[Ca2+]i Distribution and Signalling in Vascular Hypertrophy
We were initially attracted to the field of vascular hypertrophy by two themes in the hypertrophy literature. First, an extensive literature suggests that, in many different experimental models of hypertension, the consequent hypertrophy is associated with an increased contractile sensitivity to pharmacologic agents (e.g., Mulvany et al., 1981; Field and Soltis, 1985). Many authors have suggested that calcium handling might be altered in these hypertrophied vessels (for review, see Morgan and Suematsu, 1990). Alterations in calcium handling have been measured in platelets from hypertensive patients (Ernie et al., 1984) and in cultured cells from hypertensive animals (Nabika et al., 1985; Sugiyama et al., 1986), but a direct measurement of elevated intracellular ionized calcium [Ca2+]i levels in contractile hypertrophic vessels had not yet been made. Second, there is a separate literature suggesting, but again not directly showing, that growth of cultured cells requires changes in [Ca2+]i handling (Metcalfe et al., 1986). Being influenced by these two lines of investigation, we became interested in investigating [Ca2+]i levels and the changes in [Ca2+]i signalling in contractile hypertrophic vascular smooth muscle cells.
KeywordsNuclear Volume Calcium Handling Polyploid Cell Vascular Hypertrophy Aortic Cell
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