Enalapril improves systemic and renal hemodynamics and allows regression of left ventricular mass in essential hypertension

Dunn, Francis G.; Oigman, Wille; Ventura, Héctor O.; Messerli, Franz H.; Kobrin, Isaac; Fröhlich, Edward D.

doi:10.1016/0002-9149(84)90692-1

Cited by 216 publications

(66 citation statements)

References 22 publications

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“…[3][4][5][6][7][8][9][10] In addition, all components of the RAS are upregulated by pressure overload in the heart. 5,[11][12][13][14][15][16] All these results suggest that the RAS plays a critical role in the development of mechanical stressinduced cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Pressure Overload Induces Cardiac Hypertrophy in Angiotensin II Type 1A Receptor Knockout Mice

Harada

Komuro²,

Shiojima³

et al. 1998

Circulation

230

152

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Background-Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload-induced cardiac hypertrophy. Moreover, it has been reported that pressure overload-induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT 1 ) in vitro. These results suggest that the AT 1 -mediated signaling is critical for the development of mechanical stress-induced cardiac hypertrophy. Methods and Results-To determine whether AT 1 -mediated signaling is indispensable for the development of pressure overload-induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT 1A knockout (KO) mice. Quantitative reverse transcriptase-polymerase chain reaction revealed that the cardiac AT 1 (probably AT 1B ) mRNA levels in AT 1A KO mice were Ͻ10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis.

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Section: Discussionmentioning

confidence: 99%

Pressure Overload Induces Cardiac Hypertrophy in Angiotensin II Type 1A Receptor Knockout Mice

Harada

Komuro²,

Shiojima³

et al. 1998

Circulation

230

152

View full text Add to dashboard Cite

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“…Thus, from our earliest work LV mass has been shown to be reduced within three weeks by most antihypertensive agents in both SHR and in patients with essential hypertension (30,(53)(54)(55)(56)(57)(58). It is notable that, associated with ACE inhibitor-or calcium antagonist-induced reductions in LV muscle mass, there was a concomitant reduction in LV collagen; however, all calcium antagonists increased RV collagen (59) as mass or wall thickness increased (56,58,59). However, when an ACE inhibitor was administered with a calcium antagonist, the increased RV mass resulting from collagen deposition in SHR was prevented even though LV mass diminished no further (59).…”

Section: Ventricular Fibrosismentioning

confidence: 91%

Ischemia and fibrosis: the risk mechanisms of hypertensive heart disease

2000

Braz J Med Biol Res

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Mechanisms underlying risk associated with hypertensive heart disease (HHD) and left ventricular hypertrophy (LVH) are discussed in this report and provide a rationale for understanding this very common and important cause of death from hypertension and its complications. Emphasized are impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis from increased collagen deposition intramurally and perivascularly. Each is exacerbated by aging and, perhaps, also by increased dietary salt intake. These functional and structural changes promote further endothelial dysfunction, altered coronary hemodynamics, and diastolic as well as systolic ventricular contractile function in HHD. The clinical endpoints of HHD include angina pectoris (with or without atherosclerosis of the epicardial coronary arteries), myocardial infarction, cardiac failure, lethal dysrhythmias, and sudden death. The major concept to be derived from these alterations is that not all that is clinically recognized as LVH is true myocytic hypertrophy and structural remodeling. Other major co-morbid changes occur that serve to increase cardiovascular risk including impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis.

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“…[13][14][15] The mechanism for this increased efficacy with chronic administration is not clear but may involve the kallikreinkinin system or production of vasodilatory prostaglandins. 16 One of the characteristics of ACEis is that they lower peripheral vascular resistance without causing a compensatory increase in heart rate [17][18][19][20] or changing baroreceptor activity. 21 They also show lack of reflex tachycardia 22 and cause inhibition of the normal tonic influence of Ang II on the sympathetic nervous system.…”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

“…45, 46 The ACEis have been shown to reverse LV hypertrophy in patients with hypertension. 19,47,48 A meta-analysis of the effects of several antihypertensive agents suggested that ACEis were the most effective agent for reducing LV hypertrophy. 49 …”

Section: Atherosclerosismentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

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Since their inception, angiotensin-converting enzyme (ACE) inhibitors have been used as first-line therapy for the treatment of cardiovascular and renal diseases. They restore the balance between the vasoconstrictive salt-retentive and hypertrophy-causing peptide angiotensin II (Ang II) and bradykinin, a vasodilatory and natriuretic peptide. As ACE is a promiscuous enzyme, ACE inhibitors alter the metabolism of a number of other vasoactive substances. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have been proven effective in the treatment of hypertension, and reduce mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction. They inhibit ischemic events and stabilize plaques. Furthermore, they delay the progression of diabetic nephropathy and neuropathy and act as antioxidants. Ongoing studies have elucidated protective roles for them in both memory-related disorders and cancer. INTRODUCTIONIn recent years, stressful and fiercely competitive lifestyles and food habits have compounded the problems of hypertension. Long-standing and stressful, progressively rising hypertension can lead to many disorders, including myocardial infarction (MI), cerebrovascular events, congestive heart failure, peripheral arterial insufficiency, premature mortality 1 and renal dysfunction leading to glomerulosclerosis and kidney artery aneurysm. 2 A number of therapies are available, but angiotensin-converting enzyme (ACE) inhibitors have been the preferred first-line therapy for hypertension, congestive heart failure, left ventricular (LV) systolic dysfunction and MI. 3,4 ACE inhibitors (ACEis) have been in use for the past two decades, and the interest in them is still growing. Recently, the discovery of domain-selective ACEis and new members of the renin-angiotensin system (RAS) (that is, angiotensin-converting enzyme 2) have again fueled the interest of researchers. Some new studies have expanded the already impressive clinical profile of ACEis. This review traces some already known and new facets of ACE inhibition and introduces new advances in the designing of a new generation of ACEis.

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Enalapril improves systemic and renal hemodynamics and allows regression of left ventricular mass in essential hypertension

Cited by 216 publications

References 22 publications

Pressure Overload Induces Cardiac Hypertrophy in Angiotensin II Type 1A Receptor Knockout Mice

Pressure Overload Induces Cardiac Hypertrophy in Angiotensin II Type 1A Receptor Knockout Mice

Ischemia and fibrosis: the risk mechanisms of hypertensive heart disease

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

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