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Non-Receptor Mechanisms of Drug Action: Enzyme Modulation and Cell Membrane Permeability

This overview focuses on non-receptor mechanisms by which drugs exert their effects on biological systems. It highlights how enzymes function as biological catalysts that speed up chemical reactions without being altered themselves. Various drugs can modify enzyme activity, impacting processes like neurotransmitter breakdown and cellular metabolism. Additionally, it examines how certain agents, like lidocaine and calcium channel blockers, affect cell membrane permeability, influencing excitability and vascular responses. Finally, the concept of anti-metabolites is discussed, showcasing their role in disrupting normal cellular functions.

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Non-Receptor Mechanisms of Drug Action: Enzyme Modulation and Cell Membrane Permeability

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    1. Pharmacology-1 PHL 211

    11. II. Non-receptor Mechanisms Actions on Enzymes Enzymes = Biological catalysts Speed chemical reactions Are not changed themselves Some drugs alter enzyme activity & alter processes catalyzed by the enzymes Examples Cholinesterase inhibitors Monoamine oxidase inhibitors

    12. Changing Cell Membrane Permeability (Ion Channels) Lidocaine (a local anesthetic) decreases permeability of the nerve cell membrane to NA+ ? the rate of depolarization of the nerve membrane, threshold for electrical excitability, & propagation of the action potential Verapamil & nefedipine (calcium channel blockers) Block calcium channels ? Ca influx into smooth and cardiac muscle ? vasodialate vascular smooth muscle & myocardial contractility, slow AV nodal conduction Adenosine (an inhibitory neurotransmitter) Opens potassium channels

    13. Anti-metabolites An anti-metabolite is a chemical with a similar structure to a substance (a metabolite) required for normal biochemical reactions, yet different enough to interfere with the normal functions of cells, including cell division Examples: Anti-neoplastics e.g., 5-FU (5-fluorouracil) ? inhibits RNA synthesis Antimicrobials such as sulfonamide drugs, which inhibit dihydrofolate synthesis in bacteria by competing with para-aminobenzoic acid (PABA)

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