Abstract
Previous studies have shown that pharmacological doses of agonists can down-regulate beta receptors. We have shown that alteration of catecholamines within the physiological range is associated with modulation of beta receptor density. The stimulus used to alter catecholamine concentrations in vivo was change in sodium intake. In addition, administration of the beta blocker, propranolol, raised beta receptor density and the rise in receptor density was proportional to the pretreatment catecholamine concentrations. It appears that beta receptors in vivo are in a chronic state of down regulation and that this degree of down regulation parallels the catecholamine concentrations.