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 cardiac hypertrophy development, after establishment of cardiac hypertrophy and after regression of cardiac hypertrophy by an angiotensin-converting enzyme inhibitor. Left ventricular hypertrophy (LVH) was induced by abdominal aortic stenosis. After surgery, plasma norepinephrine concentrations (PNE) and left ventricular adrenergic receptors from rat hearts subjected to aortic stenosis were assessed during cardiac hypertrophy development (at 3, 7, 15, and 30 days of aortic stenosis), once cardiac hypertrophy had been established (7 and 14 weeks after the stenosis) and after regression of cardiac hypertrophy by an antihypertensive dose (200 mg/kg/day) of captopril. The presence of LVH was observed from day 7 after stenosis. PNE had significantly increased after 15 days but returned to control values 30 days after surgery. The density of alpha1-adrenoceptors was found to decrease with development of hypertrophy. Once hypertrophy had been established, 7 weeks from stenosis, PNE was not different from control; however, the density of alpha1-adrenoceptors continued to diminish, whereas PNE and the density of beta-adrenoceptors were no different from control values. Fourteen weeks after stenosis, a significant decrease in PNE was recorded, and no change in alpha1- but an increase in beta-adrenoceptors was observed. LVH was reversed by treatment with captopril; PNE was similar in control and stenosed treated animals. The density of alpha1-adrenoceptors was decreased when compared with control animals, and no change in the density of beta-adrenoceptors was observed with treatment. In conclusion, a decrease of alpha1-adrenoceptors was associated with LVH development and earlier stages of established cardiac hypertrophy. Later stages of established cardiac hypertrophy were characterized by no change in alpha1- and an increase in beta-adrenoceptors. Treatment with captopril induced LVH regression and decreased the number of alpha1-adrenoceptors without any change in beta-adrenoceptors.
Martínez
M L
ML
Institute of Pharmacology and Toxicology (Consejo Superior de Investigaciones Científicas-Universidad Complutense), School of Medicine, Universidad Complutense, Madrid, Spain.
Fernández-Tomé
P
P
López-Miranda
V
V
Colado
M I
MI
Delgado
C
C
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001013:Aorta, Thoracic / Q000601:surgery; D001794:Blood Pressure / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D004195:Disease Models, Animal; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000097:blood*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D018340:Receptors, Adrenergic, alpha-1; D011943:Receptors, Adrenergic, beta; D002216:Captopril; D009638:Norepinephrine