Abstract
Calcium causes vasoconstriction through L-type voltage-operated Ca++ channels (L-VOCCs), which mediate Ca++ influx and cell contraction in vascular cell types. Ca++ may also cause vasodilatation through stimulation of membrane-bound calcium-sensing receptors (CaRs), which mediate intracellular generation of PGE2 and decreased production of cAMP in various cell types [1]. In activated hepatic stellate cells (HSCs) from cirrhotic livers, L-VOCCs are over-expressed and responsible for HSC contraction leading to increased resistance to portal flow [2].
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