The effects of beta adrenoceptor blockade with atenolol on myocardial cellular and subcellular hypertrophy in spontaneously hypertensive rats

Lauva, Ines K.; Tomanek, Robert J.

doi:10.1002/ar.1092070409

Cited by 11 publications

(3 citation statements)

References 36 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This report supports our present experimental results. However, Lauva and Tomanek reported that atenolol reduced LV weight in male SHRs at 4 weeks of age (29). The discrepancy between these results may be related to the experimental methods used (e.g., the age and sex of rats, or the different drugs used), however, our results indicate that the inhibition of RAS plays a more important role than the suppression of the β adrenergic nervous system in the reversal of myocyte remodeling.…”

Section: Discussioncontrasting

confidence: 73%

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

et al. 2002

View full text Add to dashboard Cite

Studies have shown that the renin-angiotensin system (RAS) plays an important role in cardiac remodelinginduced by hypertension. However, the role of this system on myocyte remodeling remains unclear. In the present study, we have assessed the effect of perindopril, an angiotensin converting enzyme (ACE) inhibitor, in spontaneously hypertensive rats (SHRs) as a means to evaluate the role of RAS in myocyte remodeling. We also investigated the effect of blockade on myocyte remodeling. We used female SHRs at

show abstract

Section: Discussioncontrasting

confidence: 73%

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

et al. 2002

View full text Add to dashboard Cite

show abstract

“…Pressure-overload-induced cardiac hypertrophy has been associated with increased serum epinephrine (Womble et al, 1978), the predominant adrenal catecholamine. Treatment of spontaneously hypertensive rats with a-methyldopa, a catecholamine depleting agent, or atenolol, a cardioselective P-adrenoceptor blocking agent, did modify cardiac hypertrophy (Sen et al, 1974;Tomanek et al, 1979;Lauva and Tomanek, 1983).…”

Section: Discussionmentioning

confidence: 99%

Control of myocardial tissue components and cardiocyte organelles in pressure‐overload hypertrophy of the cat right ventricle

et al. 1986

Self Cite

View full text Add to dashboard Cite

Previous studies have demonstrated that there is a disproportionate increase in connective tissue in right ventricular myocardium subjected to pressure-overload hypertrophy associated with depressed cardiac contractility. While the myocardium is primarily responsive to load, the aim of the present study was to determine whether catecholamines also modulate the response of myocardial tissue components and cardiocyte organelles in pressure-overload-induced cardiac hypertrophy. Four experimental groups of cats were examined: a sham-operated control group, a group which had their pulmonary arteries banded in order to induce a pressure overload, a group which had been subjected to the same pressure overload, but in addition had beta-adrenoceptor blockade produced prior to and during the pressure overloading, and a group which had been subjected to the same pressure overload, but in addition had alpha-adrenoceptor blockade produced prior to and maintained during the pressure overloading. As in our previous study, there was a significant and equivalent degree of right ventricular hypertrophy in all experimental groups with pressure overload when assessed either as the ratio of right ventricular weight to body weight or as cardiocyte cross-sectional area. At the light microscopic level, the disproportionate increase in the volume density of myocardial connective tissue seen in banded animals was completely prevented by either alpha- or beta-adrenoceptor blockade. At the electron microscopic level, there was a reduction in the mitochondrial and myofibrillar volume fractions following beta-adrenoceptor blockade. The results of this study provide evidence for a modulatory role of catecholamines in the control of myocardial connective-tissue proliferation in pressure-overload-induced cardiac hypertrophy. There is also evidence to support the role of the adrenergic nervous system in regulating cardiocyte subcellular organelles, independent of the regulation of cardiocyte size.

show abstract

“…Subsequent studies employing adrenal demedullation (8), a-or P-adre-noceptor blockade ( 1 ), or chemical sympathectomy ( 17) have generally supported the view that adrenergic intervention has little or no effect on the hypertrophic response to pressure overload. Similarly, sympathectomy or P-adrenoceptor blockade does not prevent cardiac hypertrophy in spontaneously hypertensive rats (24)(25)(26), renal hypertensive rats (27), or rabbits subjected to hypoxia (28,29).…”

mentioning

confidence: 99%

Effects of Adrenoceptor Blockade on Cardiac Hypertrophy and Myocardial Phospholipids

O’Rourke

Reibel

1992

Experimental Biology and Medicine

View full text Add to dashboard Cite

Catecholamines have been proposed as a stimulus for the hypertrophic response to pressure overload of the heart and could also mediate the membrane lipid changes associated with cardiac hypertrophy. To address both of these possibilities, cardiac hypertrophy was induced by aortic constriction in the presence or absence of chronic alpha- or beta-adrenoceptor blockade. Heart weights and heart weight to body weight ratios in aortic-constricted rats of the adrenoceptor-blocked and vehicle-treated groups were elevated to the same extent when compared with values in sham-operated rats of each group. Analysis of the fatty acyl composition of the major phospholipid classes revealed that similar changes occurred in vehicle-treated, alpha-blocked, and beta-blocked aortic-constricted rats when compared with respective groups of sham-operated rats. Specifically, linoleic acid was reduced in the phosphatidylcholine, phosphatidylethanolamine (PE), and cardiolipin (CL) fractions in all groups of aortic-constricted rats. This reduction was accompanied by increased docosahexaenoic acid, arachidonic acid, or palmitic acid in phosphatidylcholine; docosahexaenoic acid in phosphatidylethanolamine; and oleic acid in cardiolipin fractions. Adrenoceptor blockade did not prevent or attenuate the major changes in the fatty acyl composition of phospholipids or the increase in heart weight associated with aortic constriction. This suggests that a change in the level of adrenoceptor stimulation is not the stimulus for cardiac hypertrophy or the observed alterations in phospholipid composition in the pressure-overloaded rat heart.

show abstract

The effects of beta adrenoceptor blockade with atenolol on myocardial cellular and subcellular hypertrophy in spontaneously hypertensive rats

Cited by 11 publications

References 36 publications

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

Control of myocardial tissue components and cardiocyte organelles in pressure‐overload hypertrophy of the cat right ventricle

Effects of Adrenoceptor Blockade on Cardiac Hypertrophy and Myocardial Phospholipids

Contact Info

Product

Resources

About