Ca2+ sources mobilized by alpha 1-receptor activation in vascular smooth muscle.
We propose the following model of Ca2+ mobilization by noradrenaline in vascular smooth muscle. Upon receptor occupation Ca2+ from a labile small intracellular store on the inner plasmalemma is released. This Ca2+ does not function as activator Ca2+ but triggers Ca2+ release from the sarcoplasmic reticulum (Ca2+-induced Ca2+ release). Simultaneously Ca2+ from an extracellularly bound store (on the external surface of the plasmalemma) is dislodged, which enters the cell through receptor linked channels. These processes are responsible for the early 'phasic' component of the noradrenaline contraction. In addition, Ca2+ from the free extracellular Ca2+ pool enters through receptor operated channels, supporting the maintained tension development.
Leijten
P
P
Cauvin
C
C
Lodge
N
N
Saida
K
K
Van Breemen
C
C
D000316:Adrenergic alpha-Agonists / Q000378:metabolism; D000818:Animals; D001011:Aorta; D002118:Calcium / Q000378:metabolism*; D008638:Mesenteric Arteries; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011817:Rabbits; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000378:metabolism*; D015016:Yohimbine / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D002118:Calcium; D009638:Norepinephrine; D011224:Prazosin