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

Abstract

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.

Contractions in guinea‐pig ventricular myocytes triggered by a calcium‐release mechanism separate from Na+ and L‐currents.

“…In other studies, similar biphasic contractions were induced by partial membrane depolarization in potassium-rich solutions containing f8-adrenergic agonists (Reiter, Vierling & Seibel, 1984;Honore, Adamantidis, Dupuis, Challice & Guilbault, 1987a, b). The first component again was sensitive to agents and manipulations which alter SR Ca2+ stores whereas the second component was sensitive to the L-type Ca2+ channel blockers, nifedipine and Cd2 .…”

“…Partial replacement of external Ca2+ with Sr2+ (Braveny & Sumbera, 1972) reveals biphasic contractions composed of an early component which can be inhibited by ryanodine and a late component which is more sensitive to the Ca2+ channel antagonist Mn2+ (King & Bose, 1983). In other studies, similar biphasic contractions were induced by partial membrane depolarization in potassium-rich solutions containing f8-adrenergic agonists (Reiter, Vierling & Seibel, 1984;Honore, Adamantidis, Dupuis, Challice & Guilbault, 1987a, b). The first component again was sensitive to agents and manipulations which alter SR Ca2+ stores whereas the second component was sensitive to the L-type Ca2+ channel blockers, nifedipine and Cd2 .…”

Utilization of fatigued and non-fatigued isolated guinea-pig papillary muscles and ventricular myocytes on the comparison of inotropic, chronotropic and intracellular calcium changes induced by monensin and digoxin

“…It has been demonstrated that 3 and 10 |jmol/l digoxin strongly enhanced PI which overlapped P2 [26]. When PI is inhibited by using a -free solution, digoxin exerts only a negative inotropic effect [29]. Thus, in agreement with Adamantidis et cd., [26], the positive inotropic effect of digoxin is thought to be mediated by an increase in activator Ca which enters the cell and causes the release of Ca from the SR. Digoxin increased the ICV of guinea-pig papillary muscles at T1 and monensin increased the ICV at T4.…”

“…of the contraction wave [29]. An increase in the rate of Ca^"^ release from the SR would increase the ICV.…”

“…The ACV is not only influenced by the rate of Ca^"^ release from the SR but also it is influenced by the Ca mflux, number of functional cross-bridges and affinity of troponin C for Ca^"^ [29]. An increase in Ca^"^ release from the SR woxild increase ACV by allowing increased binding of Ca to the contractile proteins and by increasing ATPase activity of myosin [14].…”