1. The effect of indomethacin, an inhibitor of prostaglandin synthesis, on number and sensitivity of α- and β-adrenoreceptors was studied in normal healthy volunteer subjects. 2. The subjects were studied under metabolic conditions. To achieve inhibition of prostaglandin synthesis indomethacin (2 mg day −1 kg −1 ) was given orally for 7 days. This dose decreased urinary excretion of prostaglandin E-like immunoreactivity by 70%. 3. The number of α-adrenoreceptors was measured by the specific binding of [ 3 H]dihydroergocryptine to platelet membranes and that of β-adrenoreceptors by the binding of [ 3 H]dihydroalprenolol to leucocyte membranes. 4. The number of α-adrenoreceptors did not change with indomethacin, nor did basal, prostaglandin E 1 - or noradrenaline-stimulated cyclic AMP production by platelet membranes. In contrast, the number of β-adrenoreceptors increased by 92%. Indomethacin did not affect, however, basal, 1-isoprenaline- or prostaglandin E 1 -stimulated cyclic AMP production in leucocyte membranes. 5. These results suggest that a reflex-mediated decrease in sympathetic discharge in response to an indomethacin-induced decrease in release of vasodilator prostaglandins may lead to an ‘up-regulation’ of β-adrenoreceptor sites.

1. Direct radioligand—binding techniques have been used to characterize and quantify adrenoreceptors in human peripheral lung tissue removed at thoracotomy from ten patients, nine of whom had evidence of obstructive airways disease. 2. [ 3 H]Dihydroalprenolol was used to characterize β–adrenoreceptor sites and [ 3 H]prazosin to identify α–adrenoreceptor sites. Binding of both ligands showed saturability, high affinity, rapid kinetics, reversibility and stereospecificity. The rank order of agonists and antagonists inhibiting specific binding correlated well with known physiological potencies. Specificity of [ 3 H]dihydroal-prenolol binding suggested that the population of lung β–adrenoreceptors is predominantly of the β 2 subtype.

1. The relationships between plasma noradrenaline concentration at rest and blood pressure, as well as increase in forearm blood flow in response to a brachial artery infusion of the α-adrenoreceptor-blocking agent phentolamine, were investigated in hypertensive and normotensive subjects of similar age. 2. In 44 hypertensive patients plasma noradrenaline correlated with systolic, diastolic and mean blood pressures, but no difference in the mean plasma noradrenaline concentration was found. 3. In 11 patients and 14 normotensive subjects α-adrenoreceptor blockade resulted in a similar increase in forearm blood flow. Only in the patients, however, was this increase related to plasma noradrenaline and blood pressure. 4. In patients with established essential hypertension plasma noradrenaline can be considered to be a marker of α-adrenoreceptor-mediated vasoconstriction, which, in part, determines the height of the blood pressure.