To evaluate the effects of salt and cholesterol intake on vascular responses to catecholamines, α<sub>1</sub>- and β-adrenergic receptor densities were determined in control, cholesterol-loaded, salt-loaded with desoxycorticosterone acetate (DOCA) and furosemide-loaded male rabbits, using [<sup>3</sup>H]-prazosin and (–)-[<sup>125</sup>I]-cyanopindolol as ligands, respectively. In the aortic membrane, the density of α<sub>1</sub>-adrenergic receptors (B<sub>max</sub> = 120 ± 14 fmol/mg protein, K<sub>d</sub> = 0.48 ± 0.05 nM) was higher than that of β -adrenergic receptors (B<sub>max</sub> = 10.5 ± 1.7 fmol/mg protein, K<sub>d</sub> 47.1 ± 8.6 pM). Salt loading and depletion did not alter the density or affinity of either the α<sub>1</sub>- or β -adrenergic receptors. By contrast, cholesterol loading significantly decreased αi-adrenergic receptor affinity to a K<sub>d</sub> value of 0.81 ± 0.11 nMfrom the control level of 0.48 ± 0.05 and increased the β -adrenergic receptor density to a B<sub>max</sub> of 18.7 ± 1.9 fmol/mg protein from the control level of 10.5 ± 1.7. These results showed that the density of α<sub>1</sub>-adrenergic receptors was higher than that of β-adrenergic receptors in the rabbit aortic membrane preparation, and suggested that the sensitivity of aortic membrane to catecholamines was changed by cholesterol loading.