ABSTRACT
Receptors allow cells to recognize specific extracellular signaling molecules, which we will henceforth refer to as endogenous ligands. Information encoded in the ligand-receptor recognition event is subsequently conveyed to the interior of the cell where it is transduced and amplified, resulting in altered cellular function. Many drugs used in critical care medicine are, in essence, chemical analogs of endogenous ligands that have accepted therapeutic utility. Drugs acting as agonists stimulate receptors and produce biologic responses of varying magnitudes. Like the enzyme-linked receptors discussed above, steroid receptors dimerize when bound to agonist ligands, which allows them to translocate from the cytoplasm to the nucleus where the hormone-receptor complex can bind to DNA. The excessive stimulation of receptors by endogenous ligands or through continuous drug administration in the course of some diseases may result in receptor down-regulation, whereas lack of stimulation often increases receptor numbers.
