The Contractile Apparatus of Podocytes Is Arranged to Counteract GBM Expansion

2015 ◽  
pp. 1-9 ◽  
Author(s):  
Wilhelm Kriz ◽  
Peter Mundel ◽  
Marlies Elger
Keyword(s):  
Contractile Apparatus

Inter-Filament Distance In Smooth Muscle: Implications In The Structure Of Contractile Apparatus

2011 ◽  
Author(s):  
Srboljub M. Mijailovich ◽  
Aleksandar Marinkovic ◽  
Nemanja Vujacic ◽  
Vlada Vladimirov ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Contractile Apparatus

Development and maintenance of force and stiffness in airway smooth muscle

2015 ◽  
Vol 93 (3) ◽  
pp. 163-169 ◽  
Author(s):  
Bo Lan ◽  
Brandon A. Norris ◽  
Jeffrey C.-Y. Liu ◽  
Peter D. Paré ◽  
Chun Y. Seow ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Solid State ◽  
Airway Smooth Muscle ◽  
Deep Inspiration ◽  
Contractile Apparatus ◽  
Tidal Breathing ◽  
Actomyosin Interaction ◽  
Filament Network

Airway smooth muscle (ASM) plays a central role in the excessive narrowing of the airway that characterizes the primary functional impairment in asthma. This phenomenon is known as airway hyper-responsiveness (AHR). Emerging evidence suggests that the development and maintenance of ASM force involves dynamic reorganization of the subcellular filament network in both the cytoskeleton and the contractile apparatus. In this review, evidence is presented to support the view that regulation of ASM contraction extends beyond the classical actomyosin interaction and involves processes within the cytoskeleton and at the interfaces between the cytoskeleton, the contractile apparatus, and the extracellular matrix. These processes are initiated when the muscle is activated, and collectively they cause the cytoskeleton and the contractile apparatus to undergo structural transformation, resulting in a more connected and solid state that allows force generated by the contractile apparatus to be transmitted to the extracellular domain. Solidification of the cytoskeleton also serves to stiffen the muscle and hence the airway. Oscillatory strain from tidal breathing and deep inspiration is believed to be the counter balance that prevents hypercontraction and stiffening of ASM in vivo. Dysregulation of this balance could lead to AHR seen in asthma.

scholarly journals Oxidized LDL Increases the Sensitivity of the Contractile Apparatus in Isolated Resistance Arteries for Ca2+via a Rho- and Rho Kinase–Dependent Mechanism

Circulation ◽  
2000 ◽  
Vol 102 (19) ◽  
pp. 2402-2410 ◽  
Author(s):  
Steffen-Sebastian Bolz ◽  
Jan Galle ◽  
Roland Derwand ◽  
Cor de Wit ◽  
Ulrich Pohl
Keyword(s):  
Oxidized Ldl ◽  
Rho Kinase ◽  
Contractile Apparatus ◽  
Resistance Arteries ◽  
Dependent Mechanism

Matching the Heart to Heat-Induced Circulatory Load: Heat-Acclimatory Responses

Physiology ◽  
2003 ◽  
Vol 18 (6) ◽  
pp. 215-221 ◽  
Author(s):  
Michal Horowitz
Keyword(s):  
Heart Rate ◽  
Oxygen Demand ◽  
Heat Acclimation ◽  
Regulatory Proteins ◽  
Contractile Apparatus ◽  
Cardiac Efficiency ◽  
Cross Tolerance ◽  
Altered Expression ◽  
Expression Of Genes ◽  
Cardiac Adaptation

Heat acclimation enhances cardiac efficiency by increasing stroke volume and decreasing heart rate. These adaptations involve biochemical changes in the contractile apparatus, switched on by altered expression of genes coding contractile and calcium-regulatory proteins and partially mediated by persistent low thyroxine. Heat acclimation also produces cross-tolerance to oxygen deprivation, thus reinforcing cardiac adaptation to oxygen demand/supply mismatching via energy-sparing pathways.

The Threshold for Potassium-Induced Contractures of Frog Skeletal Muscle. Potentiation of Potassium-Induced Contractures by Preexposure to Subthreshold Potassium Concentrations

1972 ◽  
Vol 50 (1) ◽  
pp. 37-44 ◽  
Author(s):  
E. C. Vos ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Potassium Concentration ◽  
Ringer Solution ◽  
Frog Skeletal Muscle ◽  
Contractile Apparatus ◽  
Tension Development ◽  
Eventual Loss ◽  
Active Processes ◽  
Muscle Potentiation ◽  
Small Bundle

A brief exposure (about 10–30 s) of a frog's toe muscle or a small bundle of fibers from the semi-tendinosus muscle to just subthreshold potassium concentrations potentiated contractures subsequently produced by exposing the muscles to a potassium concentration slightly above the threshold. The contractures thus potentiated had greater maximum tensions, and greater rates of tension development and relaxation than control contractures elicited by the same final potassium concentration. The resistance to stretch (R.T.S.) in the first few seconds of the potentiated contractures was about twice that of control contractures. Maximum potentiation occurred with preexposures of about 30 s; longer preexposures led to a decrease of potentiation and eventually to a depression of the contracture. The potentiation was not immediately abolished when the muscle was reexposed to Ringer solution but persisted for 2 min or longer (the 'washout effect'). It was concluded that exposing a muscle to low subcontracture threshold concentrations of potassium for a few seconds primes the intracellular contractile apparatus, probably by causing an increased sarcoplasmic concentration of Ca2+ ions, resulting in a potentiation of subsequently induced submaximal potassium contractures. The increase in metabolism (or 'Solandt effect') seen under these conditions is temporally related to the decline and eventual loss of the potentiation and is probably a reflection of active processes involved in reducing the sarcoplasmic concentration of Ca2+ ions.

Sign in / Sign up

Export Citation Format

Share Document