Department o f P a e d i a t r i c Nephrology, I n s t i t u t e of Child H e a l t h , London, UK. Hypertension may be due t o volume o v e r l o a d , t h e p r e s s o r e f f e c t o f c i r c u l a t i n g a g e n t s such a s r e n i n o r , t h e o r e t i c a l l y , t o reduced l e v e l s o f c i r c u l a t i n g v a s o d i l a t o r a g e n t s . C e r t a i n p r o s t a g l a n d i n s , e.8. PGE a r e known v a s o d i l a t o r s .The r e n a l medulla is known t o be a s o u r c e o?PGE , kidney damage could t h e r e f o r e r e s u l t i n reduced production and henge c o n t r i b u t e t o t h e development of h y p e r t e n s i o n . Experimental work s u g g e s t s t h a t t h e r e is decreased p r o d u c t i o n o f PGE i n a r e a s o f induced r e n a l s c a r r i n g . W e have p r e v i o u s l y e s t a b l i s h e d 2 a normal r a n g f o r t h e 24 hour u r i n a r y e x c r e t i o n o f PGE , PGF , 6 k e t o PGF and thromboxane B (TXB ) and have shown t h a z rela$?ng t h e v a l u e s l a o b t a i n e d t o u $ i n a r y 2 c r e a t i n i n e ( C r ) is t h e most u s e f u l index of PG e x c r e t i o n . We t h e r e f o r e s t u d i e d a group of c h i l d r e n w i t h secondary h y p e r t e n s i o n (due t o r e f l u x nephropathy o r r e n o v a s c u l a r d i s e a s e ) and compared them w i t h normal c h i l d r e n and with c h i l d r e n with primary hypertension.24 hour u r i n e c o l l e c t i o n s were obtained from hypert e n s i v e c h i l d r e n a t d i a g n o s i s , and random u r i n e specimens c o l l e c t e d a t follow-up c l i n i c v i s i t s . No d i f f e r e n c e s were found between hypert e n s i v e s and normals i n t h e PG:Cr r a t i o s f o r PGF , 6 k e t o PGF and TXB2 ,However, PGE :Cr r a t i o s were s u b s t a n t % l y reduced iff c h i l d r e n wlth secondary2hypertension when compared with normal (7.7 vs 17.5 nglmmol C r ) . Children with e s s e n t i a l h y p e r t e n s i o n had PGE .Cr r a t i o s a t t h e lower end of t h e normal range. Our d a t a 2 ' demonstrate reduced PGE e x c r e t i o n i n secondary h y p e r t e n s i o n , which may be a c o n t r i b u t o r y f g c t o r j n i t s development,, plasma dopmlne, noradrenallne, adrenaline and renln-activity were measured I n 39 subJects r l t h stable m l l d hypertenslon (mean age 23.9 years, 34 males), and I n 39 ag-matched normotenslve controls f r m the same opengopulatlon. Mean s l t t l n g b l m d pressure I n hypertenslves was 142/82 mug. I n normotenslves average blood pressure ras 125/74 mug. Plasma catecholmlnes were measured r l t h a CCMT radloenrymatlc assay. plasma dopmlne r a s s l g n l f l c a n t i y higher I n hypertenslves (72 + SE 7 pg/rnl) than I n normotenslves (46 + SE 4 pg/ml; p<0.01 I. The sane Tas t r u e f o r naadrenallne (302 + SE T 3 pglnl I n hypertenslves, and 157 + SE 9 pg/ml I n nwmoten?ives; p<0.0011, and for sdrenal lne (91 + SE l y p g / m l I n hypertenslves and 38 + SE 4 pg/ml I n nwmotenslves; -p'0.0...