Responses of plasma and urinary catecholamines after loading tests in patients with essential hypertension

Abstract

To investigate the role of sympathetic activity in the pathogenesis of hypertension, the responses of plasma and urinary catecholamines after quiet standing, two hours' ambulation and furosemide administration were studied in patients with essential hypertension (WHO stage I and II) and in normal subjects. Plasma renin activity (PRA), plasma arginine vaso pressin (PAVP), urinary sodium excretion and hemodynamic parameters (HR, CI and TPR) were also compared in both groups. 1) Although plasma norepinephrine (PNE) levels at rest showed a range from normal to relatively high in hypertensive subjects, the mean PNE level was significantly higher than in the normal controls. However there was no significant correlation between PNE level and blood pressure in these patients. 2) Increase in PNE levels after quiet standing for ten minutes, two hours' ambulation and the intravenous administration of 20mg furosemide was less in hypertensive subjects compared with normal controls, but there were no significant differences with respect to blood pressure, HR, CI and TRP. 3) There was no significant difference in plasma epinephrine levels at rest and after the loading tests between hypertensive subjects and normal controls. The changes in blood volume calculated from hematocrit were comparable in both groups after the loading tests. Increases in PRA and PAVP levels were also less after the loading tests in hypertensive subjects. 4) Decreases in sodium excretion and urinary dopamine excretion after two hours' ambulation in hypertensive subjects were greater than in the normal controls. These results suggested that blood pressure would be maintained by enhanced vascular reactivity to vasoactive substances, especially to norepinephrine, in essential hypertension and that the greater decrease in urinary dopamine excretion would contribute to the greater decrease of sodium excretion together with a change in the renal hemodynamics after ambulation in essential hypertension, thus contributing to the pathogenesis of essential hypertension.