B2-kinin receptor plays a key role in B1-, angiotensin converting enzyme inhibitor-, and vascular endothelial growth factor-stimulated in vitro angiogenesis in the hypoxic mouse heart

Miguel, Lourdes Sánchez de; Neysari, Shiva; Jakob, Sonja; Petrimpol, Marco; Butz, Nicole; Banfi, Andrea; Zaugg, Christian E.; Humar, Rok; Battegay, Edouard

doi:10.1093/cvr/cvn170

Cited by 26 publications

(22 citation statements)

References 40 publications

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“…The extent and morphology of endothelial sprouts is comparable to those induced by VEGF. 50 treatment normalized vascular structure and reversed microvascular rarefaction in hypertensives. Capillary density in non-diabetic hypertensive patients increased compared with that in untreated patients.…”

Section: Pro-angiogenesis Might Reduce the Development Of Hypertensionmentioning

confidence: 91%

“…ACE inhibition causes bradykinin (BK) to accumulate that increases pro-angiogenic inducers such as nitric oxide (NO) and vascular endothelial growth factor (VEGF) mainly by the BK type 2 receptor and its interaction with the VEGF receptor 2. 50,88,92 Also angiotensin II can be pro-angiogenic through the angiotensin type 2 receptor, which increases BK levels. 103 Angiotensin type 2 receptor may be specifically activated when angiotensin II type 1 receptor blockers (ARBs) block binding to the angiotensin type 1 receptor.…”

Section: Pro-angiogenesis Might Reduce the Development Of Hypertensionmentioning

confidence: 99%

“…Knockout of the BK B2 receptor blunted ACE-I-induced vascularization of mouse ischaemic legs 88 and vascularization in an in vitro model of the hypoxic heart. 50 Figure 2b depicts angiogenic activity in vitro of BK, BK1 agonist and the ACE-I enalalpril from this study. 50 Further studies in rat models suggest that ACE-I-induced neovascularization depends on both BK B1 and B2 receptors.…”

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confidence: 93%

“…42 In line, exogenous supplementation of NO by NO-donors restores ischaemia-induced angiogenesis in in vivo and in vitro models. 44,50 Thus, endothelial dysfunction in hypertension may contribute to decreased angiogenic capacity of capillaries because of an impairment of NO bioavailability.…”

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confidence: 99%

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Angiogenesis and hypertension: an update

2009

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The purpose of this review is to provide a basic understanding of the important relationship between microvascular remodelling, angiogenesis and hypertension, that is, provide an overview of recent experimental and clinical evidence from anti-hypertensive and pro-and anti-angiogenic therapy with respect to hypertension and microvascular structure. Microvascular rarefaction, that is, a loss of terminal arterioles and capillaries, is found in most forms of human and experimental arterial hypertension. This further increases peripheral resistance, and aggravates hypertension and hypertension-induced target organ damage. In some cases with a genetic predisposition, hypertension is preceded by a loss of microvessels. Therefore, new therapies aimed at reversing microvascular rarefaction potentially represent candidate treatments of hypertension. The microvasculature is formed by the continuous balance between de novo angiogenesis and microvascular regression. Imbalanced angiogenesis, in addition to functional shut-off of blood flow, contributes to microvascular rarefaction. Numerous clinical trials assessing anti-angiogenic agents in cancer patients show that this therapy leads to microvascular rarefaction and causes or aggravates hypertension. The development of specific pro-angiogenic treatment to correct hypertension or ischaemic disorders, however, it is still in its infancy. On the other hand, long-term treatment by classic anti-hypertensive therapies that present vasodilator activity can correct for hypertension-associated rarefaction in man.

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Section: Pro-angiogenesis Might Reduce the Development Of Hypertensionmentioning

confidence: 91%

Section: Pro-angiogenesis Might Reduce the Development Of Hypertensionmentioning

confidence: 99%

mentioning

confidence: 93%

mentioning

confidence: 99%

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Angiogenesis and hypertension: an update

2009

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“…Участие рецепторов кининов в процессе ангиогенеза было показано in vitro на сердцах нормальных мышей и мышей, лишенных гена Б 2 Р. В нормальных условиях эналаприл индуцировал образование сосудов, активируя оба типа кининовых рецепторов, а в условиях гипоксии усиление ангиогенеза происходило за счет индукции Б 2 Р [98].…”

Section: активация рецепторов кининов ингибиторами апфunclassified

Ace inhibitors - activators of kinin receptors

Kugaevskaya

Elisseeva

2011

BIOMED KHIM

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Angiotensin converting enzyme (ACE) inhibitors are widely used for treatment of cardiovascular diseases. The effects of ACE inhibitors on the human bradykinin receptors were investigated. The mode of action of ACE inhibitors is considered. There is evidence that ACE inhibitors exert effects on the vascular system that cannot be attributed simply to the inhibition of ACE activity and accumulation of locally produced bradykinin. ACE inhibitors augment bradykinin effects on receptors indirectly by inducing cross-talk between ACE and the B2 receptor when enzyme and receptor molecules are sterically close, possibly forming a heterodimer. ACE inhibitors activate B1 receptors directly and independently of ACE via the zink-binding consensus sequence HEXXH, which is present in B1, but not in B2 receptor. Particular structure of B2 and B1 are represented, as well as receptor amino acids coupled with the G-proteins. Activation of kinin receptors by ACE inhibitors leads to clinically beneficial effects of ACE inhibitors.

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Cardiovascular medications in angiogenesis—How to avoid the sting in the tail

Wang

Man

et al. 2012

Intl Journal of Cancer

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Cancer and cardiovascular disease are the leading causes of death worldwide. Cardiovascular medications have recently been found to have favorable effects also for the treatment of noncardiovascular diseases, including cancer. In this review, we use a reverse bedside‐to‐bench approach to investigate the effects of common cardiovascular medications on tumor angiogenesis and vascular angiogenesis. Aspirin seems to reduce the risk of developing cancer, particularly colon cancer. However, whether the protective influence of aspirin is due to antiangiogenesis effect is still unclear. β‐Blockers, which are normally used to reduce heart rate and prolong diastole, trigger an increase in stretch‐associated release of proangiogenic growth factors thereby inducing angiogenesis. However, according to other studies β‐blockers are able to inhibit angiogenesis via multiplicate mechanisms. Similarly, angiotensin converting enzyme inhibitor and angiotensin II type 1 receptor blocker have controversial effects for the regulation of cell proliferation and angiogenesis. Statins can augment collateral vascular growth in ischemic tissues and restrict the development of cancer. So this topical anti‐inflammatory drug seems to be of high value for further therapy. Finally, suggestions on how this pilot experience may guide the conduct of future preclinical investigations, and clinical trials are discussed.

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B2-kinin receptor plays a key role in B1-, angiotensin converting enzyme inhibitor-, and vascular endothelial growth factor-stimulated in vitro angiogenesis in the hypoxic mouse heart

Cited by 26 publications

References 40 publications

Angiogenesis and hypertension: an update

Angiogenesis and hypertension: an update

Ace inhibitors - activators of kinin receptors

Cardiovascular medications in angiogenesis—How to avoid the sting in the tail

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