1. In the Lyon model, genetically hypertensive (LH) rats can be compared to both normotensive (LN) and low-blood pressure (LL) control rats. 2. Using either in vitro or in vivo approaches it was observed that LH kidneys differed from LN and LL controls by a preglomerular vasoconstriction and a decreased slope of the pressure-natriuresis curve. 3. Since young LH rats exhibited an increased urinary excretion of thromboxane (Tx) B2, the stable derivative of TxA2, the role of vasoconstrictor metabolites of arachidonic acid was investigated. Using isolated kidneys, it was demonstrated that LH kidneys did not synthesize a higher amount of TxA2 than LN or LL controls in baseline conditions but after stimulation by vasoconstrictor agents. 4. This finding suggests that such an increased ability to synthesize TxA2 may amplify the normal effect of other vasoconstrictors and thus participate in the increased renal vascular resistance observed in LH rats. 5. That hypothesis was confirmed since the blockade of the TP receptors, on which both prostaglandin H2 and TxA2 act, suppressed the preglomerular vasoconstriction seen in LH kidneys. However TP receptor blockade was devoid of effect on the pressure-natriuresis abnormalities.