Tachyphylaxis (Greek ταχύς, tachys, "rapid", and φύλαξις, phylaxis, "protection") is a medical term describing an acute, sudden decrease in response to a drug after its administration (i.e., a rapid and short-term onset of drug tolerance).
It is customary that p is called a rate constant, but, since the p stands for measure of the intensity of the stimulus causing the activation, p may be variable (non-constant).
The above scheme is only the necessary condition for the rate sensitivity phenomenon, and other pathways of deactivation of B may be considered, with the subsequent return to the inactive form of the receptor/enzyme A.
Whether this is caused directly by opioid receptors modified in the past or affecting a change in some metabolic set-point is unclear.
Inhalation of an agonist for the beta-2 adrenergic receptor, such as salbutamol (albuterol — USAN), is the most common treatment for asthma.
Expression of the Gly-16 allele (glycine at position 16) results in greater receptor downregulation by endogenous catecholamines at baseline compared to Arg-16.
[10] Use of nasal decongestants (e.g., oxymetazoline) for more than three days leads to tachyphylaxis of response and rebound congestion, caused by alpha-adrenergic receptor downregulation and desensitization.
The mechanism may specifically include receptor internalisation and resistance to endogenous vasoconstrictors causing worsening in symptoms post use of medication.