Summary
It is well documented that changes in contractility of the heart can originate from alterations at the level of the sarcolemma and the intracellular Ca2+ stores. Less is known on the modulatory properties of the myofibrils. Using skinned fibres, the response of the myofibrils in terms of tension generation can be varied to a great extent at a fixed myoplasmic free [Ca2+]. TheHill equation provides a basis for characterizing the Ca2+-dependent activation in terms of co-operativity, Ca2+ sensitivity and tension at full activation. Three formally different types of activation curves are possible. Using this approach, a great number of tension vs. free [Ca2+] data were critically evaluated.
A most interesting property of the myofibrils is their ability to respond to changes in free [Ca2+] in a co-operative manner. In isolated preparations the degree ofco-operativity is apparently quite variable. By analyzing 16 published activation curves it was found that theHill n ranges between 1.0 and about 12. Beside the muscle type and probably methodological differences, also other factors contribute to this variation inHill n, such as a low [MgATP] and a low [Mg2+]. At a given intracellular Ca2+-transient, the co-operativity of the contractile system would influence both, the time-course of tension development and the extent of activation.
Among the factors which increase theCa 2+ sensitivity of the contractile system are decreasing [Mg2+] (5→0.05 mM), increasing pH (6→7), a less favourable overlap of the filaments and dephosphorylation of troponin I. It might be expected that changes in the Ca2+ sensitivity arise from the level of troponin. This holds most probably for the effects induced by Mg2+ and phosphorylation of troponin I. The effect of stretch or of H+ does probably not originate solely from the thin filaments. Alterations in Ca2+ sensitivity provide a mechanism for modulating the degree of activation at a given intracellular [Ca2+]. This mechanism plays certainly a role in changes in contractility during hypoxia, ischemia and acidosis.
The third parameter,tension at full activation is increased by a decreasing [MgATP] (4→0.03mM), increasing pH (6→7) and a more favourable overlap of the filaments. The effect of MgATP is attributed to a substrate inhibition at high [MgATP]. A decreasing sarcomere length results in a greater number of interacting sites between thin and thick filaments and so enhances maximum tension.
It should be pointed out that some of the above effects are of an opposite nature. For example, in ischemia the Ca2+ sensitivity and maximum tension is decreased due to acidosis. Concomitantly, [MgATP] is reduced resulting in a shift of the activation curve to lower [Ca2+] and an increase in maximum tension.
Thus it is difficult to predict the response of a contractile system under certain pathophysiological conditions. It should also be kept in mind that the intact cardiac cell might react in a different way due to the action of the sarcolemma or the intracellular Ca2+ stores. Nevertheless, the present approach should prove helpful in tracing changes in contractile activity of the intact myocardium to molecular events at the myofibrillar level.
Zusammenfassung
Es ist gut dokumentiert, daß Ąnderungen in der Kontraktilität des Herzens auf Vorgängen auf der Ebene des Sarkolemms und der intrazellulären Ca2+-Speicher beruhen können. Die Möglichkeit einer Modulation der Kraftenwicklung auf der Ebene der Myofibrillen ist weniger gut untersucht. Bei gehäuteten Fasern kann die Kraftentwicklung bei einer gegebenen freien [Ca2+] stark variiert werden. Die Hill-Gleichung bietet die Möglichkeit, die Ca2+-abhängige Aktivierung in bezug auf die Kooperativität, die Ca2+-Sensitivität und die Spannung bei Vollaktivierung zu charakterisieren. So gibt es drei formal verschiedene Arten von Aktivierungskurven. Mit diesem Verfahren wurde eine große Zahl von Daten (% Spannung gegen freie [Ca2+]) ausgewertet.
Von großem Interesse ist, daß Myofibrillen eine positiveKooperativität in bezug auf die Ca2+-Aktivierung aufweisen. Bei isolierten Präparaten variiert das Maß an Kooperativität ziemlich stark. Wie die Analyse von 16 publizierten Aktivierungskurven zeigt, bewegt sich der Hill-n-Wert zwischen 1,0 und ungefähr 12. Neben der Art des Muskels und methodischen Unterschieden tragen auch andere Faktoren zu dieser Variation bei, so wie niedrige [MgATP] und [Mg2+]. Bei einem gegebenen intrazellulären Ca2+-Transienten bestimmt die Kooperativität über die Steilheit der Aktivierungskurve sowohl den zeitlichen Verlauf der Spannungsentwicklung als auch den Aktivierungsgrad.
Zu den Faktoren, die dieCa 2+-Sensitivität des kontraktilen Systems erhöhen, zählen eine abnehmende [Mg2+] (5→0,05 mM), zunehmender pH-Wert (6→7), eine weniger günstige Überlappung der Filamente und die Dephosphorylierung von Troponin I. Es wäre zu erwarten, daß Veränderungen in der Ca2+-Sensitivität ihren Ursprung am Troponin haben. Dies trifft sehr wahrscheinlich zu für die Effekte, die durch Mg2+ und Phosphorylierung von Troponin I hervorgerufen werden. Die Wirkung von Dehnung und von H+ geht wahrscheinlich nicht allein von den dünnen Filamenten aus. Veränderungen in der Ca2+-Sensitivität erlauben es, den Aktivierungsgrad bei einer vorgegebenen intrazellulären [Ca2+] zu modulieren. Dieser Mechanismus spielt sicherlich eine Rolle bei Veränderungen der Kontraktilität während einer Hypoxie, Ischämie und Azidose.
Der dritte Parameter, dieSpannung bei Vollaktivierung, ist erhöht bei einer abnehmenden [MgATP] (4→0,03 mM), zunehmendem pH-Wert (6→7) und einer günstigeren Überlappung der Filamente. Der MgATP-Effekt wird einer Substrathemmung bei hoher [MgATP] zugeordnet. Eine abnehmende Sarkomerenlänge führt zu einer größeren Zahl von Interaktionsstellen zwischen dünnen und dicken Filamenten und erhöht somit die maximale Spannung.
Es soll hervorgehoben werden, daß einige der obengenannten Effekte gegenläufig sind. Zum Beispiel führt die Azidose, ausgelöst durch eine Ischämie, zu einer Abnahme der Ca2+-Sensitivität und der maximalen Spannung. Gleichzeitig ist jedoch [MgATP] erniedrigt und führt so zu einer Verschiebung der Aktivierungskurve zu niedrigeren [Ca2+] und zu einer Zunahme der maximalen Spannung.
Dies deutet die Schwierigkeit an, die Antwort eines kontraktilen Systems unter bestimmten pathophysiologischen Bedingungen vorauszusagen. Weiterhin sollte berücksichtigt werden, daß die intakte Myokardzelle in einer anderen Weise reagieren kann, zurückzuführen auf die Wirkung des Sarkolemms oder der intrazellulären Ca2+-Speicher. Trotz aller Einschränkungen sollte die hier beschriebene Analyse es ermöglichen, Veränderungen in der Kontraktilität des intakten Myokards mit molekularen Vorgängen auf der Ebene der Myofibrillen in Beziehung zu setzen.
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Rupp, H. Modulation of tension generation at the myofibrillar level—an analysis of the effect of magnesium adenosine triphosphate, magnesium, pH, sarcomere length and state of phosphorylation. Basic Res Cardiol 75, 295–317 (1980). https://doi.org/10.1007/BF01907579
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DOI: https://doi.org/10.1007/BF01907579