BETA-ADRENERGIC RECEPTORS IN RAT MYOCARDIUM DURING THE DEVELOPMENT AND REVERSAL OF HYPERTROPHY AND FOLLOWING CHRONIC INFUSIONS OF ANGIOTENSIN-II AND EPINEPHRINE

Abstract

The effect of cardiac hypertrophy on .beta.-adernergic receptor density and affinity was studied under 4 experimental conditions: in the spontaneously hypertensive rat (SHR), in the 2K-1C renal hypertensive rat (SHR), in the 2K-1C renal hypertensive rat (RHR), and following s.c. 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 wk 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 wk after clipping, returning towards normal levels following removal of the clipped kidney. Cardiac hypertrophy and hypertension were induced by s.c. infusions for up to 2 wk 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. Different models of hypertensive hypertrophy are associated with varying changes in .beta.-adrenergic receptors. Any consequential changes in myocardial function may be a result of other post receptor mechanisms.