Possible Significance of Renal Prostaglandins in Essential Hypertension

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Abstract
In vivo and in vitro studies have shown that renal formation of prostaglandins (PG), possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. Total renal PG production, especially that of PGE2 is reduced by high NaCl intake leading to a relative preponderance of PGF2α at reduced PG formation. These findings make renal PG's 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 formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal production of vasodilating and renin-stimulating PG's as reflected by a reduced urinary PGE2 excretion initially after furosemide could be the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension. Together with the observation of a positive correlation between PGF2α formation (which enhances vasoconstriction following nerve stimulation) and blood pressure in human neonates, the findings suggest that abnormalities in the production of PG's 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.