Molecular mechanisms of β-adrenergic relaxation of airway smooth muscle

Michael I. Kotlikoff, Kristine E. Kamm

Research output: Contribution to journalReview articlepeer-review

100 Scopus citations


This review summarizes recent data on the two specific mechanisms of β- adrenergic relaxation of airway smooth muscle. β2-adrenergic receptor stimulation results in the opening of large-conductance, calcium-activated potassium channels, and an attendant hyperpolarization of the myocyte. Coupling between receptor and channel occurs by phosphorylation-dependent and phosphorylation-independent mechanisms. Inhibition of channel opening by specific peptidyl toxins results in a shift in the dose-dependent relaxation of this tissue by β-adrenergic hormones. There is also evidence that β- adrenergic hormones can decrease the calcium sensitivity of contractile elements. This desensitization does not result from the phosphorylation of myosin light chain kinase but may be associated with the activation of a myosin light chain phosphatase.

Original languageEnglish (US)
Pages (from-to)115-141
Number of pages27
JournalAnnual review of physiology
StatePublished - Jan 1 1996


  • G proteins
  • calcium-activated potassium channel
  • myosin light chain kinase
  • phosphatase
  • phosphorylation

ASJC Scopus subject areas

  • Physiology


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