Vcw. Busatto et al., Differential effects of isoproterenol on the activity of angiotensin-converting enzyme in the rat heart and aorta, BRAZ J MED, 32(3), 1999, pp. 355-360
Citations number
19
Categorie Soggetti
Medical Research General Topics
Journal title
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
The excessive stimulation of beta-adrenergic receptors in the heart induces
myocardial hypertrophy. There are several experimental data suggesting tha
t this hypertrophy may also depend, at least partially, on the increase of
local production of angiotensin II secondary to the activation of the cardi
ac renin-angiotensin system. In this study we investigated the effects of i
soproterenol on the activity of angiotensin-converting enzyme (ACE) in the
heart and also in the aorta and plasma. Male Wistar rats weighing 250 to 30
5 g were treated with a dose of (+/-)-isoproterenol (0.3 mg kg(-1) day(-1),
N = 8) sufficient to produce cardiac hypertrophy without deleterious effec
ts on the pumping capacity of the heart. Control rats (N = 7) were treated
with vehicle (corn oil). The animals were killed one week later. ACE activi
ty was determined in vitro in the four cardiac chambers, aorta and plasma b
y a fluorimetric assay. A significant hypertrophy was observed in both vent
ricular chambers. ACE activity in the atria remained constant after isoprot
erenol treatment. There was a significant increase (P<0.05) of ACE activity
in the right ventricle (6.9 +/- 0.9 to 8.2 +/- 0.6 nmol His-Leu g(-1) min(
-1)) and in the left ventricle (6.4 +/- 1.1 to 8.9 +/- 0.8 nmol His-Leu g(-
1) min(-1)). In the aorta, however, ACE activity decreased (P<0.01) after i
soproterenol (41 +/- 3 to 27 +/- 2 nmol His-Leu g(-1) min(-1)) while it rem
ained unchanged;. in the plasma. These data suggest that ACE expression in
the heart can be increased by stimulation of beta-adrenoceptors. However, t
his effect is not observed on other local renin-angiotensin systems, such a
s the aorta. Our data also suggest that the increased sympathetic discharge
and the elevated plasma concentration of catecholamines may contribute to
the upregulation of ACE expression in the heart after myocardial infarction
and heart failure.