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Rho Kinase Mediates Cold-Induced Constriction of Cutaneous Arteries: Role of &agr;2C-Adrenoceptor Translocation
Cold-induced activation of Rho/Rho kinase can mediate cold-induced constriction in cutaneous arteries by enabling translocation of &agr;2C-ARs to the plasma membrane and by increasing the calcium sensitivity of the contractile process. Expand
Heme oxygenase 2: endothelial and neuronal localization and role in endothelium-dependent relaxation.
Tin protoporphyrin-9 is a selective inhibitor of HO with approximately 10-fold selectivity for HO over endothelial nitric oxide synthase (NOS) and soluble guanylyl cyclase, which implies complementary and possibly coordinated physiologic roles for these two mediators. Expand
Norepinephrine up-regulates the expression of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9 in nasopharyngeal carcinoma tumor cells.
The data suggest that catecholamine hormones produced by the sympathetic-adrenal medullary axis may affect NPC tumor progression, in part, through modulation of key angiogenic cytokines. Expand
Uninjured C-fiber nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey.
Injured cutaneous C-fiber nociceptors that innervate skin partially denervated by ligation of a spinal nerve acquire two abnormal properties: spontaneous activity and alpha-adrenergic sensitivity that may contribute to neuropathic pain. Expand
Reactive oxygen species from smooth muscle mitochondria initiate cold-induced constriction of cutaneous arteries.
The combined results suggest that cold-induced constriction is mediated by redox signaling in smooth muscle cells, initiated by mitochondrial generation of ROS, which stimulate RhoA/Rho kinase signaling and the subsequent mobilization of alpha2C-ARs to the cell surface. Expand
Silent α2C-adrenergic receptors enable cold-induced vasoconstriction in cutaneous arteries
Cold constricts cutaneous blood vessels by increasing the reactivity of smooth muscle α2-adrenergic receptors (α2-ARs) with respect to α2A-, α2B subtypes. Expand
Redox Signaling of the Arteriolar Myogenic Response
NADPH oxidase and ROS, in particular H2O2, contribute to the myogenic response of arteriolar VSMCs. Expand
Redox Regulation of Vascular Smooth Muscle Cell Differentiation
It is demonstrated that ROS can increase VSMC differentiation through a p38 MAPK–dependent pathway. Expand
Acetylcholine causes endothelium-dependent contraction of mouse arteries.
It is suggested that acetylcholine initiates two competing responses in mouse arteries: endothelium-dependent relaxation mediated predominantly by NO and endothelia-dependent contraction mediated most likely by TxA(2). Expand
Balancing prostanoid activity in the human vascular system.
  • N. Flavahan
  • Biology, Medicine
  • Trends in pharmacological sciences
  • 1 March 2007
The imbalance theory of arterial thrombosis is discussed in the context of direct studies of human vascular biology, which indicate that the imbalance theory is based on incorrect assumptions and is not plausible. Expand