Angiotensin and the remodelling of the myocardium.

Weber, K T; Janicki, J S

doi:10.1111/j.1365-2125.1989.tb03589.x

Cited by 48 publications

(15 citation statements)

References 42 publications

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“…7 These results are consistent with a deleterious effect of the hypertensive state on myocardial structure, resulting in hypertrophy of myocytes and increased connective tissue accumulation. Although the relations between these two phenomena are still unclear, 17 by unloading the left ventricular myocardium, myocardial oxygen demand should decrease, and the intramural physical stress on a per cell basis should be markedly reduced, avoiding the potential damage of physical stresses. The modest (+13%), albeit significantly higher, coronary flow rate per myocardial mass unit found in the group of treated SHR (Table 2) is consistent with the results obtained by other investigators, 18 who found that 5 months' treatment of 3-month-old SHR with the ACE-inhibitor cilazapril improved the maximal coronary flow rate in isolated perfused hearts and increased the capillary density in the myocardium.…”

Section: Discussionmentioning

confidence: 99%

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

et al. 1991

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To evaluate the effects of hypertension on cardiac hypertrophy, on myocardial structure, and on ventricular arrhythmias, 27 3-month-old spontaneously hypertensive rats were treated with enalapril (10 ing/kg) daily for 11 months and compared with 26 untreated control rats. Systolic arterial pressure was significantly decreased in treated rats, and at the end of the experiment, it was 199±3 mm Hg (treated) versus 237±3 mm Hg (controls) (p<0.001). At this time, spontaneous arrhythmias and induced arrhythmias either by programmed electrical stimulation (train of stimuli +1 or 2 extrastimuli) or by trains of eight stimuli at decreasing coupling intervals were observed in isolated heart preparations.

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Section: Discussionmentioning

confidence: 99%

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

et al. 1991

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“…50 -5 "- 59 A number of cogent arguments implicate the RAS in vascular and cardiac growth and hypertrophy (Table 3). Angiotensin provides not only a hemodynamic load by its vasoconstrictor activity, thus increasing peripheral resistance and ventricular afterload, but may have several nonhemodynamic effects on growth.…”

Section: Angiotensin Converting Enzyme In Cardiac and Vascular Hypertmentioning

confidence: 99%

Tissue angiotensin converting enzyme in cardiac and vascular hypertrophy, repair, and remodeling.

Johnston

1994

Hypertension

160

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A 52-year-old white man presented with a small full wall thickness anterior myocardial infarct. He L was given intravenous streptokinase, aspirin, and nitrates, and his course was uncomplicated.He had suffered mild essential hypertension for 10 years and had been treated over this period with moduretic (one tablet per day). His primary physician had excluded causes of secondary hypertension, and he had been told that his blood pressure control on the diuretic was satisfactory (documented at levels between 146 and 138 mm Hg systolic and 90 and 96 mm Hg diastolic). His serum cholesterol levels had been measured on several occasions, and the last reading was 6.8 mmol/dL (205 mg%).A chest radiograph performed in the hospital showed cardiomegaly, and his electrocardiogram showed high voltage over his anterior chest leads. An echocardiogram confirmed increased posterior and septal thicknesses, with normal fractional shortening. A radionuclide ventriculogram showed a left ventricular ejection fraction of 40%. Serum creatinine concentration was within normal limits, as were serum potassium and blood glucose levels.His blood pressure on presentation to the hospital with the myocardial infarction was 160/100 mm Hg and remained at this level for the first 24 hours. On the second day, 6.25 mg captopril was given and then 12.5 mg twice daily. His blood pressure fell to 150/95 mm Hg, and his captopril dose was increased to 25 mg twice daily.On discharge from the hospital, his blood pressure was 140/82 mm Hg. Six months later, on medical review, his blood pressure was 142/84 mm Hg, his cholesterol was 5.5 mg/dL, and his left ventricular hypertrophy had regressed.This man presents with a very common clinical and management problem: a middle-aged man with longstanding treated hypertension and left ventricular hypertrophy complicated by an acute myocardial infarct.Dr Johnston was an invited speaker at

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“…It has recently been suggested that activation of the renin-angiotensin-aldosterone system [31] and the alteration of myocardial high-energy phosphate levels [32] are correlated with the extent of LV remodeling. The former system plays an important role in the development of reactive myocardial hypertrophy and fibrosis that accompanies LV remodeling.…”

Section: Discussionmentioning

confidence: 99%

Nipradilol, a new β-adrenergic blocker, reduces left ventricular remodeling following myocardial infarction in spontaneously hypertensive rats

1997

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Left ventricular (LV) cavity dilation (remodeling) following myocardial infarction (MI) is a risk factor for morbidity and mortality. This study was undertaken to determine whether nipradilol, a new beta-adrenergic blocker with vasodilating action, reduces LV remodeling after MI produced by coronary ligation in spontaneously hypertensive rats. The effects on LV remodeling of the following drugs, which were administered orally for 4 weeks, were evaluated by assessing LV end-diastolic volume index (LVEDVI): (1) vehicle, (2) nipradilol, 10 mg/kg per day. (3) propranolol, 50 mg/kg per day, and (4) captopril, 30 mg/kg per day. Since LVEDVI depends on infarct size, the effects of the drugs on LVEDVI were compared between rats with a similar infarct size, i.e., moderate, 20%-40%; and large, 40%-60%, on the basis of the histological determination of infarct size. The nipradilol-treated and captopril-treated rats had significantly smaller LVEDVI than did the vehicle-treated rats with both moderate and large infarction (large infarct: 2.48 +/- 0.12 ml/kg for the vehicle group, 1.69 +/- 0.10 ml/kg for the nipradilol group, P < 0.01, and 1.79 +/- 0.14 ml/kg for the captopril group, P < 0.01). In contrast, LVEDVI-in the propranolol-treated rats was significantly greater than that in the vehicle-treated rats with a moderate infarct (2.09 +/- 0.09 ml/kg for the vehicle group versus 2.44 +/- 0.10 ml/kg for the propranolol group, P < 0.05). The results indicate that nipradilol and captopril reduce LV remodeling after MI, whereas propranolol promotes it.

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Angiotensin and the remodelling of the myocardium.

Cited by 48 publications

References 42 publications

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

Tissue angiotensin converting enzyme in cardiac and vascular hypertrophy, repair, and remodeling.

Nipradilol, a new β-adrenergic blocker, reduces left ventricular remodeling following myocardial infarction in spontaneously hypertensive rats

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