VASOCONSTRICTION OF THE AFFERENT ARTERIOLE AND DEFECTIVE RENAL SYNTHESIS OF NITRIC-OXIDE IN ESSENTIAL-HYPERTENSION

This study was designed to investigate whether some relation exists be tween afferent arteriolar resistance (AAR) and the renal production of nitric oxide (NO) and prostacyclin (PGI(2)) in 21 patients with untre ated essential hypertension and 20 normotensive controls. All subjects were studied in conditions of an unlimited Na+ diet both basally and after a four-hour amino acid infusion. AAR was calculated using Gomez' s equations. Renal production of NO and PGI(2) were assessed by radioi mmunoassay of the urinary excretion of cGMP and 6-keto-PGF(1 alpha), r espectively. Baseline AAR was higher (P < 0.01) in hypertensives than in normotensives. The baseline urinary excretion of 6-keto-PGF(1 alpha ) and cGMP were similar in the two groups of subjects. AAR diminished (P < 0.005) in normotensives and remained unchanged in hypertensives a fter amino acid infusion. Urinary excretion of 6-keto-PGF(1 alpha) was increased similarly in the two groups of subjects after infusion. Uri nary excretion of cGMP remained unchanged in normotensives and decreas ed by 31% in hypertensives after infusion. These findings suggest that afferent vasoconstriction present in hypertensive patients is unrespo nsive to the vasodilatory manoeuvre of amino acid infusion. This lack of response may be due to a defective renal synthesis of NO in these p atients.