Differences in angiotensin (1–7) between men and women

Sullivan, Jennifer C.; Rodriguez‐Miguelez, Paula; Zimmerman, Margaret A.; Harris, Ryan A.

doi:10.1152/ajpheart.00897.2014

Cited by 63 publications

(63 citation statements)

References 42 publications

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“…Importantly, previous studies have shown human plasma concentrations of ANG 1–7 to be in the range of 1–50 pmol/L, thus the concentrations of ANG 1–7 which caused measurable vasodilation were physiological. 15–18 Dilation to ANG 1–7 was also mediated by Mas receptor activation as pre-incubation with the Mas receptor antagonist A779 significantly reduced dilation in both vascular beds. Vasodilation to the direct smooth muscle activator papaverine (10 −4 mol/L) was unaffected by the presence of A779 (≥95% dilation in all groups, P>0.05 between groups; t-test; data not shown).…”

Section: Resultsmentioning

confidence: 98%

“…However, it could be surmised that long term exposure to H 2 O 2 in the vascular milieu exacerbates an already damaged vascular endothelium, thus it may be beneficial to restore NO-mediated vasodilation to promote vascular homeostasis. Previous studies have shown plasma ANG 1–7 levels positively correlate with brachial artery FMD in human subjects 7 , and recent findings by Zhang et al demonstrated that treating renal arterioles from diabetic patients with ANG 1–7 overnight restores acetylcholine mediated dilation. 8 In light of these findings, we also tested the hypothesis that exposing human atrial vessels from subjects with CAD to ANG 1–7 would restore the NO-component of the FMD response.…”

Section: Introductionmentioning

confidence: 93%

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Vascular Actions of Angiotensin 1–7 in the Human Microcirculation

Durand

Zinkevich

Riedel

et al. 2016

ATVB

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Objective This study examined vascular actions of angiotensin 1–7 (ANG 1–7) in human atrial and adipose arterioles. Approach and Results The endothelial-derived hyperpolarizing factor of flow mediated dilation (FMD) switches from anti-proliferative nitric oxide (NO) to pro-atherosclerotic hydrogen peroxide (H2O2) in arterioles from humans with coronary artery disease (CAD). Given the known vasoprotective properties of ANG 1–7, we tested the hypothesis that overnight ANG 1–7 treatment restores the NO-component of FMD in arterioles from CAD patients. Endothelial telomerase activity is essential for preserving the NO-component of vasodilation in the human microcirculation, thus we also tested whether telomerase activity was necessary for ANG 1–7 mediated vasoprotection by treating separate arterioles with ANG 1–7 ± the telomerase inhibitor BIBR-1532. ANG 1–7 dilated arterioles from patients without CAD, whereas dilation was significantly reduced in arterioles from CAD patients. In atrial arterioles from CAD patients incubated with ANG 1–7 overnight, the NO synthase inhibitor L-NAME abolished FMD while the H2O2 scavenger PEG catalase had no effect. Conversely, in vessels incubated with ANG 1–7 + BIBR-1532, L-NAME had no effect on FMD but PEG catalase abolished dilation. In cultured human coronary artery endothelial cells, ANG 1–7 significantly increased telomerase activity. These results indicate that ANG 1–7 dilates human microvessels, and dilation is abrogated in the presence of CAD. Further, ANG 1–7 treatment is sufficient to restore the NO component of FMD in arterioles from CAD patients in a telomerase-dependent fashion. Conclusion ANG 1–7 exerts vasoprotection in the human microvasculature via modulation of telomerase activity.

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Section: Resultsmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 93%

Vascular Actions of Angiotensin 1–7 in the Human Microcirculation

Durand

Zinkevich

Riedel

et al. 2016

ATVB

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“…The difference in plasma Ang-(1-7) levels between preterm adolescents and those born term was significantly greater in female participants compared with male participants. This runs counter to normal physiology as women typically exhibit decreased expression and function of the traditional RAS pathway and higher circulating Ang-(1-7) levels [43]. Estrogen can reduce ACE and AT 1 R expression, attenuate circulating Ang II, and increase circulating Ang-(1-7) [44,45].…”

Section: Discussionmentioning

confidence: 99%

Association between preterm birth and the renin−angiotensin system in adolescence

South

Nixon

Chappell

et al. 2018

Journal of Hypertension

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Objectives Preterm birth appears to contribute to early development of cardiovascular disease, but the mechanisms are unknown. Prematurity may result in programming events that alter the renin–angiotensin system. We hypothesized that prematurity is associated with lower angiotensin-(1-7) in adolescence and that sex and obesity modify this relationship. Methods We quantified angiotensin II and angiotensin-(1-7) in the plasma and urine of 175 adolescents born preterm and 51 term-born controls. We used generalized linear models to estimate the association between prematurity and the peptides, controlling for confounding factors and stratifying by sex and overweight/obesity. Results Prematurity was associated with lower plasma angiotensin II (β: −5.2 pmol/l, 95% CI: −10.3 to −0.04) and angiotensin-(1-7) (−5.2 pmol/l, 95% CI: −8.4 to −2.0) but overall higher angiotensin II:angiotensin-(1-7) (3.0 95% CI: 0.9–5.0). The preterm–term difference in plasma angiotensin-(1-7) was greater in women (−6.9 pmol/l, 95% CI: −10.7 to −3.1) and individuals with overweight/obesity (−8.0 pmol/l, 95% CI: −12.2 to −3.8). The preterm–term difference in angiotensin II:angiotensin-(1-7) was greater among those with overweight/obesity (4.4, 95% CI: 0.6–8.1). On multivariate analysis, prematurity was associated with lower urinary angiotensin II:angiotensin-(1-7; −0.13, 95% CI: −0.26 to −0.003), especially among the overweight/obesity group (−0.38, 95% CI: −0.72 to −0.04). Conclusion Circulating angiotensin-(1-7) was diminished whereas urinary angiotensin-(1-7) was increased relative to angiotensin II in adolescents born preterm, suggesting prematurity may increase the risk of cardiovascular disease by altering the renin–angiotensin system. Perinatal renin–angiotensin system programming was more pronounced in women and individuals with overweight/obesity, thus potentially augmenting their risk of developing early cardiovascular disease.

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“…In the cerebrovasculature, sex differences have been described with respect to vascular anatomy [21] and also pharmacology [60]. In the brain, arteriolar responses to vasoactive compounds, including angiotensin [19, 114] and endothelin-1 [29, 71], and nitric oxide synthase activity [88, 115], are sexually dimorphic.…”

Section: Vascular Reactivity (Vsm Dilation/constriction)mentioning

confidence: 99%

Sex-Specific Characteristics of the Microcirculation

Huxley

Kemp

2018

Advances in Experimental Medicine and Biology

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The requirements of metabolizing tissue are both continuous and variable; accordingly, the microvasculature serving that tissue must be similarly dynamic. Just as it is recognized that males and females of the same species have differing metabolic requirements, is it not likely that the microvasculature serving these tissues will differ by sex? This section focusing on the constituents of the microcirculation identifies what is known presently about the role sex plays in matching metabolic demand with microvascular function and areas requiring additional study. Many of the identified sex differences are subtle and easily ignored. In the aggregate, though, they can profoundly alter phenotype, especially under stressful conditions including pregnancy, exercise, and disease states ranging from diabetes to heart failure. Although the features presently identified to “have sex” range from differences in growth, morphology, protein expression, and intracellular signaling, males and females alike achieve homeostasis, likely by different means. Studies of microvascular sexual dimorphism are also identifying age as an independent but interacting factor requiring additional attention. Overall, attempting to ignore either sex and/or age is inappropriate and will prevent the design and implementation of appropriate interventions to present, ameliorate, or correct microvascular dysfunction.

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Differences in angiotensin (1–7) between men and women

Abstract: , women exhibit significantly higher plasma concentrations of ANG-(1-7) compared with men. In addition, this study describes a relationship between ANG-(1-7), vascular function, and diastolic blood pressure that appears to be sex dependent.

Cited by 63 publications

References 42 publications

Vascular Actions of Angiotensin 1–7 in the Human Microcirculation

Vascular Actions of Angiotensin 1–7 in the Human Microcirculation

Association between preterm birth and the renin−angiotensin system in adolescence

Sex-Specific Characteristics of the Microcirculation

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