collagenase/elastase, and allowed to reaggregate into small spheres (50-200 micron in diameter) by plating on to cellophane. These primary cultures were incubated for 5-14 days, and then impaled with microelectrodes. The mean resting potential was -55 mV, and the mean input resistance was 9.0 M omega. The cells were quiescent, electrically and mechanically, and electrical stimulation usually did not elicit responses. However, addition of Ba++ (1 mM) or tetraehtylammonium ion (TEA; 5-15 mM) induced excitability (with accompanying contractions), either as spontaneous action potentials or by allowing responses to electrical stimulation. The cells became partially depolarized (e.g., to -36 mV) by these agents, and the input resistance increased. The frequency of spontaneous firing of the Ba++-induced spikes was affected by polarizing current pulses, as expected for pacemaker behavior. Elevation of Ca++ in the bathing solution increased the amplitude (overshoot) of the action potentials, and the spikes were blocked by verapamil (10(-5) M). Electron microscopy showed that the reaggregates consisted of a tight packing of elongated small-diameter cells, some of which exhibited thick and thin myofilaments and 'dense bodies'; many cells possessed surface caveolae. The results of this study demonstrate that reaggregates of arterial smooth muscle in primary culture can maintain functional and morphological characteristics of intact arterial smooth muscle, and therefore provide a useful preparation for the study of vascular smooth muscle function and control.
Action Potentials↗
[Preparation and the properties of a highly purified preparation of myosin from smooth muscles].
Myosin was isolated from the smooth muscles of small intestine of calf with good yield and its properties were compared with the myosin's properties from the skeletal rabbit muscle. The crude myosin was purified by means of DEAE-cellulose column chromatography, using a KCl gradient. The purity of the preparations was checked spectrophotometrically by the densities of adsorption D280/D260, viscosimmetrically by the sensitivity to ATP, electrophoretically and by ultracentrifugation. By the above-mentioned properties the smooth muscle myosin was similar to the high-purified skeletal muscle myosin. A comparative study of the enzymatic properties of myosin from two types of tissues, showed the following differences: (1) in the dependence the Ca2+-ATPase activity on the KCl concentration in the incubation medium; (2) in the degree of myosin activation by actin in the presence of Mg2+; (3) in the behaviour of Ca2+-ATPase dependence on pH; (4) the different temperature optima of the ATPase activity.
Adenosine Triphosphatases↗
Ultrastructural alterations in gizzard smooth muscle of selenium-vitamin-E-deficient ducklings.
Lesions of gizzard smooth muscle were studied by light and electron microscopy in newly hatched ducklings fed a selenium-vitamin-E-deficient diet for 13-21 days. Histopathologic alterations included initial hyaline change in damaged smooth-muscle cells, subsequent mineralization of sarcoplasmic debris in necrotic smooth-muscle cells, macrophagic invasion and phagocytosis of sarcoplasmic debris, and eventual fibroblastic proliferation and scarring of damaged areas in the gizzard wall. Ultrastructurally, mild damage in smooth-muscle cells was manifested by altered mitochondria with matrical densities and disrupted membranes and dilated elements of sarcoplasmic reticulum. In smooth-muscle cells with severe injury, the alterations of mitochondria and sarcoplasmic reticulum were accompanied by myofibrillar lysis and disruption of plasma membranes and external laminae. Expanding zones of mineralization of sarcoplasmic debris in necrotic smooth muscle cells were present at dense masses of lysed myofilaments that surrounded mineralized and disrupted mitochondria. Numerous macrophages infiltrated the areas of necrosis of smooth muscle and phagocytosed sarcoplasmic debris.
Animals↗
Regulation of low density lipoprotein receptor activity by cultured human arterial smooth muscle cells.
The ability of cultured human arterial smooth muscle cells to regulate low density lipoprotein (LDL) receptor activity was tested. In contrast to human skin fibroblasts incubated with lipoprotein deficient medium under identical conditions, smooth muscle cells showed significantly reduced enhancement of 125I-labeled LDL and 125I-labeled VLDL (very low density lipoprotein) binding. Smooth muscle cells also failed to suppress LDL receptor activity during incubation with either LDL or cholesterol added to the medium, while fibroblasts shoed an active regulatory response. Thus, in comparison with the brisk LDL receptor regulation characteristic of skin fibroblasts, arterial smooth muscle cells have and attenuated capacity to regulate their LDL receptor activity. These results may be relevant to the propensity of these cells to accumulate LDL and cholesterol and form "foam cells" in the arterial wall in vivo, a process associated with atherogenesis.
Aorta, Thoracic↗