scholarly journals Effect of  -adrenergic stimulation on the relationship between membrane potential, intracellular [Ca2+] and sarcoplasmic reticulum Ca2+ uptake in rainbow trout atrial myocytes

2004 ◽  
Vol 207 (8) ◽  
pp. 1369-1377 ◽  
Author(s):  
A. Llach
Keyword(s):  
Rainbow Trout ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Atrial Myocytes ◽  
Adrenergic Stimulation ◽  
The Relationship

The function of the sarcoplasmic reticulum is not inhibited by low temperatures in trout atrial myocytes

2001 ◽  
Vol 281 (6) ◽  
pp. R1902-R1906 ◽  
Author(s):  
Leif Hove-Madsen ◽  
Anna Llach ◽  
Lluis Tort
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Low Temperatures ◽  
Experimental Temperature ◽  
Effect Of Temperature ◽  
Fast Time ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Two Temperatures ◽  
Perforated Patch Clamp ◽  
The Relationship

The effect of temperature on sarcoplasmic reticulum (SR) Ca2+ uptake and release was measured in trout atrial myocytes using the perforated patch-clamp technique. Depolarization of the myocyte for 10 s to different membrane potentials ( V m) induced SR Ca2+ uptake. The relationship between V m and SR Ca2+ uptake was not significantly changed by lowering the experimental temperature from 21 to 7°C, and the relationship between total cytosolic Ca2+and SR Ca2+ uptake was similar at the two temperatures with a pooled Vmax = 66 amol/pF and K 0.5 = 4 amol/pF. Quantification of the Ca2+ release from the SR elicited by 10-ms depolarizations to different V m showed an increasing SR Ca2+ release at more positive V mbetween −50 and +10 mV, whereas SR Ca2+ release stagnated between +10 and +50 mV. Lowering of the temperature did not affect this relationship significantly, giving an SR Ca2+ release of 1.71 and 1.54 amol/pF at 21 and 7°C, respectively. Furthermore, clearance of the SR Ca2+ content slowed down inactivation of the L-type Ca2+ current at both temperatures (the fast time constant increased significantly from 10.4 ± 1.9 to 15.0 ± 2.0 ms at 21°C and from 38 ± 15 to 73 ± 24 ms at 7°C). Thus the SR has the capacity to remove the entire Ca2+ transient at physiologically relevant stimulation frequencies at both 21 and 7°C, although it is estimated that ∼40% of the total Ca2+ transient is liberated from and reuptaken by the SR with continuous stimulation at 0.5 Hz independently of the experimental temperature.

scholarly journals The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart

2014 ◽  
Vol 307 (12) ◽  
pp. R1493-R1501 ◽  
Author(s):  
Caroline Cros ◽  
Laurent Sallé ◽  
Daniel E. Warren ◽  
Holly A. Shiels ◽  
Fabien Brette
Keyword(s):  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Adrenergic Stimulation ◽  
Relative Contribution ◽  
Safety Mechanism ◽  
Rapid Changes ◽  
Intracellular Ca ◽  
As Stress

Cardiomyocyte contraction depends on rapid changes in intracellular Ca2+. In mammals, Ca2+ influx as L-type Ca2+ current ( ICa) triggers the release of Ca2+ from sarcoplasmic reticulum (SR) and Ca2+-induced Ca2+ release (CICR) is critical for excitation-contraction coupling. In fish, the relative contribution of external and internal Ca2+ is unclear. Here, we characterized the role of ICa to trigger SR Ca2+ release in rainbow trout ventricular myocytes using ICa regulation by Ca2+ as an index of CICR. ICa was recorded with a slow (EGTA) or fast (BAPTA) Ca2+ chelator in control and isoproterenol conditions. In the absence of β-adrenergic stimulation, the rate of ICa inactivation was not significantly different in EGTA and BAPTA (27.1 ± 1.8 vs. 30.3 ± 2.4 ms), whereas with isoproterenol (1 μM), inactivation was significantly faster with EGTA (11.6 ± 1.7 vs. 27.3 ± 1.6 ms). When barium was the charge carrier, inactivation was significantly slower in both conditions (61.9 ± 6.1 vs. 68.0 ± 8.7 ms, control, isoproterenol). Quantification revealed that without isoproterenol, only 39% of ICa inactivation was due to Ca2+, while with isoproterenol, inactivation was Ca2+-dependent (∼65%) and highly reliant on SR Ca2+ (∼46%). Thus, SR Ca2+ is not released in basal conditions, and ICa is the main trigger of contraction, whereas during a stress response, SR Ca2+ is an important source of cytosolic Ca2+. This was not attributed to differences in SR Ca2+ load because caffeine-induced transients were not different in both conditions. Therefore, Ca2+ stored in SR of trout cardiomyocytes may act as a safety mechanism, allowing greater contraction when higher contractility is required, such as stress or exercise.

Na+/Ca2+-exchange activity regulates contraction and SR Ca2+ content in rainbow trout atrial myocytes

2000 ◽  
Vol 279 (5) ◽  
pp. R1856-R1864 ◽  
Author(s):  
Leif Hove-Madsen ◽  
Anna Llach ◽  
Lluis Tort
Keyword(s):  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Atrial Myocytes ◽  
Initial Value ◽  
Inhibitory Peptide ◽  
Patch Clamp Technique ◽  
Cell Shortening ◽  
Control Value ◽  
Patch Pipette ◽  
Exchange Activity

We have used the whole cell configuration of the patch-clamp technique to measure sarcolemmal Ca2+ transport by the Na+/Ca2+ exchanger (NCX) and its contribution to the activation and relaxation of contraction in trout atrial myocytes. In contrast to mammals, cell shortening continued, increasing at membrane potentials above 0 mV in trout atrial myocytes. Furthermore, 5 μM nifedipine abolished L-type Ca2+current ( I Ca) but only reduced cell shortening and the Ca2+ carried by the tail current to 66 ± 5 and 67 ± 6% of the control value. Lowering of the pipette Na+ concentration from 16 to 10 or 0 mM reduced Ca2+ extrusion from the cell from 2.5 ± 0.2 to 1.0 ± 0.2 and 0.5 ± 0.06 amol/pF. With 20 μM exchanger inhibitory peptide (XIP) in the patch pipette Ca2+extrusion 20 min after patch break was 39 ± 8% of its initial value. With 16, 10, and 0 mM Na+ in the pipette, the sarcoplasmic reticulum (SR) Ca2+ content was 47 ± 4, 29 ± 6, and 10 ± 3 amol/pF, respectively. Removal of Na+ from or inclusion of 20 μM XIP in the pipette gradually eliminated the SR Ca2+ content. Whereas I Ca was the same at −10 or +10 mV, Ca2+ extrusion from the cell and the SR Ca2+content at −10 mV were 65 ± 7 and 80 ± 4% of that at +10 mV. The relative amount of Ca2+ extruded by the NCX (about 55%) and taken up by the SR (about 45%) was, however, similar with depolarizations to −10 and +10 mV. We conclude that modulation of the NCX activity critically determines Ca2+ entry and cell shortening in trout atrial myocytes. This is due to both an alteration of the transsarcolemmal Ca2+ transport and a modulation of the SR Ca2+ content.

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.

The effect of temperature and adrenaline on the relative importance of the sarcoplasmic reticulum in contributing Ca2+ to force development in isolated ventricular trabeculae from rainbow trout

1997 ◽  
Vol 200 (11) ◽  
pp. 1607-1621 ◽  
Author(s):  
H Shiels ◽  
A Farrell
Keyword(s):  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Test Temperature ◽  
Acclimation Temperature ◽  
Relative Importance ◽  
Adrenergic Stimulation ◽  
Release Channel ◽  
Force Development ◽  
Peak Tension ◽  
Ventricular Trabeculae

The sarcoplasmic reticulum (SR) is central to intracellular Ca2+ regulation during excitation­contraction (E-C) coupling in mammalian cardiac tissue. The importance of the SR to E-C coupling in lower vertebrates is less certain. This uncertainty can be attributed, in part, to the temperature-dependency of the SR Ca2+-release channel and to interspecific differences in the ryanodine-sensitivity of ectotherm cardiac muscle. Furthermore, the relative importance of the SR in contributing intracellular Ca2+ to force development may be influenced by adrenergic stimulation, which increases trans-sarcolemmal (extracellular) Ca2+ influx. The objective of this study was to assess the relative importance of SR (intracellular) and sarcolemmal (SL; extracellular) Ca2+ fluxes during the isometric contraction of isolated ventricular trabeculae from rainbow trout Oncorhynchus mykiss. To approximate in vivo Ca2+ availability to the muscle better, a tonic level (10 nmol l-1) of adrenaline was used in all control experiments, and SL Ca2+ influx was stimulated with high levels (10 µmol l-1) of adrenaline. Ryanodine, a noted blocker of SR Ca2+ release in mammals, was used to assess SR involvement. To examine the role of temperature on the relative Ca2+ contribution from each source, experiments were performed at two temperatures (12 and 22 °C), using ventricular trabeculae from fish acclimated to both 12 and 22 °C. Under all test conditions studied, SL Ca2+ influx was the primary source of activator Ca2+, as assessed by the change in isometric force after ryanodine application. Even so, the SR contribution of activator Ca2+ was significantly greater at a test temperature of 22 °C than at 12 °C. We attribute this observation to the temperature-dependent nature of the SR Ca2+-release channel. At 22 °C and under control conditions, ryanodine reduced peak tension at all pacing frequencies (by approximately 50 % at 0.2 Hz, approximately 25 % at 1.2 Hz and approximately 20 % at 2.0 Hz), regardless of acclimation temperature. Therefore, the SR is a significant, but secondary, contributor of activator Ca2+ for tension development at warm temperatures. The magnitude of SR Ca2+ contribution was inversely related to pacing frequency, but remained significant at physiological pacing frequencies. This was a novel finding. The degree of ryanodine-sensitivity in the present study was greater than that reported previously for the rainbow trout. We attribute this difference to the use of tonic adrenergic stimulation in the present study. In contrast to the experiments at the warmer test temperature, at 12 °C and under control conditions, ryanodine significantly reduced peak tension only at low frequencies (by approximately 25 % at 0.2 Hz), regardless of acclimation temperature. These findings suggest that at cold temperatures, and at physiologically relevant pacing frequencies, the SR may not be important in supplying Ca2+ to the contractile elements of the trout heart. At both test temperatures and regardless of acclimation temperature, stimulation with 10 µmol l-1 adrenaline caused positive inotropy of sufficient magnitude to ameliorate the negative inotropic effect of ryanodine completely, with the exception of high pacing frequencies (>1.2 Hz) at 22 °C, where adrenergic stimulation did not fully compensate for the effects of ryanodine. This exception is discussed in relation to the reduced adrenergic sensitivity of the trout myocardium at warm temperatures. The adrenergically mediated compensation for the loss of the SR Ca2+ supply is a novel finding for fish hearts. Therefore, while our study clearly demonstrates that the relative importance of SR Ca2+ release is subject to temperature and frequency, adrenaline-mediated increases in SL Ca2+ influx decrease the importance of the SR in contributing Ca2+ to E-C coupling in trout ventricular myofilaments.

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