Results 81 to 90 of about 4,095,708 (243)

Long-Term Serial Exercise Stress Testing in Catecholaminergic Polymorphic Ventricular Tachycardia on Beta-Blocker and Flecainide Therapy. [PDF]

open access: yesJ Cardiovasc Electrophysiol
ABSTRACT Introduction Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially life‐threatening arrhythmic disorder typically treated with beta‐blockers and, occasionally, with flecainide. Methods All patients underwent genetic testing, electrocardiogram, echocardiogram, and exercise testing.
Wangüemert-Perez F   +9 more
europepmc   +2 more sources

TMEM16A Ca2+‐activated Cl− channel: Functional interactions with cytoskeletal and membrane‐associated proteins

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The calcium‐activated chloride (ClCa) channel TMEM16A (also known as ANO1) plays critical roles in ion transport, neurotransmission and smooth muscle contraction. Dysregulation of TMEM16A channel activity contributes to the development and progression of various diseases.
Hisao Yamamura   +4 more
wiley   +1 more source

Update on cellular expression and function of ANO1 channels in urethral smooth muscle

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Activation of ANO1 channels and resulting Cl− efflux are suggested to modulate urethral smooth muscle contractility by enhancing Ca2+ influx via voltage‐dependent Ca2+ entry and resulting contraction in urethral smooth muscle cells.
Bernard T. Drumm, Neha Gupta
wiley   +1 more source

Endothelin-Induced Sarcoplasmic Reticulum Calcium Depletion Waves in Vascular Smooth Muscle Cells [PDF]

open access: yes, 2011
Agonist-stimulated waves of elevated cytoplasmic Ca2+ concentration ([Ca2+]i ) regulate blood vessel tone and vasomotion in vascular smooth muscle. Previous studies employing cytoplasmic Ca2+ indicators revealed that these Ca2+ waves were generated by a ...
Cornelis van Breemen   +7 more
core   +1 more source

Mitochondrial Ca2+ uniporter haploinsufficiency leads to sexually dimorphic redox imbalance and metabolic remodelling in the mouse brain

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The genetic inactivation of one Mcu allele leads to sex‐specific changes in neuronal function in adult mice, that is, the firing of action potentials and the relationship between cytosolic and mitochondrial Ca2+ levels. The ability to produce NAD(P)H by stimulated neural tissue is largely preserved in male mice but delayed in ...
Jenna Gray   +16 more
wiley   +1 more source

Intramuscular pathways of maladaptation in overtraining syndrome

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The transition from adaptive overreaching to maladaptive overtraining and mechanisms through which excessive training load can lead to performance decline. Four interconnected pathophysiological domains are highlighted: neural fatigue, involving both central and peripheral components such as altered sensory feedback and reflex ...
Emily Shorter   +4 more
wiley   +1 more source

Two-pore channels and NAADP-dependent calcium signalling [PDF]

open access: yes, 2010
Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca²⁺ mobilising messenger in mammalian and non-mammalian cells. Studies on a variety of cell types suggest that NAADP evokes Ca²⁺ release from a lysosome-related store and via activation ...
Calcraft, Peter James
core   +2 more sources

Mechanisms underlying local Ca2+ signalling differences between right and left atrial myocytes at normal and increased frequencies

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Left atrial myocytes have TAT‐associated faster Ca2+ release but are more prone to maladaptation at higher frequencies due to weaker peripheral SR Ca2+ uptake and smaller trigger Ca2+ current. Abstract Changes in heart rate affect Ca2+ signalling and contractility in ventricular muscle, but the effects on atrial Ca2+ signalling ...
Joon‐Chul Kim   +6 more
wiley   +1 more source

The disease mutation A77V in Ryanodine receptor RyR2 induces changes in energy conduction pathways in the protein [PDF]

open access: yes, 2011
Energetically responsive residues of the 217 amino acid N-terminal domain of the cardiac Ryanodine receptor RyR2 are identified by a simple elastic net model. These residues lie along a hydrogen bonded path through the protein.
Nazan Walpoth, Burak Erman
core  

Inhibition of the skeletal muscle ryanodine receptor calcium release channel by nitric oxide

open access: yesFEBS Letters, 1996
NO donors were found to reduce the rate of Ca2+ release from isolated skeletal muscle sarcoplasmic reticulum (SR) and the open probability of single ryanodine receptor Ca2+ release channels (RyRCs) in planar lipid bilayers, and these effects were prevented by the NO quencher hemoglobin and reversed by 2‐mercaptoethanol.
Mészáros, LászlóG.   +2 more
openaire   +2 more sources

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