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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.
Applications of Biomaterials in Soft Tissue Replacement
Published in Yaser Dahman, Biomaterials Science and Technology, 2019
Muscle tissue functions by transforming chemical energy into mechanical energy. It can be differentiated into three types: skeletal, smooth, and cardiac (Marieb, 2006). Skeletal muscle tissues have long, striated, and multinucleate cells. They attach to bones and help in the movement and stabilization of the skeleton. Each muscle consists of many muscle fascicles (bundle of cells), and each fascicle consists of many muscle fibers (cell). Each muscle fiber consists of many myofibrils, which consist of the functional unit of the muscle (actin and myosin). Smooth muscle tissue consists of short, spindle-shaped, non-striated cells. Smooth muscle is involuntary, and can be found in the organs of the visceral region of the body such as stomach and intestines where they allow these organs to contract and expand. Cardiac muscle tissue consists of short, striated, branched cells. Cardiac muscle is only found in the heart and is responsible for the circulation of blood (Marieb, 2006).
Effects of Pressure on Vascular Smooth Muscle Cells
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Sheila Nagatomi, Harold A. Singer, Rena Bizios
Other molecular-level responses include evidence that exposure of rat smooth muscle cells to pressure induced DNA synthesis via phospholipase C activation.30 Evidence to support this claim was provided by the absence of pressure-induced DNA synthesis in rat aortic smooth muscle cells pretreated with 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (200 μM), a phospholipase C inhibitor, following exposure to sustained 80 mm Hg pressure.30 Activation of phospholipase C triggers a signal transduction pathway leading to increased intracellular calcium, which, in turn, induces smooth muscle cell contraction.8,30 An overstimulated contractile state of smooth muscle cells induces constriction of blood vessels that may contribute to hypertension.43
Effect of sub-chronic ferrous sulfate treatment on motor skills, hematological and biochemical parameters in rats
Published in Archives of Environmental & Occupational Health, 2019
Mohamed Ammari, Miryam Elferchichi, Haifa Othman, Mohsen Sakly, Hafedh Abdelmelek
Intestinal mobility was studied following the installation described below (Figure 1). A fragment of the small intestine completely disconnected and placed in a survival medium was able to make spontaneous motor activity. This activity is myogenic in nature and is an intrinsic property of smooth muscle. However, it was the gut which was the ultimate regulator of iron metabolism by intestinal absorption of the latter through the enterocytes. After decapitation of the animal by opening the abdominal cavity, five fragments of the small intestine near the duodenum (3 cm length) were taken and placed in a beaker filled with aerated Tyrode fluid and maintained at 37 °C. Rocking of isolated fragments was observed. One of these fragments was taken and one of its two ends was attached to a glass rod dipped into an incubation chamber filled with aerated Tyrode and the other end attached to a transducer connected to a recorder (voltage = 50 mA; speed = 20 mm min_1). Voltage on the line is kept constant for each test with the help of a multimeter.
Arsenic, cadmium, and mercury-induced hypertension: mechanisms and epidemiological findings
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Airton da Cunha Martins, Maria Fernanda Hornos Carneiro, Denise Grotto, Joseph A Adeyemi, Fernando Barbosa
In the same vein, As also affects contractile function in vascular smooth muscle (De Lanerolle and Paul 1991). Following phenylephrine-induced contraction, serotonin (5-HT) and/or high concentrations of potassium ions (K+) were measured as well as the mechanisms involved such as mediation by myosin light chain (MLC) phosphorylation and intracellular Ca ions influx. Vascular smooth muscle contraction occurs due to a sudden rise in intracellular free Ca2+ ions, which bind to calmodulin, resulting in a complex of Ca-calmodulin. The complex then activates myosin light chain kinase which further phosphorylates MLC resulting in vasoconstriction (De Lanerolle and Paul 1991). Lee et al. (2005) showed that As3+ enhanced vascular contraction induced by phenylephrine, 5_HT, and high K+ in a concentration-dependent manner. However, a difference regarding the mode of action was considered. Phenylephrine and 5-HT act on the α1-adrenoceptor and the 5-HT2 serotonin receptor, respectively, resulting in increases in intracellular Ca2+ levels, formation of the Ca–calmodulin complex, activation of MLC kinase and phosphorylation of MLC. High concentrations of K+, in turn, are associated with a direct elevation in intracellular Ca2+ concentrations by opening Ca2+ channels due to membrane depolarization. Although Lee et al. (2005) reported the As-induced hypercontraction effect stimulated by phenylephrine as evidenced by MLC phosphorylation, direct Ca2+ measurement also showed that As potentiated vasoconstriction induced by high K+ levels. Therefore, data suggested that, rather than direct increases in Ca2+ levels, Ca2+ sensitization may be a major contributor to the enhanced vasoconstriction induced by As. Further As-enhanced contraction is primarily due to hypercontraction of smooth muscle, since the contraction noted in aortic rings occurred without endothelium (Lee et al. 2005).