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An effect of the long-term prazosin therapy on sympathetic activity, renin plasma activity and beta-endorphin and lipid blood levels was investigated in 23 patients with the primary arterial blood hypertension. Group A included 18 patients treated with prazosin, and group B - 5 patients treated with prazosin combined with propranolol. Mean daily dose of prazosin in group A was 3.0-10.0 +/- 1.3 mg in different phases of therapy whereas in group B mean daily dose of prazosin was 3.0-6.5 +/- 1.8 mg and propranolol 50-80 mg. Significant decrease in diastolic and systolic blood pressure (p < 0.01) was achieved in both groups. Additionally significant decrease in pulse rate (p < 0.01) was seen in group B. It was found that prazosin produced significant increase in plasma noradrenaline in group A and decrease in 4-hydroxy-3-methoxyglycol excretion with the urine (p < 0.05) in both groups. Moreover, negative correlation between a decrease in blood pressure (diastolic) and noradrenaline excretion with the urine (p < 0.05) was noted in group A. No effect of prazosin therapy on plasma renin activity, beta-endorphin and lipids blood levels was observed in both groups. These results suggest that prazosin therapy in patients with the primary blood hypertension exerts an effect on sympathetic activity and does not change plasma renin activity or blood beta-endorphin and lipids levels.

An effect of the treatment with guanfacine on the activity of the adreno-sympathetic system, beta-thromboglobulin, beta-endorphin, and blood lipids was studied in 30 patients with the primary arterial blood hypertension. It was found that guanfacine significantly decreases plasma noradrenaline, adrenaline, and dopamine. Moreover, it decreases the excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy-phenylglycol. These effects correlate with the drop in both systolic and diastolic blood pressure. A decrease in plasma renin activity was also observed. It correlated with the blood pressure drops. Guanfacine increased beta-endorphin levels while beta-thromboglobulin, total cholesterol and triglycerides levels remained unaffected. The authors suggest that the hypotensive effect of guanfacine is related to the decrease in adreno-sympathetic system activity and plasma renin activity and no effect on the erythrocyte activity and lipids metabolism.

An effect of enalapril maleate on the activity of renin-angiotensin-aldosterone system and sympathetic reactivity, erythrocyte prostaglandin and sodium levels as well as blood beta-endorphin was investigated in 28 patients with the essential arterial blood hypertension. It was found that enalapril maleate significantly increased plasma renin activity, decreased plasma norepinephrine and its 24-hour excretion, and decreased erythrocyte beta-endorphin and sodium levels. Blood epinephrine and aldosterone levels and their daily excretion remained unchanged similarly to prostaglandins. The above results suggest that a decrease in sympathetic system activity and intracellular sodium concentration may play a role in the hypotensive action of enalapril maleate related to the inhibition of angiotensin II formation.