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1. The aim of these experiments was to compare the time course of changes in intracellular Ca2+ concentration ([Ca2+]i) measured in the bulk cytoplasm with those estimated to occur near the sarcolemma. Sarcolemmal Na(+)-Ca2+ exchange current and [Ca2+]i were measured in single, voltage-clamped ventricular myocytes. 2. Spontaneous Ca2+ release from the(More)
The cardiac extracellular matrix (ECM) maintains the structural and mechanical integrity of the myocardium. We determined the alterations in the composition of the ECM coincident with the transition from compensated left ventricular (LV) hypertrophy (LVH) to symptomatic congestive heart failure (CHF) and the mechanisms underlying such changes. Heart failure(More)
The control of intracellular calcium is central to regulation of contractile force in cardiac muscle. This review illustrates how analysis of the control of calcium requires an integrated approach in which several systems are considered. Thus, the calcium content of the sarcoplasmic reticulum (SR) is a major determinant of the amount of Ca(2+) released from(More)
We have investigated the effects on spontaneous SR Ca release of modulating the sarcoplasmic reticulum ryanodine receptor (RyR) with low (<0.5 mM) concentrations of caffeine. Experiments were performed on isolated rat ventricular myocytes. Intracellular Ca concentration was measured with Indo-1 or Fluo-3 in voltage-clamped cells. Spontaneous Ca release was(More)
This article reviews the consequences of the need for the cardiac cell to be in calcium flux balance in the steady state. We first discuss how this steady state condition affects the control of resting [Ca(2+)]i. The next section considers how sarcoplasmic reticulum (SR) Ca content is controlled by a feedback mechanism whereby changes of SR Ca affect the(More)
The aim of this work was to measure membrane currents activated by Ca release from the cardiac sarcoplasmic reticulum (s.r.). Intracellular Ca concentration ([Ca2+]i) was measured using fluo-3 in patch clamped cells. Calcium release from the s.r. (whether occurring spontaneously or evoked by caffeine) produced changes of membrane current which could be(More)
T he bulk of the Ca 2ϩ that activates contraction in the heart comes from the sarcoplasmic reticulum (SR). Calcium is released by the process of Ca 2ϩ-induced Ca 2ϩ release (CICR) in which the entry of a small amount of Ca 2ϩ across the cell membrane triggers the release of much more from the SR. This mechanism depends on the fact that Ca 2ϩ entry from the(More)
A method is described to activate the systolic rise of [Ca2+]i in only one region of a single, isolated cell. This is achieved by applying the calcium chelator BAPTA to the rest of the cell from a pipette. Under control conditions electrical stimulation produced a Ca transient which was uniform throughout the cell. If a BAPTA containing solution was applied(More)
This review discusses the mechanism and regulation of Ca release from the cardiac sarcoplasmic reticulum. Ca is released through the Ca release channel or ryanodine receptor (RyR) by the process of calcium-induced Ca release (CICR). The trigger for this release is the L-type Ca current with a small contribution from Ca entry on the Na-Ca exchange. Recent(More)
Age-related loss of tissue elasticity is a common cause of human morbidity and arteriosclerosis (vascular stiffening) is associated with the development of both fatal strokes and heart failure. However, in the absence of appropriate micro-mechanical testing methodologies, multiple structural remodelling events have been proposed as the cause of(More)