Prevention of structural changes in the heart in hypertension by angiotensin converting enzyme inhibition

L. B. Tan, C. Brilla, Karl Weber

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Background: The long-term effects of hypertension on the heart culminate in congestive heart failure. The underlying causes are contractile impairment due to myocyte loss and reduced compliance due to myocardial fibrosis. Newer strategies in antihypertensive therapy must, therefore, focus on prevention of myocardial damage ('cardioprotection') or, if an abnormality has occurred, on reversal towards normal myocardial structure and function ('cardioreparation'). Objective: To investigate the question of whether angiotensin converting enzyme (ACE) inhibition can influence myocardial remodelling in hypertension to produce cardioprotective and cardioreparative effects. Methods and results: Infusion of pathophysiological levels of circulating angiotensin II in rats causes cardiac myocyte necrosis, followed by fibroblast proliferation. This necrosis is not secondary to adrenergic activation or raised blood pressure. Similarly, renovascular hypertension results in cardiac myocyte necrosis, which can be prevented by pretreatment with the ACE inhibitor captopril. In established genetic hypertension in rats, sustained treatment with high-dose lisinopril normalizes the blood pressure, reverses left ventricular hypertrophy, reverses excessive interstitial and perivascular fibrosis (and consequently the impaired compliance), and reverses excessive coronary artery medial thickening (thereby normalizing coronary vascular reserve). With a low dose of lisinopril that does not reduce blood pressure significantly, only the excessive fibrosis is reversed. Conclusion: ACE inhibition has demonstrated promising myocardial remodelling effects in experimental models of hypertensive heart disease.

Original languageEnglish (US)
JournalJournal of Hypertension
Volume10
Issue numberSUPPL. 1
DOIs
StatePublished - Jun 18 1992
Externally publishedYes

Fingerprint

Peptidyl-Dipeptidase A
Lisinopril
Fibrosis
Necrosis
Blood Pressure
Hypertension
Cardiac Myocytes
Compliance
Renovascular Hypertension
Captopril
Left Ventricular Hypertrophy
Angiotensin-Converting Enzyme Inhibitors
Angiotensin II
Adrenergic Agents
Muscle Cells
Antihypertensive Agents
Blood Vessels
Heart Diseases
Coronary Vessels
Theoretical Models

All Science Journal Classification (ASJC) codes

  • Endocrinology
  • Internal Medicine

Cite this

Prevention of structural changes in the heart in hypertension by angiotensin converting enzyme inhibition. / Tan, L. B.; Brilla, C.; Weber, Karl.

In: Journal of Hypertension, Vol. 10, No. SUPPL. 1, 18.06.1992.

Research output: Contribution to journalArticle

@article{58ec2c2161114d5a88b71d38649f9960,
title = "Prevention of structural changes in the heart in hypertension by angiotensin converting enzyme inhibition",
abstract = "Background: The long-term effects of hypertension on the heart culminate in congestive heart failure. The underlying causes are contractile impairment due to myocyte loss and reduced compliance due to myocardial fibrosis. Newer strategies in antihypertensive therapy must, therefore, focus on prevention of myocardial damage ('cardioprotection') or, if an abnormality has occurred, on reversal towards normal myocardial structure and function ('cardioreparation'). Objective: To investigate the question of whether angiotensin converting enzyme (ACE) inhibition can influence myocardial remodelling in hypertension to produce cardioprotective and cardioreparative effects. Methods and results: Infusion of pathophysiological levels of circulating angiotensin II in rats causes cardiac myocyte necrosis, followed by fibroblast proliferation. This necrosis is not secondary to adrenergic activation or raised blood pressure. Similarly, renovascular hypertension results in cardiac myocyte necrosis, which can be prevented by pretreatment with the ACE inhibitor captopril. In established genetic hypertension in rats, sustained treatment with high-dose lisinopril normalizes the blood pressure, reverses left ventricular hypertrophy, reverses excessive interstitial and perivascular fibrosis (and consequently the impaired compliance), and reverses excessive coronary artery medial thickening (thereby normalizing coronary vascular reserve). With a low dose of lisinopril that does not reduce blood pressure significantly, only the excessive fibrosis is reversed. Conclusion: ACE inhibition has demonstrated promising myocardial remodelling effects in experimental models of hypertensive heart disease.",
author = "Tan, {L. B.} and C. Brilla and Karl Weber",
year = "1992",
month = "6",
day = "18",
doi = "10.1097/00004872-199204001-00007",
language = "English (US)",
volume = "10",
journal = "Journal of Hypertension",
issn = "0263-6352",
publisher = "Lippincott Williams and Wilkins",
number = "SUPPL. 1",

}

TY - JOUR

T1 - Prevention of structural changes in the heart in hypertension by angiotensin converting enzyme inhibition

AU - Tan, L. B.

AU - Brilla, C.

AU - Weber, Karl

PY - 1992/6/18

Y1 - 1992/6/18

N2 - Background: The long-term effects of hypertension on the heart culminate in congestive heart failure. The underlying causes are contractile impairment due to myocyte loss and reduced compliance due to myocardial fibrosis. Newer strategies in antihypertensive therapy must, therefore, focus on prevention of myocardial damage ('cardioprotection') or, if an abnormality has occurred, on reversal towards normal myocardial structure and function ('cardioreparation'). Objective: To investigate the question of whether angiotensin converting enzyme (ACE) inhibition can influence myocardial remodelling in hypertension to produce cardioprotective and cardioreparative effects. Methods and results: Infusion of pathophysiological levels of circulating angiotensin II in rats causes cardiac myocyte necrosis, followed by fibroblast proliferation. This necrosis is not secondary to adrenergic activation or raised blood pressure. Similarly, renovascular hypertension results in cardiac myocyte necrosis, which can be prevented by pretreatment with the ACE inhibitor captopril. In established genetic hypertension in rats, sustained treatment with high-dose lisinopril normalizes the blood pressure, reverses left ventricular hypertrophy, reverses excessive interstitial and perivascular fibrosis (and consequently the impaired compliance), and reverses excessive coronary artery medial thickening (thereby normalizing coronary vascular reserve). With a low dose of lisinopril that does not reduce blood pressure significantly, only the excessive fibrosis is reversed. Conclusion: ACE inhibition has demonstrated promising myocardial remodelling effects in experimental models of hypertensive heart disease.

AB - Background: The long-term effects of hypertension on the heart culminate in congestive heart failure. The underlying causes are contractile impairment due to myocyte loss and reduced compliance due to myocardial fibrosis. Newer strategies in antihypertensive therapy must, therefore, focus on prevention of myocardial damage ('cardioprotection') or, if an abnormality has occurred, on reversal towards normal myocardial structure and function ('cardioreparation'). Objective: To investigate the question of whether angiotensin converting enzyme (ACE) inhibition can influence myocardial remodelling in hypertension to produce cardioprotective and cardioreparative effects. Methods and results: Infusion of pathophysiological levels of circulating angiotensin II in rats causes cardiac myocyte necrosis, followed by fibroblast proliferation. This necrosis is not secondary to adrenergic activation or raised blood pressure. Similarly, renovascular hypertension results in cardiac myocyte necrosis, which can be prevented by pretreatment with the ACE inhibitor captopril. In established genetic hypertension in rats, sustained treatment with high-dose lisinopril normalizes the blood pressure, reverses left ventricular hypertrophy, reverses excessive interstitial and perivascular fibrosis (and consequently the impaired compliance), and reverses excessive coronary artery medial thickening (thereby normalizing coronary vascular reserve). With a low dose of lisinopril that does not reduce blood pressure significantly, only the excessive fibrosis is reversed. Conclusion: ACE inhibition has demonstrated promising myocardial remodelling effects in experimental models of hypertensive heart disease.

UR - http://www.scopus.com/inward/record.url?scp=0026770413&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026770413&partnerID=8YFLogxK

U2 - 10.1097/00004872-199204001-00007

DO - 10.1097/00004872-199204001-00007

M3 - Article

VL - 10

JO - Journal of Hypertension

JF - Journal of Hypertension

SN - 0263-6352

IS - SUPPL. 1

ER -