Increased Plasma Noradrenaline Concentrations in Essential Hypertension and Their Decrease after Long-Term Treatment with a β-Receptor-Blocking Agent (Prindolol)

Abstract

1. Plasma noradrenaline was measured in fiftynine patients with mild to severe essential hypertension and in fifteen normotensive control subjects under basal and orthostatic conditions. 2. In patients with essential hypertension mean plasma noradrenaline concentrations were significantly higher than in control subjects under basal and orthostatic conditions. 3. In patients with essential hypertension basal diastolic blood pressure correlated closely with the corresponding plasma noradrenaline concentrations. 4. Long-term treatment with prindolol of patients with essential hypertension led to a significant fall in diastolic and systolic blood pressure and heart rate and to a significant decrease in plasma noradrenaline concentrations under basal and orthostatic conditions. 5. The adrenergic response to upright posture, reflected by an increase in plasma noradrenaline, was not abolished by prindolol. 6. It is concluded that the anti-hypertensive effect of prindolol in patients with essential hypertension is at least partially mediated by a decrease of sympathetic nervous activity.

Beta‐adrenoceptor blockade and psychic stress in man. A comparison of the acute effects of labetalol, metoprolol, pindolol and propranolol on plasma levels of adrenaline and noradrenaline.

“…It is generally agreed that long-term treatment with ,Badrenoceptor blockers such as propranolol and labetalol causes an increase in the plasma concentration of adrenaline and noradrenaline (Christensen et al, , 1979Carlsen et al, 1980). Therefore it is of interest that Brecht et al (1976), Bonelli et al (1979) and Dominiak & Grobecker (1982) found that the plasma concentrations of catecholamines were reduced after treatment with pindolol, a nonselective 13-adrenoceptor blocker with ISA (Table 1).…”

Effect of beta‐adrenergic receptor blockade with propranolol on the response of plasma catecholamines and renin activity to upright tilting in normal subjects.

“…Perusal of published reports indicates that noradrenaline levels have been found increased (Galbo et al, 1976;Philipp, Cordes & Distler, 1977;Distler et al, 1978;Hansen, Hesse & Christensen, 1978;Rahn et al, 1978;McGrath et al, 1979;Lijnen et al, 1979), unchanged (Irving et al, 1974;de Leeuw etal., 1977) or even reduced (Brecht et al, 1976;Mueller & Ayres, 1980) after treatment with f3-adrenoceptor blocking drugs in normotensive or hypertensive subjects.…”

“…Several reports have indicated that the level of catecholamines in plasma is influenced by concurrent administration of 13-adrenoceptor blocking drugs (Irving et al, 1974;Brecht et al, 1976;Rahn et al, 1978;Distler et al, 1978). Consequences of /-adrenoceptor blockade which may affect plasma catecholamine concentration include alterations in central and baroreceptor mediated sympathetic discharge, or interference with the neuronal release and disposal of catecholamines.…”

Plasma noradrenaline concentration in essential hypertension during long‐term beta‐adrenoceptor blockade with oxprenolol.

“…Philipp, Cordes, Walter, Walter, Beyer & Distler (1976) found that with basal and dynamic exercise, plasma noradrenaline concentration increased when essential hypertensive patients were treated with atenolol; Rahn, Gierlichs, Planz, Planz & Stephany (1976) showed that there was elevation of plasma catecholamines in patients treated with propranolol for 10 days, although others have demonstrated falls in noradrenaline (Brecht, Banthien, Ernst & Schoeppe, 1976).…”