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Renal prostaglandins, kidney function and essential hypertension.

In vivo and in vitro studies have shown that renal formation of prostaglandins (PG), most probably at the juxtaglomerular complex represents an essential step for the mechanisms regulating the secretion of renin. PGs formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. Renal PG formation, especially that of PGE2, is reduced by high NaCl intake leading to a relative preponderance of PGF2 alpha at a reduced level of PG formation. These findings make renal PGs good candidates for participation in the renal regulation of sodium chloride balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG production might be involved in the etiology of high and low renin states. Thus, an impairment in the renal formation of vasodilating and renin-stimulating PGs as reflected by a blunted increase of urinary PGE2 excretion rate initially after furosemide in essential hypertensive patients could be the common denominator for both the blunted renin secretion and the increased vascular resistance which have been reported to be associated with this disease. Together with the observation of a positive correlation between PGF2 alpha formation (which enhances vasoconstriction following nerve stimulation) and blood pressure in human neonates, the findings suggest that abnormalities in the production of PGs whether due to genetic or as a result of environmental (NaCl) factors, could be involved in the development and in the natural history of essential hypertension.