Mayumi Hirano

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The contraction of smooth muscle is regulated primarily by intracellular Ca2+ signal. It is well established that the elevation of the cytosolic Ca2+ level activates myosin light chain kinase, which phosphorylates 20 kDa regulatory myosin light chain and activates myosin ATPase. The simultaneous measurement of cytosolic Ca2+ concentration and force(More)
The Ca2+-dependent, reversible phosphorylation of the 20 kDa regulatory myosin light chain (MLC) plays a primary role in regulating the contraction of smooth muscle. However, it is well known that the Ca2+ signal is not the only factor which regulates such contraction, however, the alteration of the Ca2+ sensitivity in the contractile apparatus is also(More)
Thrombin increases the cytosolic Ca(2+) concentrations and induces NO production by activating proteinase-activated receptor 1 (PAR(1)) in vascular endothelial cells. The store-operated Ca(2+) influx is a major Ca(2+) influx pathway in non-excitable cells including endothelial cells and it has been reported to play a role in the thrombin-induced Ca(2+)(More)
In smooth muscle, the cytosolic Ca2+ concentration ([Ca2+](i)) is the primary determinant of contraction, and the intracellular pH (pH(i)) modulates contractility. Using fura-2 and 2',7'-biscarboxyethyl-5(6) carboxyfluorescein (BCECF) fluorometry and rat aortic smooth muscle cells in primary culture, we investigated the effect of the increase in pH(i) on(More)
RhoA plays a critical role in regulating NO production in cultured endothelial cells. To determine its role in in situ endothelial cells, we investigated the effects of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors and a RhoA-binding domain of Rho-kinase (RB) on vascular contractility in the isolated rabbit mesenteric artery. Ex vivo treatment(More)
OBJECTIVE The goal of this study was to determine whether inhibition of transient receptor potential canonical (TRPC) channels underlies attenuation of angiotensin II (Ang II)-induced vasoconstriction by phosphodiesterase (PDE) 3 inhibition. METHODS AND RESULTS Pretreatment of rat thoracic aorta with cilostazol, a selective PDE3 inhibitor, suppressed(More)
Cerebral vasospasm determines the prognosis of subarachnoid hemorrhage (SAH). The increased vascular reactiveness has an important role in the development of cerebral vasospasm. This study analyzed the roles of the receptor-mediated signaling and the myofilament Ca(2+) sensitivity in the increased vascular reactiveness in SAH, using the basilar artery of a(More)
BACKGROUND/AIMS The effects of oxidative stress on the vascular responsiveness to the agonists of proteinase-activated receptors (PARs) were investigated. METHODS Serum-free incubation was utilized to impose oxidative stress to isolated rat aortas. Spontaneously hypertensive rats (SHR) were investigated as a model of in vivo oxidative stress. RESULTS(More)
BACKGROUND AND PURPOSE Thrombus formation is commonly associated with pulmonary arterial hypertension (PAH). Thrombin may thus play an important role in the pathogenesis and pathophysiology of PAH. Hence, we investigated the contractile effects of thrombin and its mechanism in pulmonary artery. EXPERIMENTAL APPROACH The cytosolic Ca(2+) concentrations(More)
Increased vascular smooth muscle contractility has an important role in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). Myofilament Ca(2+) sensitivity is a major determinant of smooth muscle contractility. We investigated changes in the Ca(2+)-sensitizing effect of endothelin-1 (ET-1) and the mechanisms underlying ET-1-induced(More)