Pharmacodynamics

Pharmacodynamics and pharmacokinetics are the main branches of pharmacology, being itself a topic of biology interested in the study of the interactions of both endogenous and exogenous chemical substances with living organisms.

[1] One dominant example is drug-receptor interactions as modeled by where L, R, and LR represent ligand (drug), receptor, and ligand-receptor complex concentrations, respectively.

This equation represents a simplified model of reaction dynamics that can be studied mathematically through tools such as free energy maps.

Enzyme-substrate binding is a way to alter the production or metabolism of key endogenous chemicals, for example aspirin irreversibly inhibits the enzyme prostaglandin synthetase (cyclooxygenase) thereby preventing inflammatory response.

The widest class of drugs act as ligands that bind to receptors that determine cellular effects.

In principle, a pharmacologist would aim for a target plasma concentration of the drug for a desired level of response.

Genetic factors may exist which would alter metabolism or drug action itself, and a patient's immediate status may also affect indicated dosage.

The "come up" phase can be defined as the period between the first noticeable changes in perception and the point of highest subjective intensity.

The offset phase can be defined as the amount of time in between the conclusion of the peak and shifting into a sober state.

This is colloquially known as a "hangover" for negative after effects of substances, such as alcohol, cocaine, and MDMA or an "afterglow" for describing a typically positive, pleasant effect, typically found in substances such as cannabis, LSD in low to high doses, and ketamine.

The binding of ligands (drug) to receptors is governed by the law of mass action which relates the large-scale status to the rate of numerous molecular processes.

This expression is one way to consider the effect of a drug, in which the response is related to the fraction of bound receptors (see: Hill equation).

The graph shown represents the conc-response for two hypothetical receptor agonists, plotted in a semi-log fashion.

[10] Toxicodynamics (TD) and pharmacodynamics (PD) link a therapeutic agent or toxicant, or toxin (xenobiotic)'s dosage to the features, amount, and time course of its biological action.

[12] The sort and extent of altered cellular physiology will depend on the combination of the drug's presence (as established by pharmacokinetic (PK) studies) and/or its mechanism and duration of action (PD).

[13] These cannot be accurately described in preclinical research or clinical trials due to their low incidence frequency.