Angiotensin(1–7) potentiates bradykinin-induced vasodilatation in man

Ueda, Shinichiro; Masumori-Maemoto, Satoko; Wada, Atsushi; Ishii, Masao; Kb, Brosnihan; Umemura, Satoshi

doi:10.1097/00004872-200111000-00010

Cited by 69 publications

(52 citation statements)

References 32 publications

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“…As mentioned above for vasodilation, the BK-potentiating activity of Ang- (1-7) is controversial in humans. Ueda et al (49) reported BK potentiation while Wilsdorf et al (51) were unable to show an effect at supraphysiological doses. Several mechanisms have been proposed to explain the BK-potentiating activity of Ang-(1-7) including ACE inhibition (50), non-hydrolytic interaction with ACE favoring a crosstalk between ACE and the BK-B 2 receptor (52), and AT 1-7 receptor-mediated changes in the coupling and/or signaling of BK (7,16,38,48).…”

Section: Ang-(1-7) Formation and Actions In Blood Vesselsmentioning

confidence: 97%

“…Ang- (1-7) potentiates the vasodilator and hypotensive effects of BK in normotensive (48) and hypertensive (38) rats, in the human forearm (49), and in porcine (50), dog (15) and rat coronary vessels (30). As mentioned above for vasodilation, the BK-potentiating activity of Ang- (1-7) is controversial in humans.…”

Section: Ang-(1-7) Formation and Actions In Blood Vesselsmentioning

confidence: 99%

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Cardiovascular actions of angiotensin-(1-7)

Ferreira

Santos

2005

Braz J Med Biol Res

148

114

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Section: Ang-(1-7) Formation and Actions In Blood Vesselsmentioning

confidence: 97%

Section: Ang-(1-7) Formation and Actions In Blood Vesselsmentioning

confidence: 99%

Cardiovascular actions of angiotensin-(1-7)

Ferreira

Santos

2005

Braz J Med Biol Res

148

114

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“…18 In experiments with canine coronary arteries and mesenteric arteries of rats, it was observed that Ang(1-7) potentiates the vasodilatory effects of BK, and this effect is also observed in human vessels. [19][20][21][22] Casarini et al 11 described 190 kDa and 65 kDa ACE isoforms in human urine from healthy subjects. They also analyzed the urine from mildly hypertensive untreated patients and separated 90 kDa and 65 kDa isoforms of the N-domain ACE.…”

Section: Introductionmentioning

confidence: 99%

Renin-angiotensin system may trigger kidney damage in NOD mice

Colucci

Arita

Cunha

et al. 2010

J Renin Angiotensin Aldosterone Syst

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Diabetic nephropathy is a complication of diabetes and one of the main causes of end-stage renal disease. A possible causal link between renin-angiotensin aldosterone system (RAAS) and diabetes is widely recognized but the mechanisms by which the RAAS may lead to this complication remains unclear. The aim of this study was to evaluate angiotensin-I converting enzyme (ACE) activity and expression in numerous tissues, especially kidney, of non-obese diabetic mouse. Kidney, lung, pancreas, heart, liver and adrenal tissues from diabetic and control female NOD mice were homogenized for measurement of ACE activity, SDS-PAGE and Western blotting for ACE and ACE2, immunohistochemistry for ACE and angiotensins I, II and 1-7 and bradykinin quantification. ACE activity was higher in kidney, lung and adrenal tissue of diabetic mice compared with control mice. In pancreas, activity was decreased in the diabetic group. Western blotting analysis indicated that both groups presented ACE isoforms with molecular weights of 142 and 69 kDa and a decrease in ACE2 protein expression. Angiotensin concentrations were not altered within groups, although bradykinin levels were higher in diabetic mice. The immunohistochemical study in kidney showed an increase in tubular ACE expression. Our results show that the RAAS is affected by diabetes and the elevated ACE/ACE2 ratio may contribute to renal damage.

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“…The response was attenuated by pretreatment with indomethacin and exaggerated with ACE inhibition. The potentiation of bradykinin by Ang-(1-7) was also shown in isolated dog and pig coronary arteries [13,26], rat mesenteric microvessels [27], isolated rat heart [28], and human forearm brachial arteries [29]. The vasodilator action of Ang-(1-7) was independent of acetylcholine or sodium nitroprusside mediated-vasodilation [13,30], and neither Ang I nor Ang II potentiated the bradykinin response.…”

Section: Physiologic Actions Of Angiotensin-(1-7)mentioning

confidence: 97%

Contribution of angiotensin-(1-7) to cardiovascular physiology and pathology

Ferrario

2003

Current Science Inc

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Increased understanding of the contribution of angiotensin peptides to the physiologic control of arterial pressure and cardiovascular regulation has been made possible with the introduction of agents that either inhibit the activity of angiotensins forming enzymes or block the action of the peptides at their specific receptor subtypes. This review highlights some of the lessons that have been learned from the study of the actions of angiotensin-(1-7) and its inter-relationship with other vasodilator mechanisms that modulate the control systems that determine blood pressure and tissue perfusion. The studies suggest that the renin-angiotensin system acts as a humoral mechanism for blood pressure control through the generation of several distinct forms of angiotensin peptides that may bind to diverse receptor subtypes.

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Angiotensin(1–7) potentiates bradykinin-induced vasodilatation in man

Abstract: Ang(1-7) potentiates the vasodilating effect of bradykinin, possibly through a mechanism(s) involving nitric oxide release, in human forearm resistance vessels.

Cited by 69 publications

References 32 publications

Cardiovascular actions of angiotensin-(1-7)

Cardiovascular actions of angiotensin-(1-7)

Renin-angiotensin system may trigger kidney damage in NOD mice

Contribution of angiotensin-(1-7) to cardiovascular physiology and pathology

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