URINARY PROSTAGLANDIN (PG) EXCRETION IN PRIMARY AND SECONDARY HYPERTENSION

Abstract

Hypertension may be due to volume overload, the pressor effect of circulating agents such as renin or, theoretically, to reduced levels of circulating vasodilator agents. Certain prostaglandins, e.g. PGE2 are known vasodilators. The renal medulla is known to be a source of PGE2, kidney damage could therefore result in reduced production and hence contribute to the development of hypertension. Experimental work suggests that there is decreased production of PGE2 in areas of induced renal scarring. We have previously established a normal range for the 24 hour urinary excretion of PGE2, PGF2α, 6 keto PGF1α and thromboxane B2 (TXB2) and have shown that relating the values obtained to urinary creatinine (Cr) is the most useful index of PG excretion. We therefore studied a group of children with secondary hypertension (due to reflux nephropathy or renovascular disease) and compared them with normal children and with children with primary hypertension. 24 hour urine collections were obtained from hypertensive children at diagnosis, and random urine specimens collected at follow-up clinic visits. No differences were found between hypertensives and normals in the PG:Cr ratios for PGF2α, 6 keto PGF1α and TXB2. However, PGE2:Cr ratios were substantially reduced in children with secondary hypertension when compared with normal (7.7 vs 17.5 ng/mmol Cr). Children with essential hypertension had PGE2:Cr ratios at the lower end of the normal range. Our data demonstrate reduced PGE2 excretion in secondary hypertension, which may be a contributory factor in its development.