Basic & Clinical Pharmacology by Bertram Katzung, Anthony Trevor

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 $64000 ideas scholars want to know concerning the technology of pharmacology and its program to scientific perform. collection of the subject material and order of its presentation are according to the authors’ decades adventure in educating this fabric to hundreds of thousands of clinical, pharmacy, dental, podiatry, nursing, and different well-being technological know-how scholars.

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ANP, an important regulator of blood volume and vascular tone, acts on a transmembrane receptor whose intracellular domain, a guanylyl cyclase, generates cGMP (see below). Receptors in both groups, like the receptor tyrosine kinases, are active in their dimeric forms. Cytokine Receptors Cytokine receptors respond to a heterogeneous group of peptide ligands, which include growth hormone, erythropoietin, several kinds of interferon, and other regulators of growth and differentiation. These receptors use a mechanism (Figure 2–8) closely resembling that of receptor tyrosine kinases, except that in this case, the protein tyrosine kinase activity is not intrinsic to the receptor molecule.

When the hormonal stimulus stops, the intracellular actions of cAMP are terminated by an elaborate series of enzymes. cAMPstimulated phosphorylation of enzyme substrates is rapidly reversed by a diverse group of specific and nonspecific phosphatases. cAMP itself is degraded to 5′-AMP by several cyclic nucleotide phosphodiesterases (PDE; Figure 2–13). Milrinone, a selective inhibitor of type 3 phosphodiesterases that are expressed in cardiac muscle cells, has been used as an adjunctive agent in treating acute heart failure.

If the α-adrenoceptor blockade cannot be overcome, excess effects of the drug must be antagonized “physiologically,” ie, by using a pressor agent that does not act via α receptors. Antagonists can function noncompetitively in a different way; that is, by binding to a site on the receptor protein separate from the agonist binding site, and thereby modifying receptor activity without blocking agonist binding (see Figure 1–3C and D). Although these drugs act noncompetitively, their actions are reversible if they do not bind covalently.

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