Contraction Of Guinea-pig Papillary Muscle Research Articles

Tight coupling between the rate of rise of Ca 2+ transient and peak twitch contraction in guinea-pig papillary muscle

We evaluated the relationship between cytoplasmic Ca 2+ concentration ([Ca 2+] i) and force in guinea-pig papillary muscles loaded with a fluorescent Ca 2+ indicator, fura-PE3. In the absence of ryanodine, [Ca 2+] i transient and force were altered by changing extracellular Ca 2+ concentration and stimulation frequency, and also by adding methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5-carboxylate (Bay K 8644) or ouabain. Under these conditions, the peak force correlated linearly with the maximal rate of rise of [Ca 2+] i ( γ=0.948) more than the peak [Ca 2+] i transient ( γ=0.737). Ryanodine inhibited the increase in the maximal rate of rise of [Ca 2+] i resulting in abolishment of the correlation between force and the maximal rate of rise of [Ca 2+] i. These results suggest that the maximal rate of rise of [Ca 2+] i reflects Ca 2+ release from the sarcoplasmic reticulum, and this fraction of [Ca 2+] i is crucial for determining the amplitude of twitch contractions when the sarcoplasmic reticulum is intact in guinea-pig papillary muscle.

Leukotriene D 4 increases both the force of contraction and polyphosphoinositide formation in guinea-pig papillary muscle

Leukotriene D 4 (LTD 4) increased the force of contraction in guinea-pig papillary muscle. A rapid (< 1 min), transient (< 5 min) response to LTD 4 (l μM) reached 19.3 ± 5.4% of isoproterenol maximum. A single exposure to LTD 4 resulted in complete and homologous desensitization which was not influenced by indomethacin. LTD 4 (0.1–3.0 μM) increased total inositol phosphates released from [ 3H]inositol-labeled tissue. ICI 198,615, a selective LT receptor antagonist, blocked both the increase in force of contraction and the increase in inositol phosphates by LTD 4, but had no effect on the inotropic response to isoproterenol. These data support the existence of specific functional LTD 4 receptors in myocardial tissue of guinea-pigs.

Calcium channels and excitation–contraction coupling in cardiac cells. II. A pharmacological study of the biphasic contraction in guinea-pig papillary muscle

Biphasic contractions were obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) in the presence of 0.3 microM isoproterenol. Mn2+ ions inhibited the two components of contraction in a similar way. Nifedipine and particularly Cd2+ ions specifically inhibited the second component of contraction. Isoproterenol and BAY K 8644 markedly increased the amplitude of the second component (P2) of contraction. Nevertheless, a moderate positive inotropic effect of isoproterenol was found on the first component (P1) of contraction when excitability was restored by 0.2 mM Ba instead of isoproterenol. Acetylcholine and hypoxia decreased the amplitude of the second component of contraction to a greater extent. In the presence of digoxin or Na+-free solution, P1 was strongly increased. When sarcoplasmic reticular function was hindered by 1mM caffeine or in the presence of Ca2+-free Sr2+ solution, digoxin always induced a negative inotropic effect on P2. Inversely in these conditions the transient positive inotropic effect of Na+-free solution was strongly reduced. These results are consistent with the hypothesis that the late component of contraction is triggered by the slow inward Ca2+ current and that the early component is due to Ca2+ release from the sarcoplasmic reticulum.

Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 microM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.