Role of angiotensin II in injury-induced neointima formation in rats.

Osterrieder, Wolfgang; Müller, Rita; Powell, Jerry S.; Clozel, J. P.; Hefti, Fridolin; Baumgartner, Hans R.

doi:10.1161/01.hyp.18.4_suppl.ii60

Cited by 99 publications

(51 citation statements)

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“…In vivo studies have reported that Ang II infusion induces marked intimal smooth muscle cell proliferation in rat carotid arteries [17,21], and that ACE inhibitors suppress myointimal proliferation after vascular injury [14,18]. Intimal thickening can also be prevented by Ang II receptor type-1 antagonists [66]. However, all these effects are probably also related to an action on bradykinin metabolism [67].…”

Section: Atherosclerosis and Restenosismentioning

confidence: 99%

Aspects of gene polymorphisms in cardiovascular disease: the renin‐angiotensin system

Carluccio

Soccio

Caterina

2001

Eur J Clin Investigation

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The renin-angiotensin system (RAS) plays a central role in cardiovascular homeostasis. Angiotensin is the key peptide of the RAS, and exerts its influence on the heart and blood vessels both through its haemodynamic effects (via its influence on after-load and pre-load and determining coronary vasoconstriction) and through its direct cellular effects (via its actions on cell proliferation). Numerous studies in the past 10 years have demonstrated that the pharmacological inhibition of angiotensin converting enzyme (ACE), one of the two critical enzymes of the RAS, improves the outcome in patients with several cardiovascular disorders (hypertension, heart failure, ischaemic heart disease). These studies suggest a role of the RAS as a major determinant of cardiovascular risk. Recent data suggest that genetics may in turn contribute to modulating the effects of angiotensin on coronary vascular biology and ischaemia. This paper reviews the physiologic characteristics of the RAS and recent research developments related to angiotensin cell biology and pathobiology in heart disease. In particular, this review will cover the genetic aspects of RAS and their implications in cardiovascular disease.

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Section: Atherosclerosis and Restenosismentioning

confidence: 99%

Aspects of gene polymorphisms in cardiovascular disease: the renin‐angiotensin system

Carluccio

Soccio

Caterina

2001

Eur J Clin Investigation

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“…14 Another enzyme present in mast cells is the metalloprotease, carboxypeptidase A enzyme. This enzyme cleaves the His 9 -Leu 10 bond in angiotensin I and as a result generates the fragment angiotensin [1][2][3][4][5][6][7][8][9] , which although capable of inhibiting ACE, has no known intrinsic contractile activity. 26 The human heart has been shown to possess carboxypeptidase A activity, generation of angiotensin [1][2][3][4][5][6][7][8][9] by this enzyme is sufficient to block cardiac ACE.…”

Section: Alternative Angiotensin II Generating Enzymesmentioning

confidence: 99%

“…This enzyme cleaves the His 9 -Leu 10 bond in angiotensin I and as a result generates the fragment angiotensin [1][2][3][4][5][6][7][8][9] , which although capable of inhibiting ACE, has no known intrinsic contractile activity. 26 The human heart has been shown to possess carboxypeptidase A activity, generation of angiotensin [1][2][3][4][5][6][7][8][9] by this enzyme is sufficient to block cardiac ACE. 27 It is undetermined if human blood vessels also exhibit cardoxypeptidase A activity, or if endogenous local ACE activity in the vessel wall is regulated by the synthesis of angiotensin [1][2][3][4][5][6][7][8][9] .…”

Section: Alternative Angiotensin II Generating Enzymesmentioning

confidence: 99%

“…26 The human heart has been shown to possess carboxypeptidase A activity, generation of angiotensin [1][2][3][4][5][6][7][8][9] by this enzyme is sufficient to block cardiac ACE. 27 It is undetermined if human blood vessels also exhibit cardoxypeptidase A activity, or if endogenous local ACE activity in the vessel wall is regulated by the synthesis of angiotensin [1][2][3][4][5][6][7][8][9] . Other angiotensin fragments may be generated by the action of neutral endopeptidase 24.11 and propyl-endopeptidase 24.26.…”

Section: Alternative Angiotensin II Generating Enzymesmentioning

confidence: 99%

“…[1][2][3][4] The mainstay of this therapeutic strategy is to block the formation of effector peptide, angiotensin II, by inhibition of angiotensin-converting enzyme (ACE). However, angiotensin II levels have been shown to return to pre-treatment levels following chronic ACE inhibitor therapy, and reductions in blood pressure greater than those observed with ACE inhibitors alone can be obtained by co-administration of angiotensin receptor antagonists with an ACE inhibitor.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Chymase-dependent angiotensin II formation in human blood vessels

Chester

Jaa

2000

J Hum Hypertens

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The Kallikrein‐Kinin System as a Regulator of Cardiovascular and Renal Function

Rhaleb

Yang

Carretero

2011

Comprehensive Physiology

109

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Autocrine, paracrine, endocrine, and neuroendocrine hormonal systems help regulate cardiovascular and renal function. Any change in the balance among these systems may result in hypertension and target organ damage, whether the cause is genetic, environmental or a combination of the two. Endocrine and neuroendocrine vasopressor hormones such as the renin-angiotensin system (RAS), aldosterone, and catecholamines are important for regulation of blood pressure and pathogenesis of hypertension and target organ damage. While the role of vasodepressor autacoids such as kinins is not as well defined, there is increasing evidence that they are not only critical to blood pressure and renal function but may also oppose remodeling of the cardiovascular system. Here we will primarily be concerned with kinins, which are oligopeptides containing the aminoacid sequence of bradykinin. They are generated from precursors known as kininogens by enzymes such as tissue (glandular) and plasma kallikrein. Some of the effects of kinins are mediated via autacoids such as eicosanoids, nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), and/or tissue plasminogen activator (†PA). Kinins help protect against cardiac ischemia and play an important part in preconditioning as well as the cardiovascular and renal protective effects of angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor blockers (ARB). But the role of kinins in the pathogenesis of hypertension remains controversial. A study of Utah families revealed that a dominant kallikrein gene expressed as high urinary kallikrein excretion was associated with a decreased risk of essential hypertension. Moreover, researchers have identified a restriction fragment length polymorphism (RFLP) that distinguishes the kallikrein gene family found in one strain of spontaneously hypertensive rats (SHR) from a homologous gene in normotensive Brown Norway rats, and in recombinant inbred substrains derived from these SHR and Brown Norway rats this RFLP cosegregated with an increase in blood pressure. However, humans, rats and mice with a deficiency in one or more components of the kallikrein-kinin-system (KKS) or chronic KKS blockade do not have hypertension. In the kidney, kinins are essential for proper regulation of papillary blood flow and water and sodium excretion. B2-KO mice appear to be more sensitive to the hypertensinogenic effect of salt. Kinins are involved in the acute antihypertensive effects of ACE inhibitors but not their chronic effects (save for mineralocorticoidsalt-induced hypertension). Kinins appear to play a role in the pathogenesis of inflammatory diseases such as arthritis and skin inflammation; they act on innate immunity as mediators of inflammation by promoting maturation of dendritic cells, which activate the body’s adaptive immune system and thereby stimulate mechanisms that promote inflammation. On the other hand, kinins acting via NO contribute to the vascular protective effect of ACE inhibitors during neointima formation. In myocardial i...

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Role of angiotensin II in injury-induced neointima formation in rats.

Cited by 99 publications

References 0 publications

Aspects of gene polymorphisms in cardiovascular disease: the renin‐angiotensin system

Aspects of gene polymorphisms in cardiovascular disease: the renin‐angiotensin system

Chymase-dependent angiotensin II formation in human blood vessels

The Kallikrein‐Kinin System as a Regulator of Cardiovascular and Renal Function

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