Factors modifying contraction-relaxation cycle in vascular smooth muscles

1982 ◽  
Vol 243 (5) ◽  
pp. H641-H662 ◽  
Author(s):  
H. Kuriyama ◽  
Y. Ito ◽  
H. Suzuki ◽  
K. Kitamura ◽  
T. Itoh
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Smooth Muscles ◽  
Contractile Proteins ◽  
Membrane Properties ◽  
Release Mechanism ◽  
Storage Site ◽  
Vascular Smooth Muscles ◽  
Subsequent Increase ◽  
Vascular Tissues

Contraction-relaxation cycles in vascular smooth muscles are largely dependent on the regulation of free Ca2+ in the myoplasm, as is the case in skeletal and cardiac muscles. In this article we describe the varieties of contraction-relaxation cycles of vascular smooth muscles determined at cellular and subcellular levels. To discuss the excitation-contraction and pharmacomechanical coupling mechanisms in vascular tissues, passive and active membrane properties and ionic movements measured by various procedures are briefly introduced. In vascular smooth muscles the sources of Ca2+ contributing to the activation of contractile proteins are extra- and intracellular. Influxes of Ca2+ across the membrane are enhanced by the calcium spike and electrical and chemical depolarizations or activations of autonomic receptors.l However, the Ca2+ influx during the generation of action potential does not directly increase the free Ca2+ in the cell; rather, this ion is sequestered in the storage site and activates the calcium-induced calcium-release mechanism in the storage sites with a subsequent increase in the levels of free Ca2+. In some vascular tissues depolarizations induced by activations of autonomic receptors are not a prerequisite for generation of the contraction, as these mechanical responses appear with hyperpolarization of the membrane or without a change in the membrane potential. Possible functional links between the myoplasmic membrane where the receptors are distributed and the Ca2+ storage and releasing sites (mainly sarcoplasmic reticulum) in the cell are discussed. In addition, small arteries possess possibly more than three subtypes of alpha-adrenoceptors, including the presynaptic alpha 2-adrenoceptor. The roles of sarcoplasmic reticulum and the calcium receptor of contractile proteins (calmodulin or leiotonin C) from the chemically skinned muscles of vascular tissues were compared with those of intact muscles. The relaxation of vascular tissues as induced by activations of beta-adrenoceptors, nitrites, and other chemicals is also briefly introduced.

Activation of skinned muscle fibers by calcium and strontium ions

1987 ◽  
Vol 65 (4) ◽  
pp. 642-647 ◽  
Author(s):  
C. Goblet ◽  
Y. Mounier
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Ions ◽  
Calcium Release ◽  
Muscle Fibers ◽  
Carcinus Maenas ◽  
Contractile Proteins ◽  
Calcium Atpase ◽  
Mechanical Activity ◽  
Release Mechanism ◽  
Strontium Ions

Intact and mechanically skinned skeletal muscle fibers of the crab Carcinus maenas have been used. The aim of the experiments was to determine the origin of the mechanical activity recorded in intact crab muscle fibers exhibiting an inward strontium current in strontium solution without calcium. To do so, the effect of strontium ions in inducing activation of contractile proteins and calcium release from the sarcoplasmic reticulum has been studied. The properties of the sarcoplasmic reticulum membrane towards strontium ions, i.e., the efficiency of the calcium ATPase towards strontium ions and the capability to release strontium ions have been investigated. Results show that the contractile proteins have a lower affinity for strontium than for calcium ions. However, the maximum bound strontium is identical to the maximum bound calcium. As for the sarcoplasmic reticulum, strontium ions can induce a calcium release and also can be taken up by the calcium ATPase and be released. We concluded that the mechanical activity in intact fibers bathed in a strontium medium has two origins: first, a direct and partial activation of the contractile proteins by strontium ions flowing through the calcium channel; second, a contractile proteins activation of calcium ions released by the sarcoplasmic reticulum by a "strontium-induced calcium release" mechanism.

scholarly journals Sphingosylphosphocholine modulates the ryanodine receptor/calcium-release channel of cardiac sarcoplasmic reticulum membranes

1997 ◽  
Vol 322 (1) ◽  
pp. 327-333 ◽  
Author(s):  
Romeo BETTO ◽  
Alessandra TERESI ◽  
Federica TURCATO ◽  
Giovanni SALVIATI ◽  
Roger A. SABBADINI ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptor ◽  
Calcium Release ◽  
Cardiac Tissue ◽  
Ruthenium Red ◽  
Release Mechanism ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Cardiac Sarcoplasmic Reticulum ◽  
High Calcium

Sphingosylphosphocholine (SPC) modulates Ca2+ release from isolated cardiac sarcoplasmic reticulum membranes; 50 ƁM SPC induces the release of 70Ő80% of the accumulated calcium. SPC releases calcium from cardiac sarcoplasmic reticulum through the ryanodine receptor, since the release is inhibited by the ryanodine receptor channel antagonists ryanodine, Ruthenium Red and sphingosine. In intact cardiac myocytes, even in the absence of extracellular calcium, SPC causes a rise in diastolic Ca2+, which is greatly reduced when the sarcoplasmic reticulum is depleted of Ca2+ by prior thapsigargin treatment. SPC action on the ryanodine receptor is Ca2+-dependent. SPC shifts to the left the Ca2+-dependence of [3H]ryanodine binding, but only at high pCa values, suggesting that SPC might increase the sensitivity to calcium of the Ca2+-induced Ca2+-release mechanism. At high calcium concentrations (pCa 4.0 or lower), where [3H]ryanodine binding is maximally stimulated, no effect of SPC is observed. We conclude that SPC releases calcium from cardiac sarcoplasmic reticulum membranes by activating the ryanodine receptor and possibly another intracellular Ca2+-release channel, the sphingolipid Ca2+-release-mediating protein of endoplasmic reticulum (SCaMPER) [Mao, Kim, Almenoff, Rudner, Kearney and Kindman (1996) Proc. Natl. Acad. Sci. U.S.A 93, 1993Ő1996], which we have identified for the first time in cardiac tissue.

Chemical modification of calcium release from the sarcoplasmic reticulum of mechanically skinned skeletal bullfrog muscle fibers

1986 ◽  
Vol 64 (10) ◽  
pp. 1267-1271 ◽  
Author(s):  
Takako Aoki ◽  
Toshiharu Oba ◽  
Ken Hotta
Keyword(s):  
Skeletal Muscle ◽  
Amino Acid ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Release Mechanism ◽  
Trinitrobenzenesulfonic Acid ◽  
Amino Acid Side Chains ◽  
Chloramine T ◽  
Tension Curve ◽  
Calcium Induced Calcium Release

Several types of reagents that react with amino acid side chains induced repetitive phasic contracture of skinned skeletal muscle from frogs. The presence of 10 mM procaine or 5 mM magnesium in the medium or disruption of the sarcoplasmic reticulum (SR) eliminated this contracture, indicating that the calcium-induced calcium-release mechanism of SR is involved in the contraction. Dithiothreitol inhibited the contracture induced by chloramine T, N-acetylimidazole, or p-chloromercuriphenylsulfonic acid (pCMPS) but not in the case of carbodiimide, phenylglyoxal, trinitrobenzenesulfonic acid, diethylpyrocarbonate (DEP), or N-chlorosuccinimide (NCS). Therefore, modification of groups other than the sulfhydryl ones seems to induce contractures under such conditions. The amplitude of the caffeine-induced contracture decreased after treatment with pCMPS, DEP, or NCS. NCS shifted the pCa–tension curve toward low pCa in the SR-disrupted fibers. This shift would explain the decrease in caffeine contracture. It is tentatively concluded that pCMPS and DEP release a large amount of calcium from SR.

Direct Measurement of Sarcoplasmic Reticulum Calcium Content Following Isoproterenol or Caffeine Treatment

1997 ◽  
Vol 3 (S2) ◽  
pp. 919-920
Author(s):  
Wendy E. Sweet ◽  
Christine S. Moravec
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Content ◽  
Storage Site ◽  
Calcium Store ◽  
Indirect Methods ◽  
Β Receptor ◽  
Sarcoplasmic Reticulum Calcium

The major storage site for calcium in cardiac muscle is the sarcoplasmic reticulum (SR). It has been shown using indirect methods that the amount of calcium stored in the SR can be altered by various agonists and anesthetics. The only technique to date which directly quantifies the amount of calcium in the SR is Electron Probe Microanalysis (EPMA). Using EPMA, an accurate measurement of the size of the SR calcium store can be made following treatments with known agonists.Isoproterenol (ISO) causes an increased inotropic response in cardiac muscle via the (3-adrenergic pathway. When ISO binds to the (β-receptor on the plasma membrane, it causes the activation of Protein Kinase A (PKA) through a cascade of events. PKA phosphorylates the sarcolemmal calcium channels causing an increase in the rate of calcium influx. PKA also phosphorylates Tnl, which sensitizes the myofilaments to calcium, thereby increasing the rate of calcium release from the myofilaments.

Contribution of a voltage-sensitive calcium release mechanism to contraction in cardiac ventricular myocytes

1998 ◽  
Vol 274 (1) ◽  
pp. H155-H170 ◽  
Author(s):  
Susan E. Howlett ◽  
Jie-Quan Zhu ◽  
Gregory R. Ferrier
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Ventricular Myocytes ◽  
Cardiac Contraction ◽  
Release Mechanism ◽  
Steady State Inactivation ◽  
Slope Factor ◽  
The Relationship

The contribution of a voltage-sensitive release mechanism (VSRM) for sarcoplasmic reticulum (SR) Ca2+ to contraction was investigated in voltage-clamped ventricular myocytes at 37°C. Na+ current was blocked with lidocaine. The VSRM exhibited steady-state inactivation (half-inactivation voltage: −47.6 mV; slope factor: 4.37 mV). When the VSRM was inactivated, contraction-voltage relationships were proportional to L-type Ca2+current ( I Ca-L). When the VSRM was available, the relationship was sigmoidal, with contractions independent of voltage positive to −20 mV. VSRM and I Ca-Lcontractions could be separated by activation-inactivation properties. VSRM contractions were extremely sensitive to ryanodine, thapsigargin, and conditioning protocols to reduce SR Ca2+ load. I Ca-Lcontractions were less sensitive. When both VSRM and I Ca-L were available, sigmoidal contraction-voltage relationships became bell-shaped with protocols to reduce SR Ca2+ load. Myocytes demonstrated restitution of contraction that was slower than restitution of I Ca-L. Restitution was a property of the VSRM. Thus activation and recovery of the VSRM are important in coupling cardiac contraction to membrane potential, SR Ca2+ load, and activation interval.

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