Few drugs, if any, have absolute specificity, but most features on selectivity, eg., Atropine inhibits the action of acetylcholine on smooth muscle and exocrine glands, but not the skeletal muscle. The selective action of these drugs is due to their physical-chemical bond with cellular components known as receptors. The receptors are physiological molecules involved in transmitting chemical signals between a cell and another and within cells. A molecule that binds to a receptor is defined ligand. When a ligand (hormone, neurotransmitter, drug or intracellular messenger exogenous) combines with a receptor cell function is changed, each ligand can interact with multiple receptor subtypes. The receptors activated directly or indirectly regulate cellular biochemical processes (eg., Ion conductance, protein phosphorylation, transcription of DNA). In many cases, the receptors located within the cell membrane are coupled through the guanine nucleotide binding proteins (G proteins) with different effector systems involving molecules that act as intracellular second messengers.

The receptors are dynamic structures, affected by both external factors and by intracellular regulatory mechanisms. The up-regulation and down-regulation of receptors relate phenomena of adaptation to drugs which have important clinical implications (desensitization, tolerance, acquired resistance, hypersensitivity to suspension).

The specific regions of macromolecules molecular receptor which binds the ligand recognition sites are called. A drug may interact at the same site which interacts with an endogenous agonist (hormone or neurotransmitter) or at a different site. Agonists that bind to adjacent sites or different allosteric agonists are sometimes called. The drugs are also linked in a non-specific, ie not at the molecular features of sites like receptors (eg., Plasma proteins).

The receptor theory of drug, based on the law of mass action, is somewhat comparable to kinetic analysis of interaction and inhibition of enzymes and substrates. Many biochemical mechanisms of drugs can be studied within this frame of reference. The drug receptor theory includes the concepts of kinship (the probability that a drug deal with a receptor at a given time) and intrinsic efficacy (intrinsic activity), which expresses the complex associations between the concentration of the drug or ligand states receptor activation and the functional response cell or tissue.

The physiological functions (eg., Contraction, secretion) are regulated by multiple mechanisms mediated by receptors and may be modulated by stimuli different molecular. Molecular interaction between the drug-receptor and the final answer, or organic tissue will be the interposition of various stages (involving eg., Coupling receptor and the involvement of multiple intracellular second messengers). The receptor density and efficiency of the stimulus response mechanisms vary from tissue to tissue.

The early theory of employment of drugs assumed that a drug response was directly proportional to the occupation of receptors is believed that when all the receptors were occupied or operated ceiling effect occurs. The current theory involves processes involving kinetic (speed of start / end) the occupation of receptor by ligand, activation of multiple receptor states (active / inactive) and the lack of a clear proportionality between the receptor occupancy by the ligand and the final answer tissue or organ. In these models takes into account changes in the efficiency of signal transduction (amplification mechanisms phone) and the existence of spare receptors, partial agonists and inverse agonists.

The agonists interact with receptors to alter the proportion of activated receptors, thereby altering cellular activity. Conventional agonists increase the proportion of activated receptors, inverse agonists reduce it. Many hormones and neurotransmitters (eg., Acetylcholine, histamine, norepinephrine) and many drugs (eg., Morphine, phenylephrine, isoproterenol) act as agonists.

Antagonists selectively interact with the receptors, but do not cause an observable effect, they reduce the action of another substance (agonist) at the receptor site in question. Receptor antagonists have therefore affinity but are devoid of intrinsic efficacy.

The structural analogues of molecules of agonist properties have frequently bivalent agonists and antagonists, such drugs are defined partial agonist (low efficacy). For example, receptor b – adrenergic receptors in some tissues, isoproterenol is a full agonist and prenalterolo is a partial agonist. A drug that acts as a partial agonist at a fabric can act as full agonist in another fabric.

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