Abstract
Arterial hypertension is a common health problem that is a major risk factor for many diseases, including myocardial infarction and stroke.1, 2 The pathogenesis of arterial hypertension and the basic mechanisms of blood pressure control are still insufficiently understood. An increase in the concentration of cytoplasmic free Ca2+ is thought to be the major trigger for contraction in smooth muscle (Figure 1).3 This increase in intracellular Ca2+([Ca2+]i) induces Ca2+ binding to calmodulin (CaM), and the Ca2+–CaM complex activates myosin light chain kinase to phosphorylate the myosin light chain (MLC) of myosin II. The degree of MLC phosphorylation is the determining factor in smooth muscle contraction: MLC phosphorylation promotes smooth muscle contraction, whereas MLC dephosphorylation, following a reduction in [Ca2+]i, results in muscle relaxation.
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