Calcium handling in vasoconstriction to stimulation of alpha 1- and alpha 2-adrenoceptors.
Vasoconstriction to stimulation of postsynaptic alpha 1- and alpha 2-adrenoceptors involves different mechanisms of Ca2+ mobilization. Alpha 2-adrenoceptor-mediated vasoconstriction in vivo as well as in vitro is invariably and effectively antagonized by Ca2+ channel blockers, such as nifedipine or verapamil, and is therefore primarily carried by influx of extracellular Ca2+. On the other hand, alpha 1-adrenoceptor stimulation has been linked to both influx of extracellular Ca2+ and release of Ca2+ from intracellular stores. The sensitivity of alpha 1-adrenoceptor-mediated vasoconstriction to blockade by Ca2+ channel antagonists depends on how much both mechanisms of Ca2+ mobilization contribute to the contraction process, and varies between vascular tissues and alpha 1-adrenoceptor agonists. The experimental evidence for the differential utilization of Ca2+ in vasoconstriction to alpha 1- and alpha 2-adrenoceptor stimulation is reviewed.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D002121:Calcium Channel Blockers; D011942:Receptors, Adrenergic, alpha; D002118:Calcium