[Prostaglandins in the renal vascular bed in arterial hypertension of different etiologies].

Levels of PGE2, PGF2 alpha and renin activity were measured in renal venous blood of 29 patients with essential hypertension (EH), 23 patients with renovascular hypertension (RVH) and 10 patients with unilateral pyelonephritis and high arterial hypertension. The pattern of change in renal venous PG content was found to be related to the type of renal lesion: the level of PGE2 was lowered and PGF2 alpha/PGF2 ratio increased in the blood outflow from the kidneys of EH patients and from ischemized kidneys of RVH patients as compared to similar parameters in the outflow from contralateral kidneys of patients with RVH and pyelonephritis. Venous levels of both PGs were the highest in pyelonephritis-affected kidneys. Renal venous PG levels go down in all cases as the disease grows older. An acute drop in arterial pressure is accompanied with increased withdrawal of PGF2 alpha from the kidneys and enhanced renin activity in renal veins, while PGE2 drops simultaneously. PGF2 and PGE2 showing different trends of change in response to falling arterial pressure suggests increased transition of PGE2 to PGF2 alpha under the effect of enhanced PG-9-ketodehydrogenase activity. In the abdominal aorta, the scope of drop in arterial pressure correlates to the change in PGF2 alpha level, that is an evidence of PG direct involvement in the autoregulation of renal blood flow.