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U. Pohl

Researcher at University of Freiburg

Publications -  22
Citations -  2172

U. Pohl is an academic researcher from University of Freiburg. The author has contributed to research in topics: Endothelium & Vasodilation. The author has an hindex of 15, co-authored 22 publications receiving 2152 citations.

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Journal ArticleDOI

Flow-dependent, endothelium-mediated dilation of epicardial coronary arteries in conscious dogs: effects of cyclooxygenase inhibition.

TL;DR: It is concluded that a tonic, instantaneous influence of coronary flow on the smooth muscle tone of the epicardial coronary arteries exists in vivo and it is unlikely that prostacyclin or another prostanoid is a mediator of this endothelium-mediated influence of flow on smooth muscletone.
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Differential role of extra- and intracellular calcium in the release of EDRF and prostacyclin from cultured endothelial cells.

TL;DR: EDRF production is directly controlled by extracellular Ca2+ during both receptor‐dependent and independent stimulation, and the results obtained during thimerosal stimulation indicate that there is not necessarily a tight coupling between the absolute level of [Ca2+]i and the amount of PGI2 released.
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Mechanical deformation of vessel wall and shear stress determine the basal release of endothelium-derived relaxing factor in the intact rabbit coronary vascular bed.

TL;DR: To investigate whether mechanical forces applied to the vascular wall by the myocardial contraction cycle were also a stimulus for EDRF release, cardiac arrest was induced by a continuous infusion of mepivacaine and a decrease in platelet cGMP content comparable to that after nitric oxide synthesis inhibition was observed in the arrested heart.
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EDRF-mediated shear-induced dilation opposes myogenic vasoconstriction in small rabbit arteries.

TL;DR: Myogenic responses in small mesenteric arteries can be effectively opposed by shear-induced release of EDRF, which might be a major mechanism for maintaining adequate tissue perfusion when pressure and shear stress increase simultaneously and otherwise myogenic activity would reduce vascular conductivity.
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Hypoxia stimulates release of endothelium-derived relaxant factor.

TL;DR: The results suggest that hypoxia stimulates the release of EDRF from native and cultured endothelium, and low partial pressures of oxygen, such as those that exist in small arteries and arterioles, might therefore be a physiological stimulus for continuous release ofEDRF.