Key result
Young rat aortic smooth muscle cells release ~50% less IP3-induced Ca2+ than older cells.
Maturation in rats is associated with increased responsiveness to inositol polyphosphates for intracellular calcium release in aortic smooth muscle cells, potentially affecting vascular regulation in vivo.
Caution against extrapolating rat aortic cell data to humans; leaves open IP3 signaling in age-related vascular changes.
Cells that expressed the muscle-specific intermediate filament protein desmin were cultured from the aorta of Fischer 344 rats. When the cultured cells were extracted with digitonin, they accumulated 45Ca2+ from the incubation medium in a manner that was stimulated by ATP and released subsequently by exposure to the Ca2+ ionophore A23187. Ca2+ bound in the presence of ATP was also released by exposure to inositol 1,4,5-trisphosphate (IP3). Like contraction in some kinds of smooth muscle, IP3 released Ca2+ in either the absence or the presence of the ATPase-inhibitor ruthenium red. When the responsiveness of digitonin-extracted cells cultured from 3-, 12-, and 24-month-old rats was compared, cells from the youngest group released only about one-half as much Ca2+ as cells from the 12- or 24-month-old rats. The results suggest that in the rat there are changes during maturation in the responsiveness to inositol polyphosphates of intracellular compartments that sequester Ca2+ for stimulus-contraction coupling in the aortic smooth muscle cell. These changes, characterized in smooth muscle cells in vitro, might contribute to the way vascular responsiveness is regulated in vivo.
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Fittingoff et al. (1988) studied this question. Maturation (3-month-old vs 12- or 24-month-old rats) vs. 12- or 24-month-old rats was evaluated on Ca2+ release in response to inositol 1,4,5-trisphosphate (IP3). Digitonin-extracted aortic smooth muscle cells from 3-month-old rats released only about one-half as much Ca2+ in response to IP3 compared to cells from 12- or 24-month-old rats.
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