Angiotensin-(1–9) reverses experimental hypertension and cardiovascular damage by inhibition of the angiotensin converting enzyme/Ang II axis

Ocaranza, María Paz; Moya, Jackeline; Barrientos, Víctor; Alzamora, Rodrigo; Hevia, Daniel; Morales, Cristóbal; Pinto, Melissa; Escudero, Nicolás; Garcı́a, Lorena; Novoa, Ulises; Ayala, Pedro; Díaz‐Araya, Guillermo; Godoy, Iván; Chiong, Mario; Lavandero, Sergio; Jalil, Jorge; Michea, Luis

doi:10.1097/hjh.0000000000000094

Cited by 88 publications

(95 citation statements)

References 48 publications

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“…Recientemente, Flores-Muñoz et al, mostró en su modelo experimental de ratas "strole-prone" espontáneamente hipertensas (SPSHR) que Ang-(1-9) administrada en dosis de 100 ng·Kg-1·min-1 no modificó la PAS 22 . Estos resultados difieren del efecto antihipertensivo observado para Ang-(1-9) probablemente, debido a la menor dosis de Ang-(1-9) usada en ratas SPSHR comparada con nuestros estudios de regresión de la HTA 23 . Por otra parte, los resultados del presente estudio muestran que la administración crónica de Ang-(1-9), en un modelo experimental de ratas previamente hipertensas, logró revertir la hipertrofia cardíaca, destacando que este efecto tampoco fue mediado por Ang-(1-7).…”

Section: Discussionunclassified

El efecto anti-hipertensivo de Angiotensina-(1-9) es mediado por aumento temprano de la diuresis y natriuresis

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Section: Discussionunclassified

El efecto anti-hipertensivo de Angiotensina-(1-9) es mediado por aumento temprano de la diuresis y natriuresis

et al. 2015

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“…In turn, Ang 1-9 can be converted to Ang 1-7 by ACE [36]. Angiotensin 1-9 exerts beneficial effects on the heart, which consist in reduction of blood pressure, improvement of endothelial function and limitation of hypertrophy and fibrosis [38]. It has been suggested that these beneficial effects of Ang 1-9 can be achieved via angiotensin II type 2 receptor (AT2R), independently of its conversion to Ang 1-7 [38,39].…”

Section: Apelin/apj System Vs Renin-angiotensin System (Ras)mentioning

confidence: 99%

“…Angiotensin 1-9 exerts beneficial effects on the heart, which consist in reduction of blood pressure, improvement of endothelial function and limitation of hypertrophy and fibrosis [38]. It has been suggested that these beneficial effects of Ang 1-9 can be achieved via angiotensin II type 2 receptor (AT2R), independently of its conversion to Ang 1-7 [38,39]. In addition to the favorable activity on cardiac dysfunction, ACE2 was reported to play a role in the hydrolysis of a large number of peptides, including apelin-13 and apelin-36, which are thus degraded to ineffective forms [40].…”

Section: Apelin/apj System Vs Renin-angiotensin System (Ras)mentioning

confidence: 99%

Effects of apelin on the cardiovascular system

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Apelin is an endogenous peptide acting on the APJ receptor. It consists of several isoforms characterised by different numbers of aminoacids. The number of aminoacids in the active isoforms range from 36 to 12. Apelin-13 and, to a lesser extent, apelin-36 are considered the most active isoforms with the greatest activity on the cardiovascular homeostasis. The effects normally exerted by the basal level of endogenous apelin, can be enhanced not only by its up-regulation, but may also by its exogenous administration. The present review considers the effects of apelin on various aspects of the cardiovascular function, such as cardiac development, vasomotor tone, angiogenesis, myocardial inotropy in healthy and failing hearts as well as the prevention of ischemia-reperfusion injury, cardiac fibrosis and remodeling. Also the biphasic changes of apelin level during the evolution of heart failure are considered. Although the positive inotropic effect exerted by apelin in normal and failing hearts would suggest the use of this peptide in the treatment of heart failure, the limited duration and extent of its effect do not support this possibility, unless a long lasting (6 hours) infusion is performed to overcome the limit of its short life. However, although the data on the characteristics of the inotropic activity do not provide a strong support for the treatment of active heart failure, apelin may be used in the prevention of heart failure because of its activity in limiting the consequences of myocardial ischemia such as infarct size and cardiac remodeling. KeywordsApelin/APJ system, heart failure, ischemia-reperfusion injury, contractility, cardiac protection, Reninangiotensin system 2 The apelin/APJ system Apelin In 1998 Tatemoto et al. discovered the endogenous peptide capable of binding the G protein-coupled receptor (GPCR) APJ [1,2], which at that time was considered an orphan receptor becaue its ligand was unknown. The just discovered ligand was called, apelin e.g APj Endogenous LIgaNd. Apelin is expressed in hearts, lungs, kidneys, liver, adipose tissue, gastrointestinal tract, brain, adrenal glands, endothelium, and human plasma. The gene of apelin is located on chromosome X [3] and encodes a 77 aminoacid sequence called pre-pro-apelin [4]. Upon cleavage by a family of endopeptidases, pre-pro-apelin generates several C-terminal fragments of various size, which are classified on the basis of the number of aminoacids. The active isoforms range from 36 to 12 aminoacids. As fragments shorter than 12 aminoacids are biologically inactive, it appears evident that the Cterminal 12 aminoacids are essential for receptor binding, whereas the N-terminal sequence modulates the interaction with the receptor [5]. At present it is recognized that, although different isoforms display similar functions, active isoforms differ in tissue distribution, potency and receptor binding affinity [6]. Apelin-13 and, to a lesser extent, apelin-36 have been considered the most active isoforms with the greatest activity on the cardi...

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“…5 Ang (1-9) also reduces cardiovascular damage induced both by hypertension 5 and myocardial infarction. 6 These beneficial effects of Ang (1-9) are mediated directly through binding to the AT2 receptor.…”

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confidence: 99%

“…In this issue of Hypertension, the role of dipeptidyl peptidase III (DPP III) as a new antihypertensive candidate has been characterized in the mice. 1 Similar to DPP III, the carboxy peptidase ACE2 mediates degradation from Ang II to Ang (1-7) and also from Ang I to Ang (1)(2)(3)(4)(5)(6)(7)(8)(9). Both peptides contribute to the antihypertensive/ vasoprotective effects of the counterregulatory RAAS pathway ( Figure).…”

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confidence: 99%