The present paper reviews the evidence for a possible involvement of renal eicosanoids in the pathophysiology of high blood pressure in genetically hypertensive rats of the Lyon strain. Both in vivo and in vitro experiments suggest that an increased ability to synthesize the vasoconstrictor prostaglandin H(2)and/or thromboxane A(2) in renal vessels (1) acts as an autocrine amplifier of pressor agents and (2) may contribute to resetting the pressure natriuresis curve which is a prerequisite for the development and maintenance of hypertension.

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