In patients with benign essential hypertension, distinct pathophysiological profiles (sodium excess vs. increased sympathetic activity) can be identified based on changes in plasma renin activity and pressor responsiveness during hospitalization.
May delineate hypertension subtypes by sodium vs sympathetic mechanisms; hypothesis-generating and should not yet change practice.
In 21 hospitalized patients with benign essential hypertension, pressor responses to angiotensin were significantly correlated with levels of mean blood pressure, and pressor responses to each of angiotensin, norepinephrine and tyramine were correlated significantly with urinary sodium excretion. Sixteen of the 21 patients were studied twice with an averaged interval of 21 days without changes in daily salt intake during the hospitalization. Twelve of the 16 patients exhibited a decline in blood pressure at the second study, and the blood pressure reduction was due to a decrease in total peripheral resistance. At the same time, in 7 of the 12 patients (group A), there were a significant decrease in response to angiotensin, a marked increase in plasma renin activity and insignificant decreases in urinary sodium excretion and plasma volume. The other 5 patients (group B) showed a decrease in plasma renin activity, an enhanced response to norepinephrine, insignificant increases in urinary sodium excretion and plasma volume, and invariable or rather increased responses to angiotensin, when blood pressure was declined at the time of the second study. It is suggested that the hypertension in the group A may have been related to sodium excess, while that in the group B may have been associated with an increased sympathetic activity.
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Ishii et al. (1975) studied this question.
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