Modulation of adrenergic receptors during left ventricular hypertrophy development and after regression by captopril

The objective of this study was to analyze adrenergic receptors during card iac hypertrophy development, after establishment of cardiac hypertrophy and after regression of cardiac hypertrophy by an angiotensin-converting enzym e inhibitor. Left ventricular hypertrophy (LVH) was induced by abdominal ao rtic stenosis. After surgery, plasma norepinephrine concentrations (P-NE) a nd left ventricular adrenergic receptors from rat hearts subjected to aorti c stenosis were assessed during cardiac hypertrophy development (at 3, 7, 1 5, and 30 days of aortic stenosis), once cardiac hypertrophy had been estab lished (7 and 14 weeks after the stenosis) and after regression of cardiac hypertrophy by an antihypertensive dose (200 mg/kg/day) of captopril, The p resence of LVH was observed from day 7 after stenosis. P-NE had significant ly increased after 15 days bur returned to control values 30 days after sur gery. The density of alpha(1)-adrenoceptors was found to decrease with deve lopment of hypertrophy. Once hypertrophy had been established, 7 weeks from stenosis, P-NE was not different from control; however, the density of alp ha(1)-adrenoceptors continued to diminish, whereas P-NE and the density of beta-adrenoceptors were no different from control values. Fourteen weeks af ter stenosis, a significant decrease in P-NE was recorded, and no change in alpha(1)- but an increase in beta-adrenoceptors was observed. LVH was reve rsed by treatment with captopril; P-NE was similar in control and stenosed treated animals. The density of alpha(1)-adrenoceptors was decreased when c ompared with control animals, and no change in the density of beta-adrenoce ptors was observed with treatment. In conclusion, a decrease of alpha(1)-ad renoceptors was associated with LVH development and earlier stages of estab lished cardiac hypertrophy. Later stages of established cardiac hypertrophy were characterized by no change in alpha(1)- and an increase in beta-adren oceptors. Treatment with captopril induced LVH regression and decreased the number of alpha(1)-adrenoceptors without any change in beta-adrenoceptors.