ArticleMolecular and cellular biochemistry2004
Voltage-dependence of contraction in streptozotocin-induced diabetic myocytes.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 35 citations in OpenAlex.
- Diabetes-induced chronic heart failure is due to defects in calcium transporting and regulatory contractile proteins: cellular and molecular evidence.Heart failure reviews · 2023Review
- CaPflugers Archiv : European journal of physiology · 2022Review
- Electrocardiological effects of ranolazine and lidocaine on normal and diabetic rat atrium.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021Article
- Effects of prolactin on ventricular myocyte shortening and calcium transport in the streptozotocin-induced diabetic rat.Heliyon · 2020Article
- Dapagliflozin reduces the amplitude of shortening and Ca(2+) transient in ventricular myocytes from streptozotocin-induced diabetic rats.Molecular and cellular biochemistry · 2015Article
- Streptozotocin-induced diabetes prolongs twitch duration without affecting the energetics of isolated ventricular trabeculae.Cardiovascular diabetology · 2014Article
- Structural changes in the myocardium during diabetes-induced cardiomyopathy.Heart failure reviews · 2014Review
- Novel tissue-specific mechanism of regulation of angiogenesis and cancer growth in response to hyperglycemia.Journal of the American Heart Association · 2012Article
- The chronic effects of neonatal alloxan-induced diabetes mellitus on ventricular myocyte shortening and cytosolic Ca2+.Molecular and cellular biochemistry · 2011Article
- Alloxan reduces amplitude of ventricular myocyte shortening and intracellular Ca2+ without altering L-type Ca2+ current, sarcoplasmic reticulum Ca2+ content or myofilament sensitivity to Ca2+ in Wistar rats.Molecular and cellular biochemistry · 2010Article
- Altered gene expression may underlie prolonged duration of the QT interval and ventricular action potential in streptozotocin-induced diabetic rat heart.Molecular and cellular biochemistry · 2009Article
- Effects of varying intensity exercise on shortening and intracellular calcium in ventricular myocytes from streptozotocin (STZ)-induced diabetic rats.Molecular and cellular biochemistry · 2008Article
- Effects of streptozotocin-induced diabetes on action potentials in the sinoatrial node compared with other regions of the rat heart.Molecular and cellular biochemistry · 2007Article
- Effects of carbenoxolone on heart rhythm, contractility and intracellular calcium in streptozotocin-induced diabetic rat.Molecular and cellular biochemistry · 2006Article
- The progressive effects of a fat enriched diet on ventricular myocyte contraction and intracellular Ca2+ in the C57BL/6J mouse.Molecular and cellular biochemistry · 2005Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac contractile dysfunction is frequently reported in human patients and experimental animals with type-1 diabetes mellitus. The aim of this study was to investigate the voltage-dependence of contraction in ventricular myocytes from the streptozotocin (STZ)-induced diabetic rat. STZ-induced diabetes was characterised by hyperglycaemia and hypoinsulinaemia. Other characteristics included reduced body and heart weight and raised blood osmolarity. Isolated ventricular myocytes were patched in whole cell, voltage-clamp mode after correcting for membrane capacitance and series resistance. From a holding membrane potential of -40 mV, test pulses were applied at potentials between -30 and +50 mV in 10 mV increments. L-type Ca2+ current (I Ca,L) density and contraction were measured simultaneously using a video-edge detection system. Membrane capacitance was not significantly altered between control and STZ-induced diabetic myocytes. The I Ca,L density was significantly (p < 0.05) reduced throughout voltage ranges (-10 mV to +10 mV) in myocytes from STZ-treated rats compared to age-matched controls. Moreover, the amplitude of contraction was significantly reduced (p < 0.05) in myocytes from STZ-treated rats at all test potentials between -20 mV and +30 mV. However, in electrically field-stimulated (1 Hz) myocytes, the amplitude of contraction was not altered by STZ-treatment. It is suggested that in field-stimulated myocytes taken from STZ-induced diabetic hearts, prolonged action potential duration may promote increased Ca2+ influx via the sodium-calcium exchanger (NCX), which may compensate for a reduction in Ca2+ trigger through L-type-Ca2+-channels and lead to normalised contraction.
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