Studies on the role of sympathetic nervous system in the mechanism of essential hypertension.
In order to investigate a role of sympathetic nervous system in the mechanism of blood-pressure elevation in essential hypertension, urinary catecholamines, serum dopamine-beta-hydroxylase (DBH) activity and a pressor response to infused noradrenaline (noradrenaline response) were measured, in the patients with essential hypertension, before and 2 weeks-rest after hospitalization or following salt restriction. In addition, plasma renin activity (PRA) and water-sodium contents were determined and a correlation between these variables and noradrenaline excretion, serum DBH or noradrenaline response was observed. A blood pressure fall after hospitalization was associated with a decrease of urinary noradrenaline and serum DBH, and there was a significantly positive correlation between the changes in blood pressure and those in urinary noradrenaline or in serum DBH. A significantly adverse correlation was found between plasma volume and the amounts of urinary noradrenaline excretion. The changes in noradrenaline response was negatively correlated with those in urinary noradrenaline excretion. In addition, noradrenaline response was correlated positively with plasma volume, extracellular fluid volume and total exchangeable sodium and negatively with PRA. Following salt restriction, a fall of the blood pressure was associated with an elevation of urinary noradrenaline excretion. The patients with more marked blood pressure fall showed a higher increase of urinary noradrenaline, and a significant correlation was found between the changes in these two variables. Noradrenaline response was significantly reduced, although it was not correlated significantly with noradrenaline excretion. In these experiments, adrenaline, unlike noradrenaline, did not show any obvious changes. These findings suggested that an excessive sympathetic nerve activity caused an elevation of blood pressure in the labile type of essential hypertension. It was demonstrated that a sympathetic nervous function was dependent on sodium intake and that there exisited a close relationship between noradrenaline response and water-sodium contents or PRA.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001794:Blood Pressure; D004299:Dopamine beta-Hydroxylase / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D012964:Sodium; D004299:Dopamine beta-Hydroxylase; D012083:Renin; D009638:Norepinephrine