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Therapeutic and toxic effects of the majority of drugs result from their interactions with molecular targets, that is, receptors, in the patient. The drug molecule (the ligand) interacts with the receptor and initiates the chain of biochemical and physiologic events leading to the drug’s observed effects. This ligand-receptor interaction and its results are denoted as pharmacodynamics.

The receptor concept has important practical consequences for the development of drugs. It forms the basis for understanding the actions and clinical uses of drugs described in almost every chapter of this book. These consequences may be briefly summarized as follows: First, receptors largely determine the quantitative relations between dose or concentration of drug and pharmacologic effects. The receptor’s affinity for binding a drug determines the concentration of drug required to form a significant number of ligand-receptor complexes, and the total number of receptors may limit the maximal effect a drug may produce. Second, receptors are responsible for selectivity of drug action. The molecular size, shape, and electrical charge of a drug determine whether the drug will bind to a particular receptor among the vast array of chemically different binding sites available in the patient. Accordingly, changes in the chemical structure of a drug can dramatically increase or decrease its affinities for different classes of receptors, with resulting alterations in therapeutic and toxic effects. Third, receptor activation and blockade play a key role in the mechanisms of many clinical effects of drugs.

As previously discussed (Chapter 1), receptors are specific molecules with which drugs interact to produce changes in the function of cells within the patient. Receptors must be selective in their binding characteristics in order to respond to specific chemical stimuli. The receptor site presents a unique three-dimensional configuration for the drug to bind. The complementary configuration of the drug is, in part, what creates the affinity of the drug for the receptor site (Figure 2–1). Drugs that bind to a limited group of receptor types may be classified as specific, whereas drugs binding to a larger number of receptor types may be considered nonspecific.

Figure 2–1.

Specificity of a drug for the receptor. The structure of drug “a” allows binding only to receptor “A.” In contrast, the structure of drug “b” allows binding to either receptor “A” or “B.” The conformation of drug “a” is such that this drug would be considered to be specific to receptor “A.”

Drugs interact with receptors by means of chemical bonds. The three major types of bonds are covalent, electrostatic, and hydrophobic. Covalent bonds are strong and, in many cases, not reversible under biologic conditions. Electrostatic bonds are weaker than covalent bonds, more common, and often reversible. Hydrophobic bonds are the weakest and are probably the most important in the interactions of lipid-soluble drugs and in hydrophobic “pockets” of receptors.

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