By Alex S. Evers, Mervyn Maze, Evan D. Kharasch (editors)
Lately our knowing of molecular mechanisms of drug motion and interindividual variability in drug reaction has grown tremendously. in the meantime, the perform of anesthesiology has elevated to the preoperative surroundings and diverse destinations outdoors the OR. Anesthetic Pharmacology: easy rules and scientific perform, moment variation, is a phenomenal healing source in anesthesia and important care: part 1 introduces the rules of drug motion, part 2 offers the molecular, mobile and built-in body structure of the objective organ/functional procedure and part three stories the pharmacology and toxicology of anesthetic medicines. the recent part four, Therapeutics of medical perform, offers built-in and comparative pharmacology and the sensible program of substances in day-by-day scientific perform. Edited through 3 hugely acclaimed educational anesthetic pharmacologists, with contributions from a world workforce of specialists, and illustrated in complete color, this can be a refined, straight forward source for all practitioners delivering care within the perioperative interval.
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Additional info for Anesthetic Pharmacology: Basic Principles and Clincial Practice, Second edition
Mechanisms that involve other molecules can also damp responses. Synapses such as the neuromuscular junction show altered structure and activity within hours after physiological changes such as reduced presynaptic motor neuron activity or profound blockade of postsynaptic activity . Some downstream proteins activated following GPCR agonism (receptor kinases) are feedback inhibitors that phosphorylate GPCRs and reduce their activity. Similarly, protein phosphatases (both surface receptor-linked and cytoplasmic) can be mechanisms that oppose various protein kinase enzymes.
003 Cambridge Books Online © Cambridge University Press, 2011 Chapter 2: G-protein-coupled receptors receptors coupled to different intracellular signaling pathways that respond to the same extracellular signal. Thus a single extracellular signal can elicit different effects on different target cells depending on the receptor subtype and the signaling mechanisms present. A good example is the neurotransmitter acetylcholine, which stimulates contraction of skeletal muscle, but relaxation of smooth muscle.
Likewise, G proteins consist of multiple subtypes. Sixteen homologous α-subunit genes are classified as subtypes (Gs, Gi, Gk, Gq, and so on) based on structural similarities. The different α subunits have distinct functions, coupling with different effector pathways. The different β- and g-subunit isoforms may also couple with distinct signaling pathways. Heterogeneity in effector pathways makes divergence possible within GPCR-activated pathways. This effector pleiotropy can arise from two distinct mechanisms: (1) a single receptor can activate multiple G-protein types, and/or (2) a single G-protein type can activate more than one second-messenger pathway.
Anesthetic Pharmacology: Basic Principles and Clincial Practice, Second edition by Alex S. Evers, Mervyn Maze, Evan D. Kharasch (editors)