Abstract
SEVERAL mechanisms have been proposed to account for the reactive hyperaemia which follows arterial occlusion in the kidney, including the intrarenal production of a vasodilator substance1,2. Recent work shows that the local generation of a prostaglandin can cause vasodilatation in the kidney3,4 and can contribute to autoregulation of renal blood flow5,6. We have therefore used a prostaglandin synthetase inhibitor, indomethacin7, to test whether the reactive hyperaemia which follows release of renal artery occlusion is mediated by a prostaglandin mechanism.
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HERBACZYNSKA-CEDRO, K., VANE, J. Prostaglandins as Mediators of Reactive Hyperaemia in Kidney. Nature 247, 492 (1974). https://doi.org/10.1038/247492a0
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DOI: https://doi.org/10.1038/247492a0
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