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Effects of adrenoceptor blockade on cardiac hypertrophy and myocardial phospholipids
1Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
Insights
Catecholamines do not stimulate cardiac hypertrophy or alter heart phospholipid composition in response to pressure overload. Adrenoceptor blockade did not prevent these changes in aortic-constricted rats.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Biochemistry
Background:
- Catecholamines are implicated in cardiac hypertrophy and associated membrane lipid changes.
- Pressure overload is a known trigger for cardiac hypertrophy.
Purpose of the Study:
- To investigate if catecholamines stimulate cardiac hypertrophy and phospholipid changes due to pressure overload.
- To determine the role of alpha- and beta-adrenoceptors in these responses.
Main Methods:
- Cardiac hypertrophy was induced in rats via aortic constriction.
- Adrenoceptor blockade (alpha- or beta-) was administered chronically.
- Heart weights and phospholipid fatty acyl composition were analyzed.
Main Results:
- Adrenoceptor blockade did not affect the increase in heart weight caused by aortic constriction.
- Similar changes in phospholipid fatty acyl composition (e.g., reduced linoleic acid) were observed in both blocked and unblocked rats.
- Specific fatty acid alterations included increased docosahexaenoic acid, arachidonic acid, palmitic acid, and oleic acid in various phospholipid fractions.
Conclusions:
- Adrenoceptor stimulation is not the primary stimulus for cardiac hypertrophy in pressure-overloaded hearts.
- Changes in adrenoceptor activity do not mediate the observed alterations in cardiac phospholipid composition during hypertrophy.
Abstract:
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.