470 research outputs found
Supplemental material for Safety of antithrombotic therapy for patients with acute ischemic stroke harboring unruptured intracranial aneurysm
No full textSupplemental material for Safety of antithrombotic therapy for patients with acute ischemic stroke harboring unruptured intracranial aneurysm by Yuji Shono, Hiroshi Sugimori, Ryu Matsuo, Yoshihisa Fukushima, Yoshinobu Wakisaka, Junya Kuroda, Tetsuro Ago, Masahiro Kamouchi and Takanari Kitazono: on behalf of the Fukuoka Stroke Registry Investigators: International Study of Unruptured Intracranial Aneurysms Investigators in International Journal of Stroke</p
sj-docx-1-ine-10.1177_15910199221113900 - Supplemental material for Fluid-attenuated inversion recovery vascular hyperintensity-diffusion-weighted imaging mismatch and functional outcome after endovascular reperfusion therapy for acute ischemic stroke
No full textSupplemental material, sj-docx-1-ine-10.1177_15910199221113900 for Fluid-attenuated inversion recovery vascular hyperintensity-diffusion-weighted imaging mismatch and functional outcome after endovascular reperfusion therapy for acute ischemic stroke by Keisuke Tokunaga, So Tokunaga, Kenta Hara, Masahiro Yasaka, Yasushi Okada, Takanari Kitazono and Tomoyuki Tsumoto in Interventional Neuroradiology</p
sj-pdf-1-jcb-10.1177_0271678X221145092 - Supplemental material for PDGFR<b>β</b>-positive cell-mediated post-stroke remodeling of fibronectin and laminin <b>α</b>2 for tissue repair and functional recovery
No full textSupplemental material, sj-pdf-1-jcb-10.1177_0271678X221145092 for PDGFRβ-positive cell-mediated post-stroke remodeling of fibronectin and laminin α2 for tissue repair and functional recovery by Tomoya Shibahara, Kuniyuki Nakamura, Yoshinobu Wakisaka, Masahiro Shijo, Kei Yamanaka, Masamitsu Takashima, Hayato Takaki, Masaoki Hidaka, Takanari Kitazono, Tetsuro Ago in Journal of Cerebral Blood Flow & Metabolism</p
Chloride Ions, Vascular Function and Hypertension
No full textBlood pressure is determined by cardiac output and systemic vascular resistance, and mediators that induce vasoconstriction will increase systemic vascular resistance and thus elevate blood pressure. While peripheral vascular resistance reflects a complex interaction of multiple factors, vascular ion channels and transporters play important roles in the regulation of vascular tone by modulating the membrane potential of vascular cells. In vascular smooth muscle cells, chloride ions (Cl−) are a type of anions accumulated by anion exchangers and the anion–proton cotransporter system, and efflux of Cl− through Cl− channels depolarizes the membrane and thereby triggers vasoconstriction. Among these Cl− regulatory pathways, emerging evidence suggests that upregulation of the Ca2+-activated Cl− channel TMEM16A in the vasculature contributes to the increased vascular contractility and elevated blood pressure in hypertension. A robust accumulation of intracellular Cl− in vascular smooth muscle cells through the increased activity of Na+–K+–2Cl− cotransporter 1 (NKCC1) during hypertension has also been reported. Thus, the enhanced activity of both TMEM16A and NKCC1 could act additively and sequentially to increase vascular contractility and hence blood pressure in hypertension. In this review, we discuss recent findings regarding the role of Cl− in the regulation of vascular tone and arterial blood pressure and its association with hypertension, with a particular focus on TMEM16A and NKCC1
New findings about plasma Biomarkers from the Research for Biomarkers in Ischemic Stroke. Reverse Translational Research using multiple clinical biomarkers
No full textEndothelium-Dependent Hyperpolarization (EDH) in Diabetes: Mechanistic Insights and Therapeutic Implications
No full textDiabetes mellitus is one of the major risk factors for cardiovascular disease and is an important health issue worldwide. Long-term diabetes causes endothelial dysfunction, which in turn leads to diabetic vascular complications. Endothelium-derived nitric oxide is a major vasodilator in large-size vessels, and the hyperpolarization of vascular smooth muscle cells mediated by the endothelium plays a central role in agonist-mediated and flow-mediated vasodilation in resistance-size vessels. Although the mechanisms underlying diabetic vascular complications are multifactorial and complex, impairment of endothelium-dependent hyperpolarization (EDH) of vascular smooth muscle cells would contribute at least partly to the initiation and progression of microvascular complications of diabetes. In this review, we present the current knowledge about the pathophysiology and underlying mechanisms of impaired EDH in diabetes in animals and humans. We also discuss potential therapeutic approaches aimed at the prevention and restoration of EDH in diabetes
Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels
No full textUpon stimulation with agonists and shear stress, the vascular endothelium of different vessels selectively releases several vasodilator factors such as nitric oxide and prostacyclin. In addition, vascular endothelial cells of many vessels regulate the contractility of the vascular smooth muscle cells through the generation of endothelium-dependent hyperpolarization (EDH). There is a general consensus that the opening of small- and intermediate-conductance Ca2+-activated K+ channels (SKCa and IKCa) is the initial mechanistic step for the generation of EDH. In animal models and humans, EDH and EDH-mediated relaxations are impaired during hypertension, and anti-hypertensive treatments restore such impairments. However, the underlying mechanisms of reduced EDH and its improvement by lowering blood pressure are poorly understood. Emerging evidence suggests that alterations of endothelial ion channels such as SKCa channels, inward rectifier K+ channels, Ca2+-activated Cl− channels, and transient receptor potential vanilloid type 4 channels contribute to the impaired EDH during hypertension. In this review, we attempt to summarize the accumulating evidence regarding the pathophysiological role of endothelial ion channels, focusing on their relationship with EDH during hypertension.</jats:p
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