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HORMONAL REGULATION OF RENAL FUNCTION AND BLOOD PRESSURE

Nitric oxide (NO) or endothelium-derived relaxing factor (EDRF), endothelin-1 (ET-1) and metabolites of arachidonic acid via the cytochrome P450 monooxygenase (CYP) pathway, especially 20-hydroxyeicosatetraenoic acid (20-HETE) are important humoral factors involved in the regulation of vasomotor tone, and salt and water excretion. These mediators are produced and exert profound effects in the kidney and are implicated in the genesis of hypertension and renal failure. NO is crucial in the maintenance of a state of basal systemic and renal vasodilatation, inhibiting the production and actions of ET-1 and 20-HETE, and antagonizing the vasoconstrictor tone in the renal afferent arteriole, a major site for the production and action of the vasoconstrictor, 20-HETE. The physiological actions of NO are attributed to its affinity for heme-containing enzymes including CYP enzymes. Our studies showed that NO tonically regulates the activity and production of 20-HETE and this interaction is involved in the maintenance of normal renal function and blood pressure. Thus, when NO production is inhibited, there is a disinhibition of 20-HETE effect, leading to pertubations in renal function. Inhibition of 20-HETE production therefore diminished the changes in renal and systemic hemodynamic as well as tubular effects brought about by inhibition of NO production. Our studies also provide evidence for a role for ET in NO-20-HETE interactions as administration of endothelin in the isolated perfused kidney or in the whole animal increased 20-HETE production while ETA receptor antagonism blunted 20-HETE production and attenuated the renal hemodynamic and tubular effects consequent to inhibition of NO production. A pathologic correlate for NO-20-HETE interactions was established in mineralocorticoid (volume)-dependent hypertension, an ET-sensitive model of hypertension. Thus, the attendant organ hypertrophy and renal injury in hypertension was diminished in rats treated with inhibitors of 20-HETE production and ETA receptor antagonist. In conclusion, our studies suggest that NO interacts with 20-HETE and that 20-HETE subserves a second messenger role for ET-1 in the kidney in physiological and pathological settings.


BAYO O. OYEKAN D.V.M., PH.D
Professor, Director, Center for Cardiovascular Diseases
College of Pharmacy and Health Sciences
Texas Southern University
Houston, TX 77004


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