Stimulation of the ACE2/Ang-(1–7)/Mas axis in hypertensive pregnant rats attenuates cardiovascular dysfunction in adult male offspring

Bessa, Amanda S.M.; Jesus, Érika Fernandes de; Nunes, Allancer D C; Pontes, Carolina Nobre Ribeiro; Lacerda, Ismaley Santos; Costa, Jaqueline M; Souza, Elisângela J; Lino-Júnior, Ruy S.; Biancardi, Manoel F.; Santos, Fernanda C. A.; Pedrino, Gustavo Rodrigues; Colugnati, Diego Basile; Mazaro-Costa, Renata; Mendes, Elizabeth Pereira; Castro, Carlos H.

doi:10.1038/s41440-019-0321-8

Cited by 25 publications

(29 citation statements)

References 62 publications

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“…Reprogramming strategies targeting the RAAS to prevent the developmental programming of hypertension and kidney disease that were employed in various animal models are listed in Table 2 [52,63,118,119,[147][148][149][150][151][152][153][154]. Currently, several therapeutic interventions have been reported, such as renin inhibitor [52,118,119], ACEI [63,[147][148][149][150], ARB [118,151,152], AT1R antisense [153], and ACE2 activator [154].…”

Section: Targeting On the Raas As Reprogramming Strategiesmentioning

confidence: 99%

Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins

Hsu

Tain

2021

IJMS

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The renin-angiotensin-aldosterone system (RAAS) is implicated in hypertension and kidney disease. The developing kidney can be programmed by various early-life insults by so-called renal programming, resulting in hypertension and kidney disease in adulthood. This theory is known as developmental origins of health and disease (DOHaD). Conversely, early RAAS-based interventions could reverse program processes to prevent a disease from occurring by so-called reprogramming. In the current review, we mainly summarize (1) the current knowledge on the RAAS implicated in renal programming; (2) current evidence supporting the connections between the aberrant RAAS and other mechanisms behind renal programming, such as oxidative stress, nitric oxide deficiency, epigenetic regulation, and gut microbiota dysbiosis; and (3) an overview of how RAAS-based reprogramming interventions may prevent hypertension and kidney disease of developmental origins. To accelerate the transition of RAAS-based interventions for prevention of hypertension and kidney disease, an extended comprehension of the RAAS implicated in renal programming is needed, as well as a greater focus on further clinical translation.

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Section: Targeting On the Raas As Reprogramming Strategiesmentioning

confidence: 99%

Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins

Hsu

Tain

2021

IJMS

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“…ACE2 is a human ACE-related carboxypeptidase which catalyzes the degradation of Ang II into a heptapeptide, Ang-(1-7) [12]. Numerous studies have reported that ACE2 could act as a suppressor in the progression of blood pressure [22,23].…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, our However, we did not identify the antihypertensive components in the aqueous extract of male flower. Recently, many studies demonstrated that four categories extracted from the leaf and bark of EU including lignans, iridoids, flavonoids, and terpenoids have antihypertensive action [7,27,28], and Bessa et al have separated iridoids and flavonoids from the male flowers of EU [12]; therefore, it is likely that iridoids and flavonoids may account for the antihypertensive effect of the male flowers of EU. Of course, further study will be needed to determine the antihypertensive components of the male flowers of EU.…”

Section: Discussionmentioning

confidence: 99%

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Antihypertensive Activity of Eucommia Ulmoides Oliv: Male Flower Extract in Spontaneously Hypertensive Rats

Ding

Liang

Xiao

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Eucommia ulmoides Oliv. is a traditional medical plant in Asia; however, it is still unknown whether Eucommia male flowers have an antihypertensive activity. In this study, we found that the aqueous extract of Eucommia ulmoides Oliv. male flowers can lower the blood pressure of SHR in a dose-dependent manner. Mechanistic studies suggested that the aqueous extract of male flowers can promote the mRNA and protein expressions of ACE2 in the kidney of SHR. ELISA assay showed that the plasma levels of ANG II was decreased, while ANG-(1–7) was increased in SHR treated with the aqueous extract of male flowers. ACE2 inhibitor DX600 can reverse the aqueous extract of Eucommia ulmoides Oliv. male flower-induced downregulation of Ang II and upregulation of Ang-(1–7), as well as the reduction of blood pressure in SHR. Moreover, Ang-(1–7)-Mas receptor antagonist A-779 abolished the antihypertensive effects of the aqueous extract of Eucommia ulmoides Oliv. male flower in SHR. The aqueous extract of Eucommia ulmoides Oliv. male flowers exhibited an antihypertensive action through the activation of ACE2-Ang-(1–7)-Mas signaling pathways in spontaneously hypertensive rats.

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“…Indeed, ACE2 activates the circulating endothelial progenitor cells in the blood that decreases the inflammatory cells and increases the cardiac progenitor cells in the region of peri-infarct cardiac muscles [119]. It also enhances the function of the heart and increases the level of angiotensin 1-7 in both humans and rats [120,121].…”

Section: Angiotensin (Ang)mentioning

confidence: 99%

The Rationale of Neprilysin Inhibition in Prevention of Myocardial Ischemia-Reperfusion Injury during ST-Elevation Myocardial Infarction

Bellis¹,

Mauro

Barbato³

et al. 2020

Cells

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During the last three decades, timely myocardial reperfusion using either thrombolytic therapy or primary percutaneous intervention (pPCI) has allowed amazing improvements in outcomes with a more than halving in 1-year ST-elevation myocardial infarction (STEMI) mortality. However, mortality and left ventricle (LV) remodeling remain substantial in these patients. As such, novel therapeutic interventions are required to reduce myocardial infarction size, preserve LV systolic function, and improve survival in reperfused-STEMI patients. Myocardial ischemia-reperfusion injury (MIRI) prevention represents the main goal to reach in order to reduce STEMI mortality. There is currently no effective therapy for MIRI prevention in STEMI patients. A significant reason for the weak and inconsistent results obtained in this field may be the presence of multiple, partially redundant, mechanisms of cell death during ischemia-reperfusion, whose relative importance may depend on the conditions. Therefore, it is always more recognized that it is important to consider a “multi-targeted cardioprotective therapy”, defined as an additive or synergistic cardioprotective agents or interventions directed to distinct targets with different timing of application (before, during, or after pPCI). Given that some neprilysin (NEP) substrates (natriuretic peptides, angiotensin II, bradykinin, apelins, substance P, and adrenomedullin) exert a cardioprotective effect against ischemia-reperfusion injury, it is conceivable that antagonism of proteolytic activity by this enzyme may be considered in a multi-targeted strategy for MIRI prevention. In this review, by starting from main pathophysiological mechanisms promoting MIRI, we discuss cardioprotective effects of NEP substrates and the potential benefit of NEP pharmacological inhibition in MIRI prevention.

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Stimulation of the ACE2/Ang-(1–7)/Mas axis in hypertensive pregnant rats attenuates cardiovascular dysfunction in adult male offspring

Cited by 25 publications

References 62 publications

Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins

Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins

Antihypertensive Activity of Eucommia Ulmoides Oliv: Male Flower Extract in Spontaneously Hypertensive Rats

The Rationale of Neprilysin Inhibition in Prevention of Myocardial Ischemia-Reperfusion Injury during ST-Elevation Myocardial Infarction

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