Angiotensin-Converting Enzyme Inhibition Promotes Coronary Angiogenesis in the Failing Heart of Dahl Salt-Sensitive Hypertensive Rats

Yazawa, Hisatoyo; Miyachi, Masaaki; Furukawa, Mayuko; Takahashi, K.; Takatsu, Miwa; Tsuboi, Koji; Ohtake, Masafumi; Murase, Tatsuro; Hattori, Takuya; Kato, Yosuke; Murohara, Toyoaki; Nagata, Kazuya

doi:10.1016/j.cardfail.2011.09.002

Cited by 32 publications

(24 citation statements)

References 38 publications

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“…Indeed, ACEi treatment increased VEGF expression in several experimental studies [4,[6][7][8][9]. ACEi treatment also increases tissue bradykinin levels, stimulating both bradykinin B1 receptor (BR1) and bradykinin B2 receptor (BR2) on endothelial cells [20].…”

Section: Introductionmentioning

confidence: 98%

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Polymorphisms in VEGFA gene affect the antihypertensive responses to enalapril

Oliveira-Paula

Lacchini

Fontana

et al. 2015

Eur J Clin Pharmacol

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Section: Introductionmentioning

confidence: 98%

“…The main mechanisms of action for these drugs include reduction of angiotensin II formation and prevention of bradykinin degradation [3]. Moreover, it was shown that ACEi affect other relevant mediators, such as vascular endothelial growth factor (VEGF) [4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in VEGFA gene affect the antihypertensive responses to enalapril

Oliveira-Paula

Lacchini

Fontana

et al. 2015

Eur J Clin Pharmacol

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“…Traditional nitrovasodilators increase NO˙levels but are at risk of tolerance development (16,17,44); conversely statins and ACE inhibitors enhance NOS activity (1,50,61), but concomitant increases in ADMA may also limit their NO˙-elevating ability (57). Our findings now indicate that HNO donors represent a direct means of stimulating sGC, bypassing the potential roadblocks of nitrate tolerance, ADMA and possibly also sGC oxidation state, and may thus emerge as a legitimate antihypertrophic therapy over and above ACE inhibition.…”

Section: Discussionmentioning

confidence: 72%

HNO/cGMP-dependent antihypertrophic actions of isopropylamine-NONOate in neonatal rat cardiomyocytes: potential therapeutic advantages of HNO over NO˙

Irvine

Cao

Gossain

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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RH. HNO/cGMP-dependent antihypertrophic actions of isopropylamine-NONOate in neonatal rat cardiomyocytes: potential therapeutic advantages of HNO over NO˙. Am J Physiol Heart Circ Physiol 305: H365-H377, 2013. First published May 31, 2013 doi:10.1152/ajpheart.00495.2012 is a redox congener of NO˙. We now directly compare the antihypertrophic efficacy of HNO and NO˙donors in neonatal rat cardiomyocytes and compare their contributing mechanisms of actions in this setting. Isopropylamine-NONOate (IPA-NO) elicited concentrationdependent inhibition of endothelin-1 (ET1)-induced increases in cardiomyocyte size, with similar suppression of hypertrophic genes. Antihypertrophic IPA-NO actions were significantly attenuated by L-cysteine (HNO scavenger), Rp-8-pCTP-cGMPS (cGMP-dependent protein kinase inhibitor), and 1-H-(1,2,4)-oxodiazolo-quinxaline-1-one [ODQ; to target soluble guanylyl cyclase (sGC)] but were unaffected by carboxy-PTIO (NO˙scavenger) or CGRP8-37 (calcitonin gene-related peptide antagonist). Furthermore, IPA-NO significantly increased cardiomyocyte cGMP 3.5-fold (an L-cysteine-sensitive effect) and stimulated sGC activity threefold, without detectable NO˙release. IPA-NO also suppressed ET1-induced cardiomyocyte superoxide generation. The pure NO˙donor diethylamine-NONOate (DEA-NO) reproduced these IPA-NO actions but was sensitive to carboxy-PTIO rather than L-cysteine. Although IPA-NO stimulation of purified sGC was preserved under pyrogallol oxidant stress (in direct contrast to DEA-NO), cardiomyocyte sGC activity after either donor was attenuated by this stress. Excitingly IPA-NO also exhibited acute antihypertrophic actions in response to pressure overload in the intact heart. Together these data strongly suggest that IPA-NO protection against cardiomyocyte hypertrophy is independent of both NO˙and CGRP but rather utilizes novel HNO activation of cGMP signaling. Thus HNO acutely limits hypertrophy independently of NO˙, even under conditions of elevated superoxide. Development of longer-acting HNO donors may thus represent an attractive new strategy for the treatment of cardiac hypertrophy, as stand-alone and/or add-on therapy to standard care. cardiac hypertrophy; cGMP-dependent protein kinase; nitric oxide; nitroxyl; superoxide CURRENT PHARMACOTHERAPY FOR heart failure tends to delay, but not reverse, cardiac hypertrophy. We have previously shown that NOṡ ignaling is an important antihypertrophic mechanism in the heart (44). NO˙is, however, yet to be realized as a pharmacotherapy for cardiac hypertrophy, largely a consequence of limitations at the level of myocardial asymmetric dimethylarginine (ADMA) and NO synthase (NOS; Ref. 57). HNO, a redox sibling of NO˙, is a novel regulator of cardiovascular function (26,38). NO˙and HNO share several common cardiac and vascular protective actions, ranging from potent vasodilator (2, 10, 12-14, 22, 23, 59) and antiplatelet actions (3, 4) to, more recently, antihypertrophic actions in cardiomyocytes (31). These actions are all mediated predominantly via sGC (10...

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“…Las bradiquininas son péptidos fisiológicos producidos a partir de precursores llamados quininógenos por acción de enzimas llamadas calicreínas, presentes en diversos sitios, tales como el páncreas, próstata o piel. Existen dos receptores para bradiquininas, B1 y B2, siendo este último el más importante en condiciones fisiológicas (Yazawa et al, 2011), mientras que B1 se expresa en condiciones patoló-gicas tales como inflamación o daño tisular. En relación con la angiogénesis, la unión de bradiquininas a sus receptores, principalmente B2, estimula la acción de la enzima óxido nítrico sintetasa endotelial (eNOS), y con ello, la liberación de óxido nítrico (NO), molécula que favorece tanto la secreción de VEGF como la expresión del VEFGR-2 (Li et al, 2008).…”

Section: Discussionunclassified

Efecto del Aliskireno sobre la Angiogénesis en Modelo de Membrana Alantocoriónica (MAC) de Pollo

Rosas

et al. 2016

Int. J. Morphol.

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Morphol., 34(4):1191Morphol., 34(4): -1196Morphol., 34(4): , 2016. RESUMEN:La acción antiangiogénica de los inhibidores del receptor de angiotensina II (ARA II), ha sido documentada previamente, sin embargo, no ha sido descrita la relación entre angiogénesis e inhibidores directos de la renina (DRIs), los cuales participan regulando el sistema renina-angiotensina-aldosterona (SRAA). El objetivo fue demostrar el efecto antiangiogénico de aliskireno, un DRI, en membranas alantocoriónicas (MAC) de pollo, para lo cual fueron instilados aliskireno y enalapril sobre MAC en distintas concentraciones para realizar su comparación posterior. En secciones histológicas seriadas se registró el número de vasos sanguíneos presentes en 9000 µm 2 bajo microscopio de luz a máximo aumento, y se realizó análisis estadístico utilizando ANOVA y el test de Tukey para demostrar posibles diferencias. Los receptores tratados con aliskireno, en ambas concentraciones utilizadas, presentaron menor densidad vascular, en comparación con los controles, siendo ésta estadísticamente significativa a mayor concentración. Aliskireno en concentraciones altas tiene un efecto antiangiogénico en un modelo experimental de MAC. Este hallazgo plantea la necesidad de estudios posteriores, dada la proyección que podría tener el uso inhibidores directos de la renina. A partir de estos resultados, se podría pensar en la factibilidad del uso de aliskireno para la modulación de la angiogénesis en diversas enfermedades crónicas no transmisibles.

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Angiotensin-Converting Enzyme Inhibition Promotes Coronary Angiogenesis in the Failing Heart of Dahl Salt-Sensitive Hypertensive Rats

Cited by 32 publications

References 38 publications

Polymorphisms in VEGFA gene affect the antihypertensive responses to enalapril

Polymorphisms in VEGFA gene affect the antihypertensive responses to enalapril

HNO/cGMP-dependent antihypertrophic actions of isopropylamine-NONOate in neonatal rat cardiomyocytes: potential therapeutic advantages of HNO over NO˙

Efecto del Aliskireno sobre la Angiogénesis en Modelo de Membrana Alantocoriónica (MAC) de Pollo

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