Originally Posted by velamj
I'll give it a shot. bare w me here bc its very confusing...theophyline inhibits a2 (adenosine) recep (your inhibiting an inhibitor here so its confusing...a2 is Gi) and theophyline also inhibits PDE (preventing camp breakdown). inhibited pde keeps camp elevated so pka gets activated and phosphorylates myosin light chain kinase (inactivating it) (MLCK will normally phosphorylate MLC which when combined w Ca will contract smooth muscle causing brochospasm. so thats how theophyline works in helping w asthma (ie. it prevents brochospasm by inhibiting MLCK's action on MLC)....the net effect of b2 receptor stim basically does the exact same thing...it will inc camp and prevent brochospasm...so all in all im assuming u want to inhibit b2 because w theophyline toxicity not only will u also have inc camp (like w b2 stim) but u will also be unable to get rid of elevated camp (from theophyline inhibiting pde).....so u block beta 2 to lower camp and help w theophyline tox....basically beta 2 blockage inhibits b2 receptor stimulations' potentiation of theophylines mech of action. hope i answered your q. not 100% sure im correct and i apologize for that but I'm failry confident thats y b2 is used for it. gl
I find your post very confusing and hard to read.
As I understood, the way of interfering between teophylline and beta-blockers is in the amount of intracellular cAMP. Teophyllines raise it by inhibiting phosphodiesterase and beta-blockers decrease it by inhibiting beta receptors, which are Gs coupled. This is also the way why glucagon is used in beta-blocker's intoxication.