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The mechanism of the heart's adaptation to prolonged load and dynamics of RNA synthesis in the myocardium

Der Mechanismus der Anpassung des Herzens an langdauernde Mehrbelastung und die Dynamik der RNA-Synthese im Myokard

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Summary

Calculation of RNA synthesis rate in the rat myocardium during compensatory heart hyperfunction (CHH) was based on the study of the dynamics of RNA concentration and degradation. The parallel consideration of RNA synthesis rate and phosphorylation potential ([ADP]·[Pi]/[ATP]) showed that in the early stage of CHH, RNA synthesis rate increase follows phosphorylation potential increase. With literature data having been reviewed, the paper shows that this fact corresponds to the general concept that the deficit of high energy phosphate compounds is the signal activating the genetic apparatus and “triggering” the formation of the structural basis of heart adaptation to prolonged load. The paper further shows that protein synthesis activation and heart mass increase in the process of heart hyperfunction are conditioned not only by RNA concentration and the increase in ribosome amount, but, as well, by the increase in the ratio of translating to nontranslating ribosomes. The signal activating the genetic apparatus might ensure synthesis increase of messenger RNA exceeding that of ribosomal RNA and thus explain the shift in the ratio.

The heart's adaptation to prolonged load develops incessantly as an indispensable element of the organism's adaptation to the outer environment or to a progressively developing ailment. It seems reasonable to view the mechanism of the heart's adaptation to prolonged load on the basis of a more general concept of adaptation. The paper, therefore, summarizes the general concept of the adaptation mechanism recently developed in our laboratory (10–17, 19) and presents the experimental data on RNA biosynthesis in the myocardium during compensatory hyperfunction of the heart in terms of this mechanism.

Zusammenfassung

Die RNS-Synthesegeschwindigkeit während kompensatorischer Hyperfunktion des Herzens konnte nach der Bestimmung des zeitlichen Verlaufs von RNS-Konzentration und RNS-Abbau berechnet werden. Die gleichzeitige Verfolgung von RNS-Synthesegeschwindigkeit und Phosphorylierungspotential ([ADP]·[Pi]/[ATP]) zeigte, daß im frühen Stadium der Herzhyperfunktion die Steigerung der RNS-Synthesegeschwindigkeit nach dem Anstieg des Phosphorylierungspotentials einsetzt. Zusammen mit den zitierten Daten aus der Literatur entsprechen diese Befunde dem allgemeinen Konzept, daß das Defizit an energiereichen Phosphaten das Signal für die Aktivierung des Gen-Apparates darstellt und Strukturveränderungen zur Adaptation des Herzens an erhöhte Belastung auslöst. Weiterhin wurde gezeigt, daß die Aktivierung der Proteinsynthese und die Steigerung des Herzgewichts bei Hyperfunktion nicht nur durch Erhöhung der RNS-Konzentration und der Ribosomenmenge bedingt ist, sondern auch durch die Zunahme des Verhältnisses von zur Proteinsynthese fähigen Polyribosomen zu “nichtsynthese-bereiten” Ribosomen. Dieses veränderte Verhältnis könnte dadurch bedingt sein, daß das Gen-aktivierende Signal eine vermehrte Synthese der messenger-RNS im Vergleich zur ribosomalen RNS auslöst.

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Authors and Affiliations

  1. Laboratory of experimental Cardiology of the Institute of Normal and Pathological Physiology, Academy of Medical Science, Moscow, (U.S.S.R.)

    F. Z. Meerson, M. P. Javitz, A. M. Breger & M. I. Lerman

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  1. F. Z. Meerson
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  2. M. P. Javitz
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  3. A. M. Breger
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  4. M. I. Lerman
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Meerson, F.Z., Javitz, M.P., Breger, A.M. et al. The mechanism of the heart's adaptation to prolonged load and dynamics of RNA synthesis in the myocardium. Basic Res Cardiol 69, 484–499 (1974). https://doi.org/10.1007/BF01906981

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