The effect of cardiac hypertrophy on beta-adrenergic receptor density and affinity was studied under 4 experimental conditions: in the spontaneously hypertensive rat (SHR), in the 2K-1C renal hypertensive rat (RHR), and following subcutaneous infusions of 2 pressor agents; epinephrine (E) and angiotensin II(AII). Using the antagonist 3H-dihydroalprenolol [( 3H]-DHA), the number of binding sites was shown to significantly decrease at both 13 and 24 weeks of age in the SHR when compared to age-matched WKY, with no change in affinity. In the RHR a significant increase in binding sites was observed at both 6 and 10 weeks after clipping, returning towards normal levels following removal of the clipped kidney. Cardiac hypertrophy and hypertension were induced by subcutaneous infusions for up to 2 weeks of both E and AII. E caused an alteration in receptor density, causing a significant decrease with no change in affinity. In contradistinction, although the degree of hypertrophy was the same following AII, no changes in receptor density or affinity were seen. These present experiments confirm our hypothesis that different models of hypertensive hypertrophy are associated with varying changes in beta-adrenergic receptors. This suggests that any consequential changes in myocardial function may be a result of other post receptor mechanisms.