Evidence for t-tubular conduction failure in frog skeletal muscle induced by elevated extracellular calcium concentration

1987 ◽  
Vol 8 (3) ◽  
pp. 229-241 ◽  
Author(s):  
J. N. Howell ◽  
Anuraj Shankar ◽  
S. G. Howell ◽  
Frank Wei
Keyword(s):  
Skeletal Muscle ◽  
Calcium Concentration ◽  
Extracellular Calcium ◽  
Frog Skeletal Muscle ◽  
Extracellular Calcium Concentration ◽  
Conduction Failure

Inhibition of tetanus tension by elevated extracellular calcium concentration

1981 ◽  
Vol 240 (5) ◽  
pp. C193-C200 ◽  
Author(s):  
J. N. Howell ◽  
K. W. Snowdowne
Keyword(s):  
Skeletal Muscle ◽  
Action Potentials ◽  
Calcium Concentration ◽  
Extracellular Calcium ◽  
Frog Skeletal Muscle ◽  
Transverse Tubular System ◽  
Microelectrode Recordings ◽  
Tubular System ◽  
Osmotic Effects ◽  
Reversible Reduction

Extracellular [Ca2+] in the range of 5-20 mM produces a concentration-dependent reversible reduction in tetanus tension in single frog skeletal muscle fibers. Both peak tension and ability to sustain tension during tetanus is reduced. The effect is unrelated to osmotic effects and independent of stimulation frequency in the range 100-200 Hz. The effect occurs both at 8 and 24 degrees C. Tetanus tension is most strongly inhibited by elevated extracellular [Ca2+] at short muscle lengths, but the effect can be seen at all lengths. Microelectrode recordings during tetanus indicate that action potentials remain undiminished in amplitude and duration throughout the tetanus. The evidence suggests that the inhibition results from a failure of action potentials propagation within the transverse tubular system.

Effects of repetitive activity, ruthenium red, and elevated extracellular calcium on frog skeletal muscle: implications for t-tubule conduction

1987 ◽  
Vol 65 (4) ◽  
pp. 691-696 ◽  
Author(s):  
John N. Howell ◽  
Hans Oetliker
Keyword(s):  
Calcium Concentration ◽  
Ruthenium Red ◽  
Extracellular Calcium ◽  
Frog Skeletal Muscle ◽  
Contraction Coupling ◽  
Force Development ◽  
High Calcium ◽  
Conduction Failure ◽  
New Evidence ◽  
T System

In this report we review evidence that indicates that experimental elevation of t-tubular calcium can lead to failure of action potential propagation within the t system and we present some new evidence suggesting that t-tubular calcium concentration may rise during repetitive activity. The evidence for t-tubular conduction failure consists of comparisons of the effects of high calcium and of ruthenium red on excitation and excitation–contraction coupling as well as morphological observations of wavy myofibrils in the axial core of fibers contracting tetanically in solutions containing elevated calcium concentrations. Evidence for elevation of t-tubular calcium concentration during repetitive activity comes from the following. During twitches, the early, large birefringence signal and force development arc delayed in onset if the extracellular calcium and (or) potassium concentrations are above normal or if the fiber has been stimulated tetanically just prior to the test twitch. The delays that occur in twitches following tetanic contractions are attenuated when the extracellular and, therefore, the t-tubular calcium concentration is buffered with citrate.

scholarly journals Rare diseases caused by abnormal calcium sensing and signalling

Endocrine ◽  
2021 ◽  
Vol 71 (3) ◽  
pp. 611-617
Author(s):  
Judit Tőke ◽  
Gábor Czirják ◽  
Péter Enyedi ◽  
Miklós Tóth
Keyword(s):  
Calcium Homeostasis ◽  
Calcium Concentration ◽  
Gene Mutations ◽  
Cell Types ◽  
Bartter Syndrome ◽  
Extracellular Calcium ◽  
Calcium Signal ◽  
Extracellular Calcium Concentration ◽  
Calcium Sensing ◽  
Increased Risk

AbstractThe calcium-sensing receptor (CaSR) provides the major mechanism for the detection of extracellular calcium concentration in several cell types, via the induction of G-protein-coupled signalling. Accordingly, CaSR plays a pivotal role in calcium homeostasis, and the CaSR gene defects are related to diseases characterized by serum calcium level changes. Activating mutations of the CaSR gene cause enhanced sensitivity to extracellular calcium concentration resulting in autosomal dominant hypocalcemia or Bartter-syndrome type V. Inactivating CaSR gene mutations lead to resistance to extracellular calcium. In these cases, familial hypocalciuric hypercalcaemia (FHH1) or neonatal severe hyperparathyroidism (NSHPT) can develop. FHH2 and FHH3 are associated with mutations of genes of partner proteins of calcium signal transduction. The common polymorphisms of the CaSR gene have been reported not to affect the calcium homeostasis itself; however, they may be associated with the increased risk of malignancies.

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