scholarly journals The role of the sarcoplasmic reticulum in the response of ferret and rat heart muscle to acidosis.

1987 ◽  
Vol 384 (1) ◽  
pp. 431-449 ◽  
Author(s):  
C H Orchard
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Heart Muscle ◽  
Rat Heart

scholarly journals Brain natriuretic peptide secretion in adult rat heart muscle cells: The role of calcium channels

2008 ◽  
Vol 101 (7-8) ◽  
pp. 459-463 ◽  
Author(s):  
Laurence Nader ◽  
Viviane Smayra ◽  
Victor Jebara ◽  
Patrick Bois ◽  
Daniel Potreau ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Heart Muscle ◽  
Rat Heart ◽  
Muscle Cells ◽  
Adult Rat ◽  
Heart Muscle Cells ◽  
Peptide Secretion

scholarly journals Pyruvate carboxylation in the rat heart. Role of biotin-dependent enzymes

1989 ◽  
Vol 257 (3) ◽  
pp. 913-916 ◽  
Author(s):  
K E Sundqvist ◽  
J K Hiltunen ◽  
I E Hassinen
Keyword(s):  
Heart Muscle ◽  
Malic Enzyme ◽  
Rat Heart ◽  
Pyruvate Carboxylase ◽  
Mass Action ◽  
Kinetic Properties ◽  
Biotin Deficiency ◽  
Perfused Rat Heart ◽  
Pyruvate Carboxylation

Pyruvate carboxylation in the isolated perfused rat heart was studied under steady-state conditions. A biotin deficiency resulting in a 90% decrease in myocardial pyruvate carboxylase left the pyruvate carboxylation rate unchanged. Pyruvate carboxylation in heart muscle must therefore take place by means of an enzyme which does not contain biotin. The kinetic properties and mass-action ratio of the NADP-linked malic enzyme in heart muscle can be taken as circumstantial evidence in favour of the role of malic enzyme in pyruvate carboxylation in myocardium.

scholarly journals Intracellular calcium transients and developed tension in rat heart muscle. A mechanism for the negative interval-strength relationship.

1985 ◽  
Vol 86 (5) ◽  
pp. 637-651 ◽  
Author(s):  
C H Orchard ◽  
E G Lakatta
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Heart Muscle ◽  
Rat Heart ◽  
Calcium Transients ◽  
Time Dependent ◽  
Papillary Muscles ◽  
Stimulation Rate ◽  
Age Related ◽  
Old Rats ◽  
Strength Relationship

The purposes of the present study were to determine (a) whether changes of intracellular [Ca2+] (Cai) can account for the decrease of developed tension observed in rat heart muscle when stimulation rate is increased, and (b) whether the effect of stimulation rate on Cai is altered in conditions in which the rate of repriming of the sarcoplasmic reticulum (SR) is altered, as when perfusate [Ca2+] (Cao) is increased, and in heart muscle from senescent animals. The photoprotein aequorin was used to monitor Cai in rat papillary muscles. In muscles from 6-mo-old rats, increasing the stimulation rate in the range 0.2-0.66 Hz led to parallel decreases of both the aequorin light transient and developed tension when Cao was 2 mM. When Cao was increased to 4 mM, changes in the stimulation rate had less effect on both the light transient and tension. At 8 mM Cao, changing the stimulation rate had no effect on either the light transient or developed tension. Papillary muscles from 24-mo-old rats, in which SR function is likely to be depressed, exhibited a prolonged Ca2+ transient and twitch. At a Cao of 4 or 8 mM, increasing the stimulation rate from 0.33 to 0.66 Hz still led to decreases in the size of the aequorin light transient and developed tension in these muscles. Developed tension and aequorin light responded to increases of Cao in the same way in both groups of muscles. We conclude that under the conditions of our experiments, developed tension is determined by Cai. The negative interval-strength relationship observed when Cao is in the physiological range can be accounted for by a time-dependent recycling of Ca2+ by the SR. The effects of increasing Cao and the age-related differences observed at high Cao can also be accounted for using this model.

Effects of cocaine on sarcoplasmic reticulum in skinned rat heart muscle

1993 ◽  
Vol 264 (3) ◽  
pp. H845-H850 ◽  
Author(s):  
F. Tomita ◽  
A. L. Bassett ◽  
R. J. Myerburg ◽  
S. Kimura
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Heart Muscle ◽  
Rat Heart ◽  
Cardiac Toxicity ◽  
Contractile Proteins ◽  
Left Ventricular ◽  
Simultaneous Application ◽  
Contractile System ◽  
Uptake Studies ◽  
Tension Experiments

We examined the effects of cocaine on the ability of the sarcoplasmic reticulum (SR) to release and accumulate Ca2+ and on the Ca2+ sensitivity of the contractile proteins using chemically skinned rat left ventricular muscles. The preparations were treated with saponin (40 micrograms/ml for Ca2+ release and uptake studies and 200 micrograms/ml for Ca(2+)-tension experiments). The SR was loaded with 10(-6) M Ca2+ solution; SR Ca2+ release was induced by application of 5 or 25 mM caffeine. The amount of Ca2+ released from the SR was estimated by the area under the caffeine-induced transient contraction. After 1 min of SR Ca2+ loading, simultaneous application of 50 microM cocaine and 5 mM caffeine increased caffeine-induced Ca2+ release by 15.7 +/- 3.1% (P < 0.05). However, when Ca(2+)-loaded preparations were treated with cocaine for 1 min before application of 5 mM caffeine, caffeine-induced Ca2+ release was reduced by 17.1 +/- 3.0% (P < 0.05). When cocaine was applied during the Ca2+ loading periods, the amount of Ca2+ accumulated by the SR (the area under the 25 mM caffeine-induced contraction) increased for both 1-min (10.9 +/- 1.7%, P < 0.05) and 3-min (15.5 +/- 4.4%, P < 0.05) Ca2+ loading periods. Cocaine (50 microM) had no effect on the Ca2+ sensitivity of the contractile system. We conclude that cocaine at a concentration of 50 microM can directly alter the ability of the SR to release and accumulate Ca2+. These effects of cocaine, especially those on SR Ca2+ release, may play a role in its potential for induction of cardiac toxicity.

Sign in / Sign up

Export Citation Format

Share Document