Enhanced renal PGE2 in hypertensives with increased red cell Na(+)-Li+ countertransport

In this study, maximal velocities of Na(+)-Li+ countertransport were measured in red blood cells of 50 untreated essential hypertensives and 30 normotensive controls. In addition, urinary excretion of renal prostaglandins (PG) and plasma renin activity (PRA) was measured in each subject. Maximal velocity of Na(+)-Li+ countertransport was above the upper limit in controls of 525 mumol.l cell-1.h-1 in seven patients and was normal in the remaining patients. Patients with increased countertransport did not differ significantly from controls and from patients with normal countertransport with regard to urinary excretion of 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and thromboxane B2 (TxB2) (the stable metabolite of thromboxane A2). In contrast, mean values of PGE2 were significantly higher (P less than 0.01) in patients with increased countertransport (411 +/- 39 pg/min) compared with patients with normal countertransport (181 +/- 15 pg/min) and controls (146 +/- 13 pg/min). In addition, six patients with increased countertransport exhibited urinary levels of PGE2 higher than the upper limit in controls. Hypertensives with increased countertransport showed enhanced PRA when compared with the remaining patients (2.96 +/- 0.50 vs. 1.30 +/- 0.52 ng.ml-1.h-1, P less than 0.05) and with controls (1.86 +/- 0.08 ng.ml-1.h-1, P less than 0.05). Finally, the relationship between PGE2 and PRA was found to be significant in patients with increased countertransport (r = 0.776, P less than 0.05). These results indicate that renal synthesis of PGE2 is enhanced in essential hypertensives with increased Na(+)-Li+ countertransport activity and hyperreninemia.