Excretion of 3H-norepinephrine in the urine of hypertensives

Abstract

The role of catecholamine-sympathetic nervous system on the genesis of essential hypertension has long been investigated, but unsettled. Ikoma reported an increase of norepinephrine excretion in the urine of patients with essential hypertention without renal insufficiency, whereas Euler demonstrated elevated levels of urinary excretion of norepinephrine in only 16.4 per cent of 500 hypertensive patients. There were also no significant differences in urinary excretion of the metabolites of catecholamines between normal controls and hypertensive patients. On the other hand, the fact that most antihypertensive agents currently used are involved in some way with catecholamine metabolism, suggests an intimate relationship between hypertension and sympathetic nervous system. Gitlow was the first who investigated the catecholamine metabolism of the essential hypertension with use of dl-beta-H3-norepinephrine. It was assumed that the accelerated turnover of norepinephrine may be present in the essential hypertensive patients. However, De'Quattro could not confirm the accelerated turnover in the hypertensive patients. This discrepancy may be the reflection of the absence of a uniform sympathetic nervous response in the different varieties of hypertension. There are posturated two stages of essential hypertension, i.e., labile and fixed. A heightened sympathetic and circulatory activity may be more characteristic in the early labile than in the fixed phase of essential hypertension. The purpose of this study was to compare the rate of norepinephrine turnover in labile hypertension and fixed hypertension and to study on the effect of fusaric acid, a potent inhibitor of dopamine beta hydroxylase, on the catecholamine turnover in the hypertensive patients.