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Radioactive receptor ligands have been used to confirm this occupancy assumption in many drug-receptor systems buy viagra sublingual online now erectile dysfunction treatment in mumbai. In these systems purchase viagra sublingual cheap online erectile dysfunction caused by medications, drug bound to receptors (B) relates to the concentration of free (unbound) drug (C) as depicted in Figure 2–1B and as described by an analogous equation: in which Bmax indicates the total concentration of receptor sites (ie buy online viagra sublingual erectile dysfunction at age 50, sites bound to the drug at infinitely high concentrations of free drug) and K (the equilibrium dissociation constant) represents the concentration of free drug at which half-maximald binding is observed buy generic dapoxetine from india. This constant characterizes the receptor’s affinity for binding the drug in a reciprocal fashion: If the Kd is low order cialis professional pills in toronto, binding affinity is high order genuine cialis professional line, and vice versa. This transformation is convenient because it expands the scale of the concentration axis at low concentrations (where the effect is changing rapidly) and compresses it at high concentrations (where the effect is changing slowly), but otherwise has no biologic or pharmacologic significance. Maximal responsiveness is preserved, however, because the remaining available receptors are still in excess of the number required. In curve C, produced after treatment with a larger concentration of antagonist, the available receptors are no longer “spare”; instead, they are just sufficient to mediate an undiminished maximal response. Still higher concentrations of antagonist (curves D and E) reduce the number of available receptors to the point that maximal response is diminished. The overall transduction process that links drug occupancy of receptors and pharmacologic response is called coupling. The relative efficiency of occupancy-response coupling is determined, in part, at the receptor itself; full agonists tend to shift the conformational equilibrium of receptors more strongly than partial agonists (described in the text that follows). Coupling is also determined by “downstream” biochemical events that transduce receptor occupancy into cellular response. For some receptors, such as ligand-gated ion channels, the relationship between drug occupancy and response can be simple because the ion current produced by a drug is often directly proportional to the number of receptors (ion channels) bound. For other receptors, such as those linked to enzymatic signal transduction cascades, the occupancy-response relationship is often more complex because the biologic response reaches a maximum before full receptor occupancy is achieved. Many factors can contribute to nonlinear occupancy-response coupling, and often these factors are only partially understood. Receptors are said to be “spare” for a given pharmacologic response if it is possible to elicit a maximal biologic response at a concentration of agonist that does not result in occupancy of the full complement of available receptors. Experimentally, spare receptors may be demonstrated by using irreversible antagonists to prevent binding of agonist to a proportion of available receptors and showing that high concentrations of agonist can still produce an undiminished maximal response (Figure 2–2). For example, the same maximal inotropic response of heart muscle to catecholamines can be elicited even when 90% of the β adrenoceptors are occupied by a quasi-irreversible antagonist. In some cases, receptors may be simply spare in number relative to the total number of downstream signaling mediators present in the cell, so that a maximal response occurs without occupancy of all receptors. Here, maximal response is elicited by activation of relatively few receptors because the response initiated by an individual ligand-receptor-binding event persists longer than the binding event itself. Irrespective of the biochemical basis of receptor reserve, the sensitivity of a cell or tissue to a particular concentration of agonist depends not only on the affinity of the receptor for binding the agonist (characterized by the K ) but also on thed degree of spareness—the total number of receptors present compared with the number actually needed to elicit a maximal biologic response. The concept of spare receptors is very useful clinically because it allows one to think precisely about the effects of drug dosage without having to consider biochemical details of the signaling response. The K of the agonist-receptord interaction determines what fraction (B/Bmax) of total receptors will be occupied at a given free concentration (C) of agonist regardless of the receptor concentration: Imagine a responding cell with four receptors and four effectors.

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