Sarcoplasmic reticulum and mitochondria as cation accumulation sites in smooth muscle

1973 ◽  
Vol 265 (867) ◽  
pp. 17-23 ◽  
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Divalent Cation ◽  
Electromechanical Coupling ◽  
Surface Membrane ◽  
Smooth Muscles ◽  
Relative Volume ◽  
Electron Dense Material ◽  
Tubular System ◽  
Central Elements

A tubular system of sarcoplasmic reticulum that is not penetrated by extracellular markers is described in vertebrate smooth muscles. The sarcoplasmic reticulum forms fenestrations around the surface vesicles and also forms close appositions (an approximately 10 to 12 nm gap traversed by periodic electron dense material) with the non-specialized surface membrane. The morphological couplings are considered to be the most probable sites of electromechanical coupling of the action potential to the twitch contraction. The relative volume of the sarcoplasmic reticulum varies in functionally different (tonic and phasic) smooth muscles, and correlates with the ability of the different smooth muscles to contract in the absence of extracellular calcium. Electron opaque deposits of strontium are accumulated by peripheral and central elements of the sarcoplasmic reticulum. The accumulation of strontium and barium by mitochondria raises the possibility that, in addition to the sarcoplasmic reticulum, mitochondria may play a role in the regulation of intracellular divalent cation levels in vertebrate smooth muscle.

scholarly journals SARCOPLASMIC RETICULUM AND THE TEMPERATURE-DEPENDENT CONTRACTION OF SMOOTH MUSCLE IN CALCIUM-FREE SOLUTIONS

1971 ◽  
Vol 51 (3) ◽  
pp. 722-741 ◽  
Author(s):  
Andrew P. Somlyo ◽  
Carrick E. Devine ◽  
Avril V. Somlyo ◽  
Stanley R. North
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Extracellular Space ◽  
Room Temperature ◽  
Electromechanical Coupling ◽  
Contractile Response ◽  
Surface Membrane ◽  
Smooth Muscles ◽  
Smooth Muscle Contraction ◽  
Free Cell

The contractile response of turtle oviduct smooth muscle to acetylcholine after 30 min of incubation of muscles in Ca-free, 4 mM ethylene (bis) oxyethylenenitrilotetraacetic acid (EGTA) solutions at room temperature was greater than the contractile response after 30 min of incubation in the Ca-free medium at 37°C. Incubation in Ca-free solution at 37°C before stimulation with acetylcholine in Ca-free solutions at room temperature also reduced the contractile response, suggesting that activator calcium was lost from the fibers at a faster rate at higher temperatures. Electron micrographs of turtle oviduct smooth muscle revealed a sarcoplasmic reticulum (SR) occupying approximately 4% of the nucleus- and mitochondria-free cell volume. Incubation of oviduct smooth muscle with ferritin confirmed that the predominantly longitudinally oriented structures described as the SR did not communicate with the extracellular space. The SR formed fenestrations about the surface vesicles, and formed close contacts (couplings) with the surface membrane and surface vesicles in oviduct and vena caval smooth muscle; it is suggested that these are sites of electromechanical coupling. Calculation of the calcium requirements for smooth muscle contraction suggest that the amount of SR observed in the oviduct smooth muscle could supply the activator calcium for the contractions observed in Ca-free solutions. Incubation of oviduct smooth muscle in hypertonic solutions increased the electron opacity of the fibers. A new feature of some of the surface vesicles observed in oviduct, vena caval, and aortic smooth muscle was the presence of approximately 10 nm striations running approximately parallel to the openings of the vesicles to the extracellular space. Thick, thin, and intermediate filaments were observed in turtle oviduct smooth muscle, although the number of thick filaments seen in the present study appeared less than that previously found in mammalian smooth muscles.

Coupling mechanisms in airway smooth muscle

1990 ◽  
Vol 258 (4) ◽  
pp. L119-L133 ◽  
Author(s):  
R. F. Coburn ◽  
C. B. Baron
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Airway Smooth Muscle ◽  
Electromechanical Coupling ◽  
Cell Function ◽  
Surface Membrane ◽  
Smooth Muscles ◽  
Membrane Receptors ◽  
Airway Smooth Muscle Cells ◽  
Coupling Mechanisms

This review documents available information about coupling mechanisms involved in airway smooth muscle force development and maintenance and relaxation of force. Basic concepts, obtained from experiments performed on many different mammalian cell types, are in place regarding coupling between surface membrane receptors and cell function; these concepts are considered as a framework for understanding coupling between receptors and contractile proteins in smooth muscles and in airway smooth muscles. We have divided various components of coupling mechanisms into those dependent on changes in the surface membrane potential (electromechanical coupling) and those independent of the surface membrane potential (pharmacomechanical coupling). We have, to some degree, emphasized modulation of coupling mechanisms by intrasurface membrane microprocessing or by second messengers. A challenge for the future is to obtain a better understanding of how coupling mechanisms are altered or modulated during different phases of contractions evoked by a single agonist and under conditions of multiple agonist exposure to airway smooth muscle cells.

scholarly journals SARCOPLASMIC RETICULUM AND EXCITATION-CONTRACTION COUPLING IN MAMMALIAN SMOOTH MUSCLES

1972 ◽  
Vol 52 (3) ◽  
pp. 690-718 ◽  
Author(s):  
Carrick E. Devine ◽  
Avril V. Somlyo ◽  
Andrew P. Somlyo
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Pulmonary Artery ◽  
Mesenteric Artery ◽  
Electromechanical Coupling ◽  
Surface Membrane ◽  
Main Pulmonary Artery ◽  
Smooth Muscles ◽  
Taenia Coli ◽  
Virtual Absence ◽  
Mesenteric Vein

The sarcoplasmic reticulum (SR) was studied in the smooth muscles of rabbit main pulmonary artery, mesenteric vein, aorta, mesenteric artery, taenia coli, guinea pig mesenteric artery, and human uterus, and correlated with contractions of the smooth muscles in Ca-free media. SR volumes were determined in main pulmonary artery (5.1%), aorta (5%), portal-anterior mesenteric vein (2.2%), taenia coli (2%), and mesenteric artery (1.8%): because of tangentially sectioned membranes these estimates are subject to a correction factor of up to +50% of the values measured. Smooth muscles that contained a relatively large volume of SR maintained significant contractile responses to drugs in the virtual absence of extracellular calcium at room temperatures, while smooth muscles that had less SR did not. The unequal maximal contractions of main pulmonary artery elicited by different drugs were also observed in Ca-free, high potassium-depolarizing solution, indicating that they were secondary to some mechanism independent of changes in membrane potential or calcium influx. Longitudinal tubules of SR run between and are fenestrated about groups of surface vesicles separated from each other by intervening dense bodies. Extracellular markers (ferritin and lanthanum) entered the surface vesicles, but not the SR. The peripheral SR formed couplings with the surface membrane: the two membranes were separated by gaps of approximately 10 nm traversed by electron-opaque connections suggestive of a periodicity of approximately 20–25 nm. These couplings are considered to be the probable sites of electromechanical coupling in twitch smooth muscles. Close contacts between the SR and the surface vesicles may have a similar function, or represent sites of calcium extrusion. The presence of both thick and thin myofilaments and of rough SR in smooth muscles supports the dual, contractile and morphogenetic, function of smooth muscle.

scholarly journals ELECTROMECHANICAL COUPLING IN TUBULAR MUSCLE FIBERS

1972 ◽  
Vol 52 (3) ◽  
pp. 626-638 ◽  
Author(s):  
Arieh Gilai ◽  
I. Parnas
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cell Membrane ◽  
Electromechanical Coupling ◽  
Surface Membrane ◽  
Hexagonal Array ◽  
Thin Filaments ◽  
Transverse Tubular System ◽  
The Core ◽  
Tubular System ◽  
Terminal Cisternae

The tubular fibers of the claw-closer muscle of the scorpion have a central core containing nuclei and mitochondria. The myofibrils have the shape of thin lamellae (1 µ) extending radially from the core to the surface membrane (20 µ). The thick myofilaments are organized in a hexagonal array with orbits of 10–13 thin myofilaments. The ratio of thick-to-thin filaments is 1:5. Transverse tubular system (TS) openings are located between lamellated myofibrils. In each sarcomere two TS's are found, one on each side of the H band. The TS is composed of a transverse tubule and tubular pockets (TP). The TP's form diadic contact with the terminal cisternae of the sarcoplasmic reticulum. The TS can be traced from the cell membrane down to the cell core. The surface area of the TS was calculated to be six times that of the outer surface membrane.

Sarcoplasmic Reticulum Function in Smooth Muscle

2010 ◽  
Vol 90 (1) ◽  
pp. 113-178 ◽  
Author(s):  
Susan Wray ◽  
Theodor Burdyga
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Physiological Activity ◽  
Smooth Muscles ◽  
Outward Current ◽  
Integrated Approach ◽  
Transient Outward Current ◽  
Coupling Mechanism ◽  
Striated Muscles ◽  
Development And Aging

The sarcoplasmic reticulum (SR) of smooth muscles presents many intriguing facets and questions concerning its roles, especially as these change with development, disease, and modulation of physiological activity. The SR's function was originally perceived to be synthetic and then that of a Ca store for the contractile proteins, acting as a Ca amplification mechanism as it does in striated muscles. Gradually, as investigators have struggled to find a convincing role for Ca-induced Ca release in many smooth muscles, a role in controlling excitability has emerged. This is the Ca spark/spontaneous transient outward current coupling mechanism which reduces excitability and limits contraction. Release of SR Ca occurs in response to inositol 1,4,5-trisphosphate, Ca, and nicotinic acid adenine dinucleotide phosphate, and depletion of SR Ca can initiate Ca entry, the mechanism of which is being investigated but seems to involve Stim and Orai as found in nonexcitable cells. The contribution of the elemental Ca signals from the SR, sparks and puffs, to global Ca signals, i.e., Ca waves and oscillations, is becoming clearer but is far from established. The dynamics of SR Ca release and uptake mechanisms are reviewed along with the control of luminal Ca. We review the growing list of the SR's functions that still includes Ca storage, contraction, and relaxation but has been expanded to encompass Ca homeostasis, generating local and global Ca signals, and contributing to cellular microdomains and signaling in other organelles, including mitochondria, lysosomes, and the nucleus. For an integrated approach, a review of aspects of the SR in health and disease and during development and aging are also included. While the sheer versatility of smooth muscle makes it foolish to have a “one model fits all” approach to this subject, we have tried to synthesize conclusions wherever possible.

CaM kinase II and phospholamban contribute to caffeine-induced relaxation of murine gastric fundus smooth muscle

2005 ◽  
Vol 288 (6) ◽  
pp. C1202-C1210 ◽  
Author(s):  
Minkyung Kim ◽  
Sang Yun Cho ◽  
In Soo Han ◽  
Sang Don Koh ◽  
Brian A. Perrino
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Muscle Tone ◽  
Smooth Muscles ◽  
Cyclopiazonic Acid ◽  
Gastric Fundus ◽  
Cam Kinase Ii ◽  
Cam Kinase ◽  
Camkii Activation

Caffeine has been shown to increase the Ca2+ release frequency (Ca2+ sparks) from the sarcoplasmic reticulum (SR) through ryanodine-sensitive stores and relax gastric fundus smooth muscle. Increased Ca2+ store refilling increases the frequency of Ca2+ release events and store refilling is enhanced by CaM kinase II (CaMKII) phosphorylation of phospholamban (PLB). These findings suggest that transient, localized Ca2+ release events from the SR may activate CaMKII and contribute to relaxation by enhancing store refilling due to PLB Thr17 phosphorylation. To investigate this possibility, we examined the effects of caffeine on CaMKII, muscle tone, and PLB phosphorylation in murine gastric fundus smooth muscle. Caffeine (1 mM) hyperpolarized and relaxed murine gastric fundus smooth muscle and activated CaMKII. Ryanodine, tetracaine, or cyclopiazonic acid each prevented CaMKII activation and significantly inhibited caffeine-induced relaxation. The large-conductance Ca2+-activated K+ channel blocker iberiotoxin, but not apamin, partially inhibited caffeine-induced relaxation. Caffeine-induced CaMKII activation increased PLB Thr17, but not PLB Ser16 phosphorylation. 3-Isobutyl-1-methylxanthine increased PLB Ser16 phosphorylation, but not PLB Thr17 phosphorylation. The CaMKII inhibitor KN-93 inhibited caffeine-induced relaxation and PLB Thr17 phosphorylation. These results show that caffeine-induced CaMKII activation and PLB phosphorylation play a role in the relaxation of gastric fundus smooth muscles.

Sarcoplasmic reticulum Ca2+ uptake is impaired in coronary smooth muscle distal to coronary occlusion

2001 ◽  
Vol 281 (1) ◽  
pp. H223-H231 ◽  
Author(s):  
Cristine L. Heaps ◽  
Michael Sturek ◽  
Elmer M. Price ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Exercise Training ◽  
Coronary Occlusion ◽  
Smooth Muscles ◽  
Cyclopiazonic Acid ◽  
Coronary Smooth Muscle ◽  
Protein Levels ◽  
Chronic Occlusion ◽  
Plasmic Reticulum

After chronic occlusion, collateral-dependent coronary arteries exhibit alterations in both vasomotor reactivity and associated myoplasmic free Ca2+ levels that are prevented by chronic exercise training. We tested the hypotheses that coronary occlusion diminishes Ca2+ uptake by the sarcoplasmic reticulum (SR) and that exercise training would prevent impaired SR Ca2+ uptake. Ameroid constrictors were surgically placed around the proximal left circumflex (LCx) artery of female swine 8 wk before initiating 16-wk sedentary (pen confined) or exercise-training (treadmill run) protocols. Twenty-four weeks after Ameroid placement, smooth muscles cells were enzymatically dissociated from both the LCx and nonoccluded left anterior descending (LAD) arteries of sedentary and exercise-trained pigs, and myoplasmic free Ca2+ was studied using fura 2 microfluorometry. After the SR Ca2+ store was partially depleted with caffeine (5 mM), KCl-induced membrane depolarization produced a significant decrease in the time to half-maximal ( t ½) myoplasmic free Ca2+ accumulation in LCx versus LAD cells of sedentary pigs. Furthermore, inhibition of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA; 10 μM cyclopiazonic acid) significantly reduced t ½ in cells isolated from the LAD but not from the LCx. Exercise training did not prevent the differences in t ½ myoplasmic free Ca2+ accumulation observed between LCx and LAD cells. Occlusion or exercise training did not alter SERCA protein levels. These results support our hypothesis of impaired SR Ca2+ uptake in coronary smooth muscle cells isolated distal to chronic occlusion. Impaired SR Ca2+ uptake was independent of SERCA protein levels and was not prevented by exercise training.

scholarly journals Simultaneous measurement of Ca2+ release and influx into smooth muscle cells in response to caffeine. A novel approach for calculating the fraction of current carried by calcium.

1994 ◽  
Vol 104 (2) ◽  
pp. 395-422 ◽  
Author(s):  
A Guerrero ◽  
J J Singer ◽  
F S Fay
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Smooth Muscle Cells ◽  
Surface Membrane ◽  
Ryanodine Receptors ◽  
Preceding Paper ◽  
Muscle Cells ◽  
Ionic Currents ◽  
Membrane Channels

Activation of ryanodine receptors on the sarcoplasmic reticulum of single smooth muscle cells from the stomach muscularis of Bufo marinus by caffeine is accompanied by a rise in cytoplasmic [Ca2+] ([Ca2+]i), and the opening of nonselective cationic plasma membrane channels. To understand how each of these pathways contributes to the rise in [Ca2+]i, one needs to separately monitor Ca2+ entry through them. Such information was obtained from simultaneous measurements of ionic currents and [Ca2+]i by the development of a novel and general method to assess the fraction of current induced by an agonist that is carried by Ca2+. Application of this method to the currents induced in these smooth muscle cells by caffeine revealed that approximately 20% of the current passing through the membrane channels activated following caffeine application is carried by Ca2+. Based on this information we found that while Ca2+ entry through these channels rises slowly, release of Ca2+ from stores, while starting at the same time, is much faster and briefer. Detailed quantitative analysis of the Ca2+ release from stores suggests that it most likely decays due to depletion of Ca2+ in those stores. When caffeine was applied twice to a cell with only a brief (30 s) interval in between, the amount of Ca2+ released from stores was markedly diminished following the second caffeine application whereas the current carried in part by Ca2+ entry across the plasma membrane was not significantly affected. These and other studies described in the preceding paper indicate that activation of the nonselective cation plasma membrane channels in response to caffeine was not caused as a consequence of emptying of internal Ca2+ stores. Rather, it is proposed that caffeine activates these membrane channels either by direct interaction or alternatively by a linkage between ryanodine receptors on the sarcoplasmic reticulum and the nonselective cation channels on the surface membrane.

scholarly journals THE SARCOPLASMIC RETICULUM AND ITS ASSOCIATION WITH THE T SYSTEM IN AN INSECT

1967 ◽  
Vol 32 (3) ◽  
pp. 535-545 ◽  
Author(s):  
Martin Hagopian ◽  
David Spiro
Keyword(s):  
Fine Structure ◽  
Sarcoplasmic Reticulum ◽  
Cell Surface ◽  
Osmium Tetroxide ◽  
Surface Membrane ◽  
Transverse Tubular System ◽  
Leucophaea Maderae ◽  
Tubular System ◽  
Femoral Muscle ◽  
T System

The fine structure of the sarcoplasmic reticulum and the transverse tubular system of the femoral muscle of the cockroach, Leucophaea maderae, was studied after prefixation in glutaraldehyde, postfixation in osmium tetroxide, and embedding in Epon. The sarcoplasmic reticulum in this muscle reveals features not previously reported. The sarcoplasmic reticulum is abundant, consisting mainly of a fenestrated envelope which surrounds each myofibril at all levels in the sarcomere. This sarcoplasmic reticulum envelope is continuous transversally as well as longitudinally along the myofibrils. Dyadic junctions are formed by a single T system element which contacts the unfenestrated sarcoplasmic reticulum of adjacent myofibrils in an alternating manner at the ends of the A band. At the dyads, regularly spaced thickenings of the sarcoplasmic reticulum membranes bordering the dyadic spaces are noted. These thickenings, however, do not contact the T tubule membrane. Typical dyadic contacts also are seen between the cell surface membrane and sarcoplasmic reticulum. Z line-like material is seen in contact with the membranes of the cell surface and longitudinal branches of the T systems.

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