The Na+, K+ pumps keep us going : how passive and active transport of sodium (Na+) and potassium (K+) control performance and fatigue in skeletal muscle /
Clasificación: | Libro Electrónico |
---|---|
Autor principal: | |
Autor Corporativo: | |
Formato: | Electrónico eBook |
Idioma: | Inglés |
Publicado: |
Aarhus, Denmark :
Aarhus University Press,
2016.
|
Temas: | |
Acceso en línea: | Texto completo |
Tabla de Contenidos:
- The Na+, K+ pump and its discovery
- The transport and distribution of Na+ and K+ in skeletal muscle and how they are quantified
- Rapid passive fluxes of Na+ and K+ start muscle contraction and set a limit to excitability
- The definition, structure and function of the Na+, K+-pump
- The synthesis and localization of the Na+, K+ pumps in skeletal muscle
- Measurements of the content of [3H]ouabain binding sites indicate that in skeletal muscle, the major part of these binding sites of the Na+, K+ pumps are localized on the outer surface of sarcolemma and in the t-tubules
- The content of Na+, K+ pumps in skeletal muscles and how it can be quantified
- Muscle contractions, Na+, K+ transport and sodium potassium fatigue
- The rate of [³H]ouabain binding to sarcolemma can be quantified and what information may this provide?
- Measurements of [3H]ouabain binding to other cell types and preparations
- Acute and long-term regulation of Na+, K+ pumps in skeletal muscle
- Catecholamines and caffeine
- Peptide hormones stimulating the Na+, K+ pumps
- Insulin-like growth Factore-I (IGF-I)
- CGRP and other calcitonins
- Amylin, related peptides, and other stimuli for the Na+, K+ -pumps
- The importance of Na+-influx in causing depolarization and muscle fatigue
- Effect of varying Na+, K+-pump stimulating agents on intracellular Na+ in rat soleus muscles and how this may compensate functional defects caused by plasma membrane leakage
- Long-Term regulation of Na+, K+ pump content
- Training, inactivity and denervation
- Muscular dystrophy and McArdle disease
- Hyperkalemic periodic paralysis in horses, human subjects and mutant mice with a similar geneti anomaly
- K+ deficiency and K+ restoration
- Thyroid hormones ans starvation
- Thermogenic actions of thyroid hormones and malignant hyperthermia (MH)
- Diabetes
- Steroid hormones, glucocorticoids, aldosterone
- Major conclusions and general perspectives.