Plasma epinephrine and norepinephrine concentrations in primary and secondary human hypertension.

Supine plasma concentrations of epinephrine and norepinephrine were measured by a radioenzymatic method in 69 patients with essential hypertension and were compared with the levels found in 40 patients with hypertension resulting from chronic parenchymatous renal disease and in 18 normotensive controls. Mean plasma levels of epinephrine and norepinephrine were not statistically different in primary and secondary hypertension and comparable to levels in normotenstve controls. If the upper confidence limit is taken to be 0.4 ng/ml of plasma norepinephrine in renal hypertension, only three of 69 patients with essential hypertension (4%) had a slightly raised plasma norepinephrine and, with an upper confidence limit of 0 3 ng/ml in normal subjects, only four of 69 patients (6%) had a definitely raised plasma norepinephrine. Plasma norepinephrine was significantly higher in high-renin as compared to low-renin essential hypertension; it correlated neither with age nor blood pressure. Plasma epinephrine was suppressed in about 30% of the patients with primary and secondary hypertension and correlated significantly with heart rate and pulse pressure. On the basis of the present results, differences in the sympathetic tone in primary hypertension and secondary hypertension of renal origin are not obvious. Supine plasma catecbolamine levels do not add any new evidence to the concept that increased activity of the sympathetic nervous system is involved in the pathogeoesis of essential hypertension. In fact, plasma epinephrine is suppressed in a substantial number of patients with primary and secondary hypertension. Furthermore, since plasma reoin correlated with plasma norepinephrine only in essential but not in renal hypertension, it appears that the sympathetic nervous system contributes to basal renin release only in primary hypertension. In secondary hypertension resulting from chronic renal disease, basal renin release is probably maintained by the renal baroreceptors of the diseased kidneys. (Hypertension 3: 373-379, 1981)