Renin-hyporesponsiveness in essential hypertension dissociation between plasma renin and catecholamines or aldosterone following furosemide

Summary The influences of sequential stimulation with upright posture and sodium depletion by intravenous furosemide on blood levels of norepinephrine, epinephrine, dopamine, renin and aldosterone was studied in 26 normal subjects and 45 patients with borderline (N=20) or established (N=25) essential hypertension. Basal 24-h urinary sodium, norepinephrine and epinephrine excretion rates and basal (supine) plasma catecholamine, renin and aldosterone levels and the body sodium-volume state were comparable between the three groups. Assumption of the upright posture for 10 to 60 min caused significant increases in plasma norepinephrine (P<0.001), epinephrine (P<0.001) or dopamine (P<0.05) levels. Upright plasma catecholamine concentrations were similar in normal and hypertensive subjects and they were not modified further by furosemide. In contrast upright posture as well as furosemide induced each a successive significant (P<0.02) increase in plasma renin and aldosterone levels. Furosemide-stimulated renin was significantly (P<0.05) lower in patients with established hypertension than in normal or borderline hypertensive subjects; however, plasma aldosterone levels were comparable. These findings suggest that renin release induced by furosemide is not mediated by increased adrenergic activity. Consequently, renin-hyporesponsiveness in established hypertension cannot be explained by decreased sympathetic activity. In contrast to the altered renin regulation, aldosterone-responsiveness to upright posture or furosemide as well as adrenergic activity under these conditions appear to be usually normal in borderline or established hypertension.Supported by the Swiss National Science Foundation