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Journal ArticleDOI

Synergistic effect of angiotensin-(1-7) on bradykinin arteriolar dilation in vivo.

TLDR
The potentiation of BK-induced vasodilation by Ang-(1-7) is a receptor-mediated phenomenon dependent on cyclooxygenase-related products and NO release.
About
This article is published in Peptides.The article was published on 1999-10-01. It has received 113 citations till now. The article focuses on the topics: Angiotensin II & Vasodilation.

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Citations
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Journal ArticleDOI

Angiotensin-converting enzyme 2, angiotensin-(1-7) and Mas: new players of the renin-angiotensin system

TL;DR: Recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism are discussed.
Journal ArticleDOI

Angiotensin-(1-7): an update.

TL;DR: The evidence that Ang-(1-7) takes an important part of the mechanisms aimed to counteract the vasoconstrictor and proliferative effects of Ang II is summarized.
Journal ArticleDOI

Potential influence of COVID-19/ACE2 on the female reproductive system.

TL;DR: The available evidence suggests that ACE2 is widely expressed in the ovary, uterus, vagina and placenta, and it is believed that apart from droplets and contact transmission, the possibility of mother-to-child and sexual transmission also exists.
Journal ArticleDOI

Identification and characterization of prolylcarboxypeptidase as an endothelial cell prekallikrein activator.

TL;DR: PKA did not correct the coagulant defect in factor XI deficient plasma, was purified from HUVEC cultured in factor XII-deficient serum, was not detected by antibody to factor XII, did not activate FXI, and was not inhibited by a neutralizing antibody to FXII.
Journal ArticleDOI

Angiotensin-(1-7): Cardioprotective Effect in Myocardial Ischemia/Reperfusion

TL;DR: The results suggest that the antiarrhythmogenic effect of low concentrations of Ang-(1-7) is mediated by a specific receptor and that release of endogenous prostaglandins contributes to the alleviation of reversible and/or irreversible ischemia-reperfusion injury.
References
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Journal ArticleDOI

Angiotensin-(1-7) Dilates Canine Coronary Arteries Through Kinins and Nitric Oxide

TL;DR: The results suggest that increases in circulating levels of Ang-(1-7) accompanying long-term administration of converting enzyme inhibitors or Ang II receptor blockers may contribute to the cardioprotective actions of these drugs.
Journal ArticleDOI

Metabolism of Angiotensin-(1–7) by Angiotensin-Converting Enzyme

TL;DR: It is suggested that increased levels of Ang-(1-7) following ACE inhibition may be due, in part, to decreased metabolism of the peptide.
Journal ArticleDOI

N-Domain–Specific Substrate and C-Domain Inhibitors of Angiotensin-Converting Enzyme: Angiotensin-(1–7) and Keto-ACE

TL;DR: Keto-ACE inhibited bradykinin and Ang I hydrolysis by C-ACE in approximately a 38- to 47-times lower concentration than by N-ACE; this potentiation of kinins at the receptor level can explain some of the well-documented kininlike actions of Ang-(1-7).
Journal ArticleDOI

Angiotensin-(1-7) augments bradykinin-induced vasodilation by competing with ACE and releasing nitric oxide

TL;DR: This study evaluated whether the potentiation of the BK-induced vasodilation by Ang-(1-7) may be attributable to inhibition of BK metabolism, release of nitric oxide, or both, and how this affects canine coronary artery rings.
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