Prolonged Clonidine Treatment: Catecholamines, Renin Activity and Aldosterone Following Exercise in Hypertensives

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Abstract
Eight patients with essential hypertension, WHO grade I-III, were studied under standardized conditions in a metabolic ward, before and after 8-20 wk of treatment with clonidine in a maintenance dose of 300-600 .mu.g/24 h. Before clonidine, plasma noradrenaline [norepinephrine] concentration (PNA), plasma adrenaline [epinephrine] concentration (PA), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) increased in response to standing and submaximal exercise for 20 min. PNA was positively correlated to pulse rate in the supine position (R [regression coefficient] = 0.74, P < 0.05) and the increase in PNA to the increase in pulse rate during exercise (min 10, R = 0.73, P < 0.05; min 15, R = 0.79, P < 0.05; min 20, R = 0.74, P < 0.05). No other significant correlations were found between PNA, PA, PRA and PAC and blood pressure (BP) and pulse rate. Clonidine reduced BP, pulse rate, PNA and PRA under all conditions studied. PA was reduced in the upright position and in connection with exercise. PAC was reduced during clonidine after exercise but otherwise unaltered. The clonidine-induced decrease in PNA was positively correlated to the decrease in diastolic BP in the supine (R = 0.76, P < 0.05) and in the upright (R = 0.80, P < 0.05) position. Long-term clonidine treatment lowered the BP and pulse rate, at least partly by reducing sympathetic activity via a central mechanism. However, clonidine did not block the sympathetic reflex mechanisms engaged in the maintenance of BP in the upright position. During clonidine, the adrenaline values were lower than before treatment in the supine and in the upright position and also following exercise, indicating that clonidine exerts an inhibitory effect on the sympatho-adreno-medullary system.