1. In order to assess the pathophysiological role of renal prostacyclin in genetic hypertension, the urinary excretion of its main stable metabolite, 6-ketoprostaglandin F1α, was followed in 12 hypertensive, normotensive and low blood pressure female rats of the Lyon strains at the ages of 5,9, 21, 32 and 45 weeks.
2. The urinary excretion of 6-ketoprostaglandin F1α, which progressively decreased in the three strains between 5 and 21 weeks of age, was found to be increased in 5- and 9-week-old hypertensive rats and it was reduced in 5-week-old low blood pressure rats, compared with age-matched normotensive controls.
3. The urinary 6-ketoprostaglandin F1α was found to be significantly related to the systolic blood pressure in 5- and 9-week-old rats of the three strains (r = 0.42; n = 71; P<0.001).
4. These results exclude a primary role in the development of hypertension for a genetically determined defect in the renal biosynthesis of prostacyclin in the spontaneous hypertensive rat of the Lyon strain.