During further development the ability of sarcoplasmic reticulum to accumulate Ca2+ increases and there is a progressive maturation of Ca2+ release from the sarcoplasmic reticulum . Growth retardation in offspring of diabetic mothers thus seems to be connected with the slower development of systems responsible for calcium handling in cardiac muscle. Whether these changes may also represent some delayed effect of disturbances in prenatal development remains, however, a matter of speculation. Similar retardation of cardiac maturation was observed following other prenatal interventions, such as hypoxia or administration of retinoic acid .It has been repeatedly reported that adult rats made diabetic with streptozotocin exhibit depressed cardiac contractile function . Experimental studies at the cellular level have provided data for several possible explanations for this dysfunction. Among these, an abnormal intracellular Ca2+ homeostasis and trans-sarcolemmal receptor signalling defects have been suggested . You can find best quality treatment now – buy zoloft online to see how cheap it is.
Two kinds of Ca2+-dependent alterations may affect contractility of the diabetic heart : changing the availability of Ca2+ to the myofilaments; and modifying the responsiveness of the myofilaments to activation by intracellular Ca2+. There has, however, been no consistent finding regarding the sensitivity of the myofilaments to Ca2+: the sensitivity of isolated myofibrils has been reported to be unchanged , increased or decreased during diabetes. Although these experiments were performed under different conditions, the data appear to suggest that altered intracellular Ca2+ transients are not the only cause of cardiac dysfunction.