Abstract
The basis for different observed effects of norepinephrine (NE) on 45Ca fluxes was investigated by characterizing changes in binding of various distinct Ca++ fractions. The presence of a sufficiently high concentration of Sr++ (5.0 mM) prevents 45Ca uptake at high affinity Ca++ binding sites, whereas that at low affinity Ca++ binding sites is unaffected. Addition of Sr++ after equilibration with 45Ca also specifically displaces high affinity 45Ca. Efflux of 45Ca is increased by 10(-6) M NE when muscles are washed out with 1.5 mM Ca++ solution and decreased by NE when washed out in a O-Ca plus 0.05 mM EDTA solution. NE releases a portion (approximately 20 nmol/g of tissue) of the La+++-resistant high affinity Ca++, decreases La+++-sensitive high affinity Ca++ efflux, increases La+++-sensitive low affinity Ca++ efflux and increases La+++-inaccessible low affinity Ca++ uptake in muscles previously depolarized with a 160 mM K+-substituted solution. Of these four differing actions, Sr++ only affects the first two by preventing high affinity Ca++ binding (including that fraction of Ca++ released by NE). The interrelationships that exist between these Ca++ components are not clear, but the use of combinations of Sr++, La+++ and varied Ca++ concentrations can establish conditions under which a specific type of Ca++ binding predominates. Correlations between mobilization of specific Ca++ fractions and contractile responsiveness in vascular smooth muscle can then be examined.
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