In 44 patients undergoing coronary artery bypass grafting, the effect of chronic administration of the fi-adrenoceptor antagonists sotalol, propranolol, pindolol, metoprolol and atenolol on fiadrenoceptor density in right atria (containing 70% PB-and 30% P2-adrenoceptors) and in lymphocytes (having only f2-adrenoceptors) was studied.2 fl-Adrenoceptor density in right atrial membranes and in intact lymphocytes was assessed by (-)[1225I]-iodocyanopindolol (ICYP) binding; the relative amount of right atrial P,-and #2-adrenoceptors was determined by inhibition of ICYP binding by the selective #2-adrenoceptor antagonist ICI 118,551 and analysis of the resulting competition curves by the iterative curve fitting programme LIGAND. 3 With the exception of pindolol, all f-adrenoceptor antagonists increased right atrial ,Badrenoceptor density compared to that observed in atria from patients not treated with fadrenoceptor antagonists. 4 All f-adrenoceptor antagonists increased right atrial fi-adrenoceptor density; on the other hand, only sotalol and propranolol also increased right atrial f2-adrenoceptor density, whereas metoprolol and atenolol did not affect it and pindolol decreased it. 5 Similarly, in corresponding lymphocytes, only sotalol or propranolol increased fi2-adrenoceptor density, while metoprolol and atenolol did not affect it and pindolol decreased it.6 It is concluded that P-adrenoceptor antagonists subtype-selectively regulate cardiac and lymphocyte ,B-adrenoceptor subtypes. The selective increase in cardiac fi1-adrenoceptor density evoked by metoprolol and atenolol may be one of the reasons for the beneficial effects observed in patients with end-stage congestive cardiomyopathy following intermittent treatment with low doses of selective fl-adrenoceptor antagonists.

We have determined simultaneously the density of beta-adrenoceptors in human myometria (by (-)-[125I]iodopindolol binding) derived from 36 women undergoing cesarean section and in the corresponding circulating lymphocytes (by (-)-[125I]iodocyanopindolol binding). In myometrial membranes about 80% to 85% of the beta-adrenoceptors were of the beta 2-subtype. The density of myometrial and lymphocyte beta-adrenoceptors in women treated with the beta 2-adrenoceptor agonist hexoprenaline to prevent preterm labor was about 65% to 70% lower than that in nontreated women. Concomitantly, in hexoprenaline-treated women the 10 mumol/L isoproterenol-evoked increase in lymphocyte cyclic adenosine monophosphate content (as index for lymphocyte beta-adrenoceptor responsiveness) was diminished to a similar extent. Combining all data resulted in a significant positive correlation between myometrial and lymphocyte beta-adrenoceptor densities (r = 0.7303; n = 36; p less than 0.001). It is possible that determination of beta-adrenoceptor function in circulating lymphocytes may be a useful model to monitor myometrial beta-adrenoceptor changes during tocolytic therapy.