Why the study?
Does sympathetic activity, as measured by urinary catecholamine excretion, change in patients with renovascular hypertension following sodium restriction?
Does sympathetic activity, as measured by urinary catecholamine excretion, change in patients with renovascular hypertension following sodium restriction?
Altered urinary excretion of catecholamines and their metabolites suggests that increased sympathetic activity may play a role in the pathogenesis of renovascular hypertension.
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May implicate sympathetic overactivity in high-renin renovascular hypertension; hypothesis-generating for sodium restriction effects on catecholamines.
Urinary excretion of catecholamines, vanillylmandelic acid, and methoxycatecholamines was studied in 50 patients with renovascular hypertension. The urinary excretion of noradrenaline was increased in patients with elevated peripheral plasma renin activity and in those with elevated renal vein renin ratio in comparison with the patients with normal plasma renin activity. The urinary excretion of dopamine was diminished and vanillylmandelic acid increased in the entire group of patients with renovascular hypertension. In the investigated group, following sodium restriction, the mean urinary excretion of noradrenaline increased while dopamine excretion decreased. These results suggest that the increased sympathetic activity may play a role in the pathogenesis of renovascular hypertension.
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Januszewicz et al. (1978) studied this question.
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