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- W2489124920 abstract "The alteration of cardiovascular myocytes is an important compensatory response to hypertension; however the pressor effect of angiotensin-II (A-II) on the correlation of myocyte morphological adaptation and collagen/parenchyma distribution in the ventricles has not been determined. Previous observations that the AII peptide is involved in the etiology of hypertension, suggested that ventricular collagen remodeling and associated pathophysiological alterations may be induced by a dysfunctional renin-angiotensin system. The objectives of this study were to 1) determine the contribution and distribution of collagen and parenchyma remodeling in the left ventricles after chronic exposure to subpressor (Sd) or pressor doses (Pd) of angiotensin II (A-Il); and 2) correlate the morphological adaptations of cardiomyocytes to weight changes of the entire heart after A-Il. The increase was 0.03 to 0.11 in the Pd-treated rats which was accompanied by a higher level of hypertrophic response than with the Sd treatment. Left-ventricular cell lengths (CL) of Pd-treated rats increased by 13%, while the heart weight to body weight ratio (HW/BW) increased by 22%. The myocardial interstitium response to the hypertrophic stimulation by A-Il included disproportionate collagen/parenchyma distribution to myocyte enlargement that is more pronounced with larger doses of A-Il and level of hypertrophy. This suggests that the A-II peptide is involved in the etiology of hypertension and a local increase is a primary factor of sustained myocardial remodeling." @default.
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- W2489124920 date "2009-01-01" @default.
- W2489124920 modified "2023-10-17" @default.
- W2489124920 title "Left Ventricular Hypertrophy, Cardiac Myocyte Adaptation, and Collagen/Parenchymal Distribution in Response to Subpressor and Pressor Doses of Angiotensin II in Sprague-Dawley Rats" @default.
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- W2489124920 doi "https://doi.org/10.5580/10d9" @default.
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