ACE2, angiotensin-(1–7), and Mas: the other side of the coin

Bäder, Michael

doi:10.1007/s00424-012-1120-0

Cited by 141 publications

(121 citation statements)

References 101 publications

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“…Nevertheless, the survival rate in MasR knockout mice was higher than in wild type, which as authors point out is surprising because MasR typically plays a protective role in vascular disease. 3 Interestingly, the findings of this work are supported by preliminary data from a similar study by Shimada et al 8 also indicating that Ang (1-7) infusion significantly reduces the rate of aneurysm rupture. However, in contrast to the study by Silva et al, 6 the results of Shimada et al 8 suggest that the beneficial effects of Ang (1-7) may be mediated via the angiotensin receptor type 2 (AT2R), as opposed to the MasR.…”

Section: See Related Article Pp 362-368supporting

confidence: 83%

“…Angiotensin-converting enzyme-2 converts angiotensin II, an 8-aa peptide with oxidative and vasoconstrictor properties, into the 7-aa Ang (1-7). 3 The latter has vasodilator and antioxidant properties and is known to act via the Mas receptor (MasR; Figure). The protective actions of both angiotensin-converting enzyme-2 and Ang (1-7) present a novel therapeutic target for cardiovascular and metabolic diseases.…”

Section: See Related Article Pp 362-368mentioning

confidence: 99%

“…The protective actions of both angiotensin-converting enzyme-2 and Ang (1-7) present a novel therapeutic target for cardiovascular and metabolic diseases. 3 The specific role of renin-angiotensin system in the pathogenesis of intracranial aneurysms is unclear, with evidence both for and against its involvement in aneurysm formation. 4 It is speculated that injury inflicted on artery walls because of shear stress can result in the activation of the reninangiotensin system and, therefore, an inflammatory cascade ultimately leading to aneurysm formation.…”

Section: See Related Article Pp 362-368mentioning

confidence: 99%

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Angiotensin (1–7) as a Therapy to Prevent Rupture of Intracranial Aneurysms?

et al. 2014

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Section: See Related Article Pp 362-368supporting

confidence: 83%

Section: See Related Article Pp 362-368mentioning

confidence: 99%

Section: See Related Article Pp 362-368mentioning

confidence: 99%

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Angiotensin (1–7) as a Therapy to Prevent Rupture of Intracranial Aneurysms?

et al. 2014

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“…This could in turn lower the blood pressure. [46][47][48] With regard to kidney AT2 receptor activation, it has been shown to suppress renin biosynthesis. Because renin plasma levels were not significantly affected by the present protocol, it seems unlikely that peripheral renal AT2 receptors were activated in the present setting.…”

Section: Discussionmentioning

confidence: 99%

“…Because renin plasma levels were not significantly affected by the present protocol, it seems unlikely that peripheral renal AT2 receptors were activated in the present setting. 46,49,50 The reduction in blood pressure after intranasal ANGII sustained during the first hour but faded as plasma levels of aldosterone increased. Aldosterone influences the salt-water homeostasis of the body via the kidneys and may elevate blood pressure with some delay.…”

Section: Discussionmentioning

confidence: 99%

Intranasal Angiotensin II in Humans Reduces Blood Pressure When Angiotensin II Type 1 Receptors Are Blocked

et al. 2014

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T he peptide hormone angiotensin II (ANGII) displays a wide range of regulatory actions on blood pressure. Besides its systemic effects on the blood vessels and different organ systems, local ANGII is crucially involved in the central nervous regulation of blood pressure.1-6 ANGII receptors, mainly type 1 receptors (AT1) and also type 2 receptors (AT2), are expressed in several cerebral nuclei where they mediate effects of locally produced ANGII.7-10 Inhibition of central nervous ANGII synthesis reversed hypertension in spontaneously hypertensive rats. 11The differentiation of central nervous and peripheral actions of ANGII is important for understanding blood pressure homeostasis and the development of essential hypertension in humans. Peripheral ANGII increases blood pressure but cannot surpass the blood-brain barrier, except via the circumventricular organs (area postrema, organum vasculosum laminae terminalis).12,13 These structures express a magnitude of AT1 receptors and seem to serve as an interface gating effects of circulating ANGII to brain stem and hypothalamic nuclei (ie, nucleus tractus solitarius, supraoptic nucleus, and paraventricular nuclei). Such humoral ANGII input is known to increase tonic blood pressure levels by an upward resetting of the sympathetic baroreceptor reflex activity 2,14-17 and may also activate intrinsic hypothalamic neurohypophysial fiber pathways, inducing the release of vasopressin. 3,[18][19][20] When ANGII is directly injected into the nucleus tractus solitarius, the baroreceptor reflex is suppressed via activation of AT1 receptors. After intracerebral administration, however, pressor effects of ANGII were revealed to be variable and even contradictory depending on dose and location of the injection, therefore suggesting differential effects on blood pressure regulation. 3,4,9,10,19,[21][22][23][24] The intranasal administration of small peptide molecules represents an established approach to bypass the bloodbrain barrier in humans and to achieve direct central nervous effects. [25][26][27][28][29] These studies demonstrate that peptide molecules such as ANGII directly enter the cerebrospinal fluid after their intranasal administration without previous uptake to the blood but instead via diffusion along neuronal clefts in the nasal mucosa. Importantly, because of the relatively great amounts of substance administered to achieve central nervous effects of the peptide, it cannot be prevented that, rather than directly accessing the cerebrospinal fluid compartment, some portion of the substance spills over into the circulation. Peptide that enters the circulation might then mask direct central nervous effects after intranasal peptide administration. Thus, a viable approach to unravel direct brain effects of intranasal peptide administration is to combine this treatment with a peripherally acting receptor blocker of the peptide.Abstract-Intranasal administration of angiotensin II (ANGII) affects blood pressure in a mode different from intravenously administered ANGII via a d...

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