By Bertram Katzung, Anthony Trevor
Equipped to mirror the syllabi in lots of pharmacology classes and in built-in curricula, uncomplicated & scientific Pharmacology, 12e covers the real innovations scholars want to know in regards to the technological know-how of pharmacology and its software to medical perform. collection of the subject material and order of its presentation are in response to the authors’ a long time event in educating this fabric to hundreds of thousands of clinical, pharmacy, dental, podiatry, nursing, and different healthiness technology scholars.
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Extra resources for Basic & Clinical Pharmacology
Upon removal of agonist, GRK activation is terminated, and the desensitization process can be reversed by cellular phosphatases. For β adrenoceptors, and many other GPCRs, β-arrestin binding also accelerates endocytosis of receptors from the plasma membrane. Endocytosis of receptors promotes their dephosphorylation by a receptor phosphatase that is present at high concentration on endosome membranes, and receptors then return to the plasma membrane. This helps explain the ability of cells to recover receptor-mediated signaling responsiveness very efficiently after agonist-induced desensitization.
Ligand-Regulated Transmembrane Enzymes Including Receptor Tyrosine Kinases hsp90 Transcriptionactivating domain DNA-binding domain Altered transcription of specific genes FIGURE 2–6 Mechanism of glucocorticoid action. The glucocorticoid receptor polypeptide is schematically depicted as a protein with three distinct domains. A heat-shock protein, hsp90, binds to the receptor in the absence of hormone and prevents folding into the active conformation of the receptor. Binding of a hormone ligand (steroid) causes dissociation of the hsp90 stabilizer and permits conversion to the active configuration.
For example, protamine, a protein that is positively charged at physiologic pH, can be used clinically to counteract the effects of heparin, an anticoagulant that is negatively charged. In this case, one drug acts as a chemical antagonist of the other simply by ionic binding that makes the other drug unavailable for interactions with proteins involved in blood clotting. Another type of antagonism is physiologic antagonism between endogenous regulatory pathways mediated by different receptors. For example, several catabolic actions of the glucocorticoid hormones lead to increased blood sugar, an effect that is physiologically opposed by insulin.