POSTNATAL DEVELOPMENT OF CALCIUM (Ca) RELEASE FROM CARDIAC SARCOPLASMIC RETICULUM(SR)

Abstract

Potentiation of contractile force of the first stimulated contraction following a rest interval (rest potentiation; RP)has been attributed to enhanced SR Ca release. Postnatal development of SR Ca release was assessed by evaluating RP in oxygenated left atrial strips isolated from immature (I;14-21 day old; n=11) and adult (A; n=9) rabbits. Isometric developed tension (DT) and dT/dt (pH=7.4;@30°C) were determined while pacing at 1 Hz (control) and following 2-90 sec. rest intervals (RI). RP was maximal at 60 sec. RI. Ryanodine (10⁻⁸M), a putative blocker of SR Ca release, abolished RP in both age groups. At 2.5mM extracellular Ca (Ca)_e, DT was potentiated 176% in I and 287% in A while dT/dt was potentiated 163% in I and 295% in A (A>I; p<0.05). However, at 5mM (Ca)_e, DT was potentiated 310% in I but only 215% in A(I>A;p<0.05). Mechanisms whereby the increase in (Ca)_e increased RP in I might include either an increase in the action potential-mediated Ca influx that triggers SR Ca release or an increase in SR Ca loading. To evaluate these mechanisms, (Ca)_e was increased from 2.5 to 5mM during the RI. RP was increased comparably in both age-groups, although the increase was small (≤25%) when compared with the 176% increase in RP in I when (Ca)_e was increased to 5mM prior to RI. These results indicate that the immature heart requires a higher (Ca)_e to optimize SR Ca loading as compared to the adult, and this difference may be a functional correlate of the recognized morphologic maturation of cardiac SR during postnatal development.

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