Potentiation of the hypotensive effect of bradykinin by angiotensin-(1–7)-related peptides

Paula, Renata Dutra de; Lima, Celso V.; Britto, Raquel Rodrigues; Campagnole‐Santos, Maria José; Khosla, M. C.; Santos, Robson Augusto Souza

doi:10.1016/s0196-9781(99)00031-5

Cited by 46 publications

(47 citation statements)

References 31 publications

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“…One may argue that A-779 could interfere with the binding of Ang-(1-7) to ACE. However, we have recently shown that A-779 does not inhibit ACE and does not prevent Ang-(1-7) from inhibiting this enzyme (15).…”

Section: Discussionmentioning

confidence: 88%

“…The mechanism of the interaction between Ang-(1-7) and BK is very complex (12,15). Deddish and colleagues (12) have provided evidence for an interaction of Ang-(1-7) with ACE that, independently of the enzymatic inhibition, would facilitate a crosstalk between ACE and the BK B 2 receptor leading to BK potentiation.…”

Section: Discussionmentioning

confidence: 99%

“…Several reports have described a BKpotentiating activity for Ang-(1-7) (10)(11)(12)(13)(14)(15) that could contribute to the cardiovascular effects of ACE inhibition and AT 1 receptor blockers (16). The Ang-(1-7)-BK interaction has been studied in vivo (10,11), in cell culture (12) or in isolated vessels (14).…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart

Almeida

Frábregas

Madureira

et al. 2000

Braz J Med Biol Res

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It has been shown that angiotensin-(1-7) (Ang-(1-7)) infusion potentiates the bradykinin (BK)-induced hypotensive response in conscious rats. The present study was conducted to identify Ang-(1-7)-BK interactions in the isolated rat heart perfused according to the Langendorff technique. Hearts were excised and perfused through the aortic stump under a constant flow with Krebs-Ringer solution and the changes in perfusion pressure and heart contractile force were recorded. Bolus injections of BK (2.5, 5, 10 and 20 ng) produced a dosedependent hypotensive effect. Ang-(1-7) added to the perfusion solution (2 ng/ml) did not change the perfusion pressure or the contractile force but doubled the hypotensive effect of the lower doses of BK. The BK-potentiating Ang-(1-7) activity was blocked by pretreatment with indomethacin (5 mg/kg, ip) or L-NAME (30 mg/kg, ip). The Ang-(1-7) antagonist A-779 (50 ng/ml in Krebs-Ringer) completely blocked the effect of Ang-(1-7) on BK-induced vasodilation. These data suggest that the potentiation of the BK-induced vasodilation by Ang-(1-7) can be attributed to the release of nitric oxide and vasodilator prostaglandins through an Ang-(1-7) receptor-mediated mechanism.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

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Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart

Almeida

Frábregas

Madureira

et al. 2000

Braz J Med Biol Res

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“…Indeed, a bradykinin-potentiating effect of Ang-(1-7) was reported in certain rodent models. 72,73 This peptide evokes endotheliumdependent relaxation in several vascular beds. [74][75][76] In addition, Ang-(1-7) improves endothelial function in vivo, 77 induces coronary vasodilation by NO release 72,78 and activates eNOS in Chinese hamster ovary cells.…”

Section: Redox-sensitive Signaling By the Ace2-ang-(1-7)-mas Axismentioning

confidence: 99%

ACE2–angiotensin-(1–7)–Mas axis and oxidative stress in cardiovascular disease

2010

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The renin-angiotensin-aldosterone system (RAAS) is a pivotal regulator of physiological homeostasis and diseases of the cardiovascular system. Recently, new factors have been discovered, such as angiotensin-converting enzyme 2 (ACE2), angiotensin-(1-7) and Mas. This newly defined ACE2-angiotensin-(1-7)-Mas axis was shown to have a critical role in the vasculature and in the heart, exerting mainly protective effects. One important mechanism of the classic and the new RAAS regulate vascular function is through the regulation of redox signaling. Angiotensin II is a classic prooxidant peptide that increases superoxide production through the activation of NAD(P)H oxidases. This review summarizes the current knowledge about the ACE2-angiotensin-(1-7)-Mas axis and redox signaling in the context of cardiovascular regulation and disease. By interacting with its receptor Mas, angiotensin-(1-7) induces the release of nitric oxide from endothelial cells and thereby counteracts the effects of angiotensin II. ACE2 converts angiotensin II to angiotensin-(1-7) and, thus, is a pivotal regulator of the local effects of the RAAS on the vessel wall. Taken together, the ACE2-angiotensin-(1-7)-Mas axis emerges as a novel therapeutic target in the context of cardiovascular and metabolic diseases.

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“…This is based on pharmacological and physiological evidence suggesting that Ang II (1-7) is capable of mediating differential and opposing actions to Ang II, such as eliciting vasorelaxation in porcine, 27 canine 28 and feline 29 vessels, possibly via nitric oxide (NO) and/or prostaglandins. [30][31][32][33][34] Ang II (1-7) has also been shown to potentiate bradykinin-induced vasodilatation in rats, 35,36 as well as in canine 28 and porcine 37 coronary arteries. These actions are possibly mediated by a number of mechanisms, involving B 2 receptors, the novel Ang II (1-7) binding site, 35 regulation of ACE activity 38,39 and/or NO and prostaglandin production.…”

Section: Ang II (1-7)mentioning

confidence: 99%

Bioactive angiotensin peptides: focus on angiotensin IV

Mustafa

Lee

Chai

et al. 2001

J Renin Angiotensin Aldosterone Syst

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The ability of Ang II (1-7) to mediate and oppose Ang II actions has been recently reviewed. [46][47][48][49] Angiotensin 1-9 and ACE2 Recently, a novel ACE-related enzyme (ACE2) has also been discovered, that catalyses carboxypeptidase cleavage of Ang I to generate Ang (1-9), which subsequently serves as a substrate for the generation of Ang II (1-7). ACE2 is found on the endothelium of coronary and intrarenal vessels and renal tubular epithelium, raising the possibility that the formation of Ang II (1-7) may be important in regulating cardiac and renal function. 50,51 Angiotensin IV Angiotensin IV (Ang IV), originally considered to be biologically inactive, has attracted recent attention because of its ability to elicit many biological actions. Ang IV binds with high affinity to a pharmacologically-distinct binding site, designated the AT 4 receptor. 52,53 This binding site shows highest selectivity for Ang IV, with approximately 10-fold lower affinity for Ang III. Affinities for Ang II and [Sar 1 -Ile 8 ] Ang II are markedly lower, while losartan, PD 123177 and CGP 42112A show no activity. [54][55][56][57][58] The AT 4 -receptor has a distinct distribution pattern in the brain, being found in regions associated with cognitive, sensory and motor function in the guinea pig, 55 sheep 59 and monkey. 60 We recently localised the AT 4 receptor in human forebrain, midbrain, and pons, using an iodinated Ang IV analogue, Norleucine 1 -Ang IV (Nle 1 -Ang IV), a more stable analogue of Ang IV with higher affinity for the AT 4receptor. The distribution of the AT 4 -receptor in the human brain was similar to that reported in other species. 61 The AT 4 -receptor is also found in abundance in peripheral tissues, such as the heart, adrenal cortex, kidney, vascular smooth muscle cells and numerous other tissues. 62 REVIEW Figure 1 Schematic representation of the enzymatic events leading to the formation of angiotensin peptides.

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Potentiation of the hypotensive effect of bradykinin by angiotensin-(1–7)-related peptides

Cited by 46 publications

References 31 publications

Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart

Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart

ACE2–angiotensin-(1–7)–Mas axis and oxidative stress in cardiovascular disease

Bioactive angiotensin peptides: focus on angiotensin IV

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