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26 (Notes) Chapter 2. Pharmacokinetics Chapter 3. Pharmacodynamics Pharmacodynamics starts where pharmacokinetics left off – it assumes that the drug has managed to reach its target, and looks at the principles that govern the interaction between the two. remained largely experimental, despite considerable efforts in the last 10-15 years. • Membranes: Inhalation anaesthetics (diethylether, chloroform, and their more modern replacements). The mode of action of these was enshrouded in mystery for a long time, but accumulating evidence now supports direct interaction with several ion channels.
The voltage-gated Na+ channels are closed, whereas the K+ ‘leak’ channels are open. A diffusion potential only exists for K+, rendering the interior is electrically negative. b: Opening of a voltage-gated Na+ channel in response to an externally triggered depolarization (=reversal of the potential). c: Propagation of the action potential by successive sodium channel opening events. larization spike (duration ~1-3 msec) that approaches but does not quite reach the Na+ equilibrium potential, followed by a slightly longer lasting depression below the level of the resting potential.
An important aspect of competitive inhibition is that, with sufficiently high concentrations of physiological ligand, the receptor can still be maximally activated. Competitive inhibition thus reduces the receptor’s sensitivity to the agonist but does not diminish the maximum effect that can be attained at very high agonist concentrations. This means that, in case of an accidental overdose of the inhibitor, the endogenous agonist or a drug that mimics it could be used to overcome the inhibition.