Letter | Published:

Prostaglandins as Mediators of Reactive Hyperaemia in Kidney

Naturevolume 247page492 (1974) | Download Citation



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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    Present address: Experimental and Clinical Medical Research Centre, Polish Academy of Sciences, Dwarkowa, 3, Warsaw

    • J. R. VANE

    Present address: Wellcome Research Laboratories, Langley Court, Beckenham, Kent


  1. Department of Pharmacology, Institute of Basic Medical Sciences, Royal College of Surgeons of England, Lincoln's Inn Fields, London, WC2A 3PN

    •  & J. R. VANE


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