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Hormonal Regulation of Sodium, Potassium, Calcium, and Magnesium Ions
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
The cAMP system stimulates target effects in the following hormonal systems:59 (1) adrenocorticotropin, (2) thyroid-stimulating hormone, (3) luteinizing hormone, (4) follicle-stimulating hormone, (5) vasopressin (also known as antidiuretic hormone), (6) parathyroid hormone, (7) glucagon, (8) catecholamines (epinephrine, norepinephrine), (9) secretin, and (10) the hypothalamic-releasing hormones. In some instances, hormone-receptor binding releases another second messenger known as cyclic guanosine monophosphate (cGMP), which is a nucleotide like cAMP. Still another second messenger system involves the hormone binding to a receptor that causes the passage of calcium ions into the target cell. These internalized Ca++ bind with a protein called calmodulin. The Ca++–calmodulin complex activates various intracellular biochemical processes in a manner similar to that of cAMP or cGMP. An example of the Ca++–calmodulin system is found in the induced contraction of smooth muscle.
Pulsed Electromagnetic Fields
Published in Marko S. Markov, James T. Ryaby, Erik I. Waldorff, Pulsed Electromagnetic Fields for Clinical Applications, 2020
PEMF signals with a vast range of waveform parameters have been reported to reduce pain and inflammation (Ross and Harrison, 2013b) and enhance healing (Pilla, 2006). Using the ECM model, a common unifying mechanism has been proposed, which involves Ca2+-dependent NO signaling, to quantify the relation between signal parameters and bioeffect (Pilla et al., 2011). Intracellular calcium ions play an important role in the signal transduction pathways a cell utilizes to respond to external challenges, for example, cell growth and division, apoptosis, metabolism, synaptic transmission, and gene expression (Bootman et al., 2001; Mellstrom et al., 2008). Regulation of cytosolic Ca2+ concentration is orchestrated by an elaborate system of pumps, channels, and binding proteins found both in the plasma membrane and on intracellular organelles such as the endoplasmic reticulum (Harzheim et al., 2010). High-affinity proteins (e.g., CaM, troponin) mediate the multiple physiological responses regulated by changes in intracellular Ca2+ concentrations produced by challenges that cause free Ca2+ to increase above its normal and tightly regulated value of approximately 100 nM in mammalian cells (Konieczny et al., 2012). In terms of PEMF mechanism, CaM is of particular interest because it is the first responder to changes in cytosolic Ca2+ and because of the many roles it plays in cell signaling and gene regulation pathways once activated by bound Ca2+ (Faas et al., 2011). In an immediate response to stress or injury, activated CaM binds to its primary enzyme target, constitutive nitric oxide synthase (cNOS, neuronal [nNOS], and/or endothelial [eNOS]), which, in turn, binds to and catalyzes L-arginine resulting in the release of the signaling molecule NO. As a gaseous free radical with an in-situ half-life of about 5 s (Ignarro et al., 1993), NO can diffuse through membranes and organelles and act on molecular targets at distances up to about 200 µm (Tsoukias, 2008). Low transient concentrations of NO activate its primary enzyme target, soluble guanylyl cyclase (sGC), which catalyzes the synthesis of cyclic guanosine monophosphate (cGMP) (Cho et al., 1992). The CaM/NO/cGMP signaling pathway is a rapid response cascade that can modulate peripheral and cardiac blood flow in response to normal physiologic demands as well as to inflammation and ischemia (Bredt and Snyder, 1990). This same pathway also modulates the release of cytokines, such as interleukin-1beta (IL-1β), which is proinflammatory (Ren and Torres, 2009), and growth factors, such as basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF), which are important for angiogenesis, a necessary component of tissue repair (Werner and Grose, 2003).
The impact of beetroot juice supplementation on muscular endurance, maximal strength and countermovement jump performance
Published in European Journal of Sport Science, 2021
Kristin L. Jonvik, Daan Hoogervorst, Harmen B. Peelen, Mark de Niet, Lex B. Verdijk, Luc J. C. van Loon, Jan-Willem van Dijk
Beetroot juice has become a popular supplement among athletes due to the recent research on the ergogenic properties of dietary nitrate. The effects of dietary nitrate ingestion have been attributed to its reduction to nitrite by oral bacteria, and the further reduction in the circulation to nitric oxide (NO), particularly in environments of low oxygen availability and low pH (Lundberg, Weitzberg, & Gladwin, 2008). NO is important for several physiological processes associated with exercise, including the regulation of blood flow and skeletal muscle contraction (Stamler & Meissner, 2001). NO has the ability to stimulate the conversion of cyclic guanosine monophosphate (cGMP), which causes relaxation of smooth muscle (i.e. vasodilation) (Katsuki, Arnold, Mittal, & Murad, 1977). Furthermore, an increase in cGMP increases the contraction velocity of skeletal muscle fibers and could, as such, increase peak power (Morrison, Miller, & Reid, 1996).