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→Full and Partial Agonists
===Full and Partial Agonists===
===Full and Partial Agonists===
* A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.
* A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.
The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist.
It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.
===Inverse Agonists===
These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therfore have a negative efficacy.
===Effector Linkage Mechanisms===
Once the agonist binds to the receptor the cell response can be formed in three different ways:
* By the opening of a ligand gated ion channel
* By an intracellular second messenger system
* By DNA transcription
==Antagonists==