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In 11 healthy untrained volunteers the increase in plasma dopamine-beta-hydroxylase (DBH) activity during graded physical exercise has been examined as a true measure of increased activity of the sympathetic nervous system. The correlation between DBH activity, catecholamine concentration (CA) in plasma and heart rate was studied. When work on an electrically braked bicycle ergometer was gradually increased from 12.5 to 100, 200 and 300 watts there was a linear increase in DBH activity and heart rate; the increase in CA concentrations followed an exponential function. The peak values for DBH activity and CA concentration in plasma after the 300 watt work load (as percentages of the resting levels) were 130+/-3% and 820+/-71%, respectively; the adrenaline concentration in plasma increased only to 150+/-19% (p less than 0.05). There were significant correlations between heart rate and work load, DBH and work load and log CA and work load. The data imply direct correlations between heart rate and DBH, heart rate and log CA and DBH and log CA. The exponential increase in noradrenaline concentration in plasma might be due either to a greater net ""overflow'' from sympathetic nerve endings, and/or to increased secretion by the adrenal medulla. In the latter case, the release of noradrenaline would not be accompanied by secretion either of adrenaline or DBH. After work ceased there were sharp falls in heart rate and CA concentration, which indicate an immediate drop in sympathetic activity. DBH activity in plasma returned to normal very slowly; it reached half maximum values after 20-22 min. It is concluded that increased sympathetic activity in man can be estimated in vivo as changes in DBH and/or CA concentration in plasma. In contrast, a rapid decrease in sympathetic activity is directly reflected only by a rapid fall in the plasma concentrations of CA.

1 This study was designed to follow changes in plasma catecholamine concentrations during ,B-adrenoceptor blockade using doses of antagonists which decreased the mean arterial pressure (MAP) by about 15 mm Hg. Noradrenaline, adrenaline and dopamine were radioenzymatically determined in 34 patients with moderate essential hypertension during an 8 week course of treatment with either pindolol (with intrinsic sympathomimetic activity, ISA) or propranolol (without ISA). Plasma catecholamines were determined before and 1, 7, 28 and 56 days after commencement of treatment and 1 week after discontinuation of treatment. 2 After one day of pindolol therapy plasma catecholamine concentrations were decreased, but no decrease in MAP was observed. After one day of propranolol therapy, however, MAP was decreased, but except for increased levels of adrenaline, plasma catecholamines showed no changes. 3 On the 56th day of therapy both 0-adrenoceptor blockers had decreased the MAP. Pindolol therapy had caused a decrease in all three catecholamines whereas propranolol had caused no change except for decreased dopamine levels. 4 One week after cessation of propranolol therapy catecholamines were decreased but the MAP had begun to return to initial values; after cessation of pindolol therapy however, the MAP remained decreased. 5 The dissimilar relationships between blood pressure and catecholamine concentration during pindolol and propranolol therapy are evidence for multiple and different modes of action for P-adrenoceptor blockers with and without ISA. This study demonstrates that catecholamine concentrations were generally decreased during low-dose P-adrenoceptor blocker therapy, with lower catecholamine levels during pindolol treatment than during propranolol treatment.

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