Journal ArticleDOI
Vasoconstriction and increased flow: two principal mechanisms of shear stress-dependent endothelial autacoid release.
TLDR
The mechanisms of which nitric oxide and prostacyclin are released from endothelium-intact rabbit femoral arteries under resting conditions and after stimulation by either shear stress or acetylcholine were investigated.Abstract:
The mechanisms of which nitric oxide (NO) and prostacyclin (PGI2) are released from endothelium-intact rabbit femoral arteries under resting conditions and after stimulation by either shear stress or acetylcholine (ACh) were investigated. The concentration of NO in the effluate was determined by monitoring the NO-mediated stimulation of purified soluble guanylyl cyclase, and that of PGI2 was done using a specific radioimmunoassay for its stable hydrolysis product, 6-ketoprostaglandin F1 alpha, NO release under static (no-flow) conditions and in the absence of a stimulus accounted for 10-15% of the maximum release of NO from luminally perfused segments stimulated with ACh and was attenuated by removal of extracellular Ca2+. A six- to sevenfold increase in shear stress (from 0.15 to 1 dyn/cm2), generated either by vasoconstriction at constant flow or by an increase in flow at constant diameter, elicited a five- to sevenfold increase in NO release, which was correlated with increasing shear stress. The same increase in shear stress also enhanced the release of PGI2 from the femoral artery segments by 11- to 12-fold. Removal of extracellular Ca2+ abolished the shear stress-dependent PGI2 released but did not affect that of NO. In contrast, the ACh-stimulated NO release was strongly inhibited in the absence of extracellular Ca2+ (78% inhibition). Charybdotoxin, an inhibitor of Ca(2+)-activated K+ channels, and glibenclamide, an inhibitor of the ATP-sensitive K+ channel, had no effect on the shear stress-dependent release of NO.(ABSTRACT TRUNCATED AT 250 WORDS)read more
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Journal ArticleDOI
Nitric Oxide Is Responsible for Flow-Dependent Dilatation of Human Peripheral Conduit Arteries In Vivo
Robinson Joannides,Walter E. Haefeli,Lilly Linder,Vincent Richard,El Hassan Bakkali,Christian Thuillez,Thomas F. Lüscher +6 more
TL;DR: No, but not prostacyclin, is essential for flow-mediated dilatation of large human arteries, and this response can be used as a test for the L-arginine/NO pathway in clinical studies.
Journal ArticleDOI
The Structure and Function of the Endothelial Glycocalyx Layer
TL;DR: The mechanical and biochemical properties of the EGL and the latest studies on the interactions of this layer with red and white blood cells are examined, including its deformation owing to fluid shear stress, its penetration by leukocyte microvilli, and its restorative response after the passage of a white cell in a tightly fitting capillary.
Journal Article
Calcium Movements, Distribution, and Functions in Smooth Muscle
Hideaki Karaki,Hiroshi Ozaki,Masatoshi Hori,Minori Mitsui-Saito,Ken-ichi Amano,Ken-ichi Harada,Shigeki Miyamoto,Hiroshi Nakazawa,Kyung-Jong Won,Koichi Sato +9 more
TL;DR: Contraction of smooth muscle is regulated by the cytosolic Ca2+ level ([Ca2+]i)b, and the sensitivity of the contractile elements in response to changes in the environment surrounding the cell.
Journal ArticleDOI
The role of mechanical forces in tumor growth and therapy.
TL;DR: Shear stresses exerted by flowing blood and interstitial fluid modulate the behavior of cancer and a variety of host cells, and taming these physical forces can improve therapeutic outcomes in many cancers.
Journal ArticleDOI
Angiogenesis in skeletal and cardiac muscle
TL;DR: The role that mechanical factors deriving from blood flow play in the growth of blood vessels was most probably mentioned for the first time by John Hunter in his “Treatise on the Blood Flow, Inflammation and Gunshot Wounds,” published in 1794 and later shown in tadpole tails by Clark.