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(Circulation Research. 2006;98:579.)
© 2006 American Heart Association, Inc.

Editorials

A New Insight Into the Pathogenesis of Coronary Vasospasm

Hiroshi Hibino, Yoshihisa Kurachi

From the Division of Molecular and Cellular Pharmacology, Department of Pharmacology, Graduate School of Medicine, Osaka University, Japan.

Correspondence to Dr Yoshihisa Kurachi, Division of Molecular and Cellular Pharmacology, Department of Pharmacology, Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan. E-mail ykurachi@pharma2.med.osaka-u.ac.jp

See related article, pages 682–689

Key Words: ATP-sensitive K⁺ (K_ATP) channels • coronary spasm • vascular constriction • K⁺ channel opening drugs (KCO)

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To elucidate the control mechanisms of coronary vascular tone is one of the central interests in cardiac pathophysiology, because ischemic heart disease is one of the major causes of death in many countries. Although the coronary vascular tone is finally determined by the contractile state of smooth muscle, exo-smooth muscle mechanisms including autonomic nerves, endothelial cells, and blood cells have been shown indispensable for the control. Particular types of receptors, ion channels, and intracellular signal-cascades exist in coronary smooth muscle cells and mediate the controls by exo-smooth muscle elements (Figure). For example, stimulation of ₁-adrenergic receptor, which is physiologically achieved by noradrenaline (NA) released from sympathetic presynapses, increases the intracellular Ca²⁺ (Ca²⁺_i) via phosphatidylinositol (PI)-turnover and also probably via opening of receptor-activated Ca²⁺-permeable TRP channel. Membrane depolarization does so via opening voltage-dependent Ca²⁺ channels. The augmentation of Ca²⁺_i results in contraction of the smooth muscle cells and thus constriction of the coronary artery.¹ Activation of ß₂-adrenergic receptor, in turn, inhibits the coronary smooth muscle contraction through protein-kinase A pathway.² The contraction is also suppressed by protein-kinase G activated by a dilating factor, nitric oxide (NO), which is produced in the endothelial cells.

View larger version (29K): [in this window] [in a new window]   The mechanism for control of vascular tone. Activation of voltage-gated Ca2+ channel at the presynapse of sympathetic nerve increases intracellular Ca2+, which triggers a release of norepinephrine (NE). NE stimulates adrenergic 1 receptor (1R) in the smooth muscle cells and drives PI-turnover as described in this scheme. The intracellular Ca2+, . . . [Full Text of this Article]

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