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Receptors 1
Published in James E. Ferrell, Systems Biology of Cell Signaling, 2021
The largest class of receptors in humans is the G-protein-coupled receptors (GPCRs), a diverse family of proteins that are evolutionarily related to bacterial rhodopsin proteins and that share a common topology—they span the plasma membrane seven times, with the N-terminus of the protein outside the cell and the C-terminus inside. Probably the best-studied of the GPCRs are the adrenergic receptors, so-named because one of the hormones that activates them—epinephrine or adrenaline—is synthesized and released by cells in the medulla of the adrenal glands. Adrenergic receptors function in the central nervous system, the peripheral nervous system, and in organs such as the heart and the lung. In humans there are nine types of adrenergic receptors, which are divided into two groups (α and β) based on their pharmacology. Adrenergic receptors regulate blood pressure, cardiac contractility, pupil size, the smooth muscles in the bronchial tree, and intermediary metabolism. Studies of adrenergic signaling, from the late 19th century through the present day, have yielded and continue to yield enormous insights into physiology, disease, and the general principles of cellular regulation.
Syncope: Physiology, Pathophysiology and Aeromedical Implications
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
David A. Low, Christopher J. Mathias
There are specific neurotransmitters in each pathway that influence ganglionic and post-ganglionic activity (Figure 13.2). Acetylcholine is the preganglionic neurotransmitter for both the parasympathetic and sympathetic pathways, and is also the post-ganglionic neurotransmitter of parasympathetic neurons that stimulate muscarinic receptors. In contrast, sympathetic post-ganglionic neurons release noradrenaline, along with other co-transmitters, such as adenosine triphosphate, that act on alpha- or beta-adrenergic receptors. One exception is at the adrenal cortex where there is no post-synaptic neuron, though the presynaptic neuron releases acetylcholine to act on nicotinic receptors which stimulates the release of adrenaline and noradrenaline into the circulation as hormones that can also act on the adrenergic receptors.
Imaging of Beta-Receptors in the Heart
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Jeanne M. Link, John R. Stratton, Wayne C. Levy, Jeanne Poole, James H. Caldwell
The adrenergic system plays the major role in modulation of heart rate and contractility (1). Adrenergic signaling is initiated by the binding of the adrenergic agonists, norepinephrine, and epinephrine, to adrenergic receptors. Three types of adrenergic receptors, alpha 1, alpha 2, and beta receptors, are known, and each of these has three subtypes. (β-ARs also have a fourth “putative” subtype. All the types of adrenergic receptors are found in the heart, but the ratio of β to α receptors in the heart is 10:1 (1,2) and approximately 75% to 80% of the cardiac β-AR are the β1 subtype. Binding of adrenergic agonists to the active β-AR (β1 and β2) on the outer surface of the sarcolemma causes a conformational change in the transmembrane receptor G-coupled protein that initiates a series of secondary intracellular molecular interactions. Specifically, cyclic AMP production and a number of cellular events including phosphorylation of the calcium channel and the release of calcium by the sarcoplasmic reticulum (2–4). In the healthy heart, the β-AR are part of an exquisitely balanced and complex regulatory system. While we are far from understanding all the details, in addition to contraction, the system includes myocyte growth and apoptosis (2). The β-AR are the receptors with the greatest effect on augmenting or maintaining contractility; despite the need for a maximal response from all of the available β-AR to induce the required inotropic response (1–3).
β-Agonist in the environmental waters: a review on threats and determination methods
Published in Green Chemistry Letters and Reviews, 2022
Usman Armaya’u, Marinah Mohd Ariffin, Saw Hong Loh, Wan Mohd Afiq Wan Mohd Khalik, Hanis Mohd Yusoff
β-agonists are made up of phenylethanolamine backbone containing aromatic group, aliphatic nitrogen groups, and beta-hydroxyl group (1). These compounds are referred to as β-adrenergic agonists because they emulate the actions of catecholamines that occur naturally such as dopamine, norepinephrine, and epinephrine (adrenaline). The catecholamines are responsible for regulating physiological (body) functions like breathing rate as well as the heartbeat. They can also activate regulatory proteins (protein kinase) by binding to β-receptors on skeletal muscle cells, resulting in muscle development, increased muscle protein synthesis as well as feed transformation (2–5). Almost all group members have the common -CH-(OH)-CH2-NH side chain bonded to the aromatic ring, but with unique substituent groups on the phenylethanolamine at the amino nitrogen (typically tert.-butyl or isopropyl group) and yet another substituent group at different locations throughout the phenylic ring. (–OH, –Cl, –NH2, –CN, and –CF3) (6,7). They have typical modes of operations such as chemical composition, efficiency, and side effects with various pharmacokinetics which take account of changes in dosage planning and duration of action. The common chemical structure of β-agonists showing the different substituent groups (R1, R2, R3, R4, and R5) is presented in Table 1 showing the actual structures and other physiochemical parameters of the four β-agonists. They have comparable physical and chemical characteristics, with the majority of the members consisting of white crystalline particles or powders that are odorless and bitter. β-agonists can be dissolved in a wide range of organic polar solvents as well as inorganic solvents with low acidity or alkalinity when they are in their free form. In addition to being readily soluble in alcohol, methanol, and water; they are also somewhat soluble in acetone; however, they are not soluble in ether due to their high electrostatic attraction. Based on the benzene ring structure, β-stimulants are produced as parent molecules that can absorb light in the ultraviolet and visible ranges of wavelengths between 220-310 nm (8). They are synthetic derivatives of naturally produced molecules (catecholamines) which (as the name implies) bind β-receptors to nerve cells to cause instant detectable physiological effects e.g. increase in heart rate (9). Their mode of action resembles that of norepinephrine and epinephrine (endogenous agonists of the β-adrenergic receptor), which, when activated at nerve endings in the bloodstream, constitute an important part of the function of the autonomic (involuntary) nervous system (10–12). The process regulates multiple organs like cardiovascular, gastrointestinal, etc., and metabolic processes (13).