Newly Discovered Components and Actions of the Renin–Angiotensin System

Carey, Robert M.

doi:10.1161/hypertensionaha.113.01111

Cited by 59 publications

(44 citation statements)

References 48 publications

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“…Recently, new Mas-related genes (Mrg) have been explored, many of them coding orphan receptors [43,3]. Alamandine is a heptapetide, structurally and functionally similar to ANG-(1-7), with a N-terminal Ala marking the difference between the two [44].…”

Section: Discussionmentioning

confidence: 99%

“…It is mainly formed from angiotensin A by the catalytic enzyme ACE-2 [44]. Interestingly, alamandine-induced vasodilation is not abolished by A-779 but by a Mrg type D (MrgD) inhibitor (D-Pro-Ang (1-7)), suggesting that this membrane receptor may specifically mediate alamandine effects in a NO dependent pathway [3,44]. Additionally, some studies have shown that in certain circumstances ANG-(1-7) effects are not blocked by A-779, but are nonetheless endothelium-dependent [44,45].…”

Section: Discussionmentioning

confidence: 99%

“…Classically, the RAS was viewed as a linear enzymatic cascade resulting in angiotensin II (ANG II) formation, one of the most important mediators involved in cardiovascular diseases, including hypertension and heart failure [2]. However, further investigation provided a new insight into this system, revealing a more complex and dynamic network formed by numerous molecular pathways [3]. Among these, angiotensin-(1-7) (ANG-(1-7)) emerged as an important mediator able to counter-regulate ANG II deleterious cardiovascular effects, holding the promise of new therapeutic strategies [4].…”

Section: Introductionmentioning

confidence: 99%

“…Some evidence suggests that the AT 2 receptor may contribute to vasodilation induced by ANG- (1)(2)(3)(4)(5)(6)(7) in mouse coronary artery. Regarding this, Castro et al observed that in the presence of a specific AT 2 receptor inhibitor (PD123319), ANG-(1-7) treatment did not reduce coronary perfusion pressure [20] and, more recently, a similar effect was demonstrated in a model of rat heart hypertrophy [21].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

Mendonça

Mendes-Ferreira

Bento-Leite

et al. 2014

Cardiovasc Drugs Ther

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

Mendonça

Mendes-Ferreira

Bento-Leite

et al. 2014

Cardiovasc Drugs Ther

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“…9,10 Within the brain, however, AT2 receptors are expressed at substantial levels, and novel binding sites are still being identified. 36,41,42 Their activation may protect from cerebral ischemia or hypertension. [43][44][45] Our findings in healthy humans show that intranasal ANGII combined with systemic AT1 receptor blockade reduces blood pressure.…”

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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Neurohumoral and Autonomic Regulation of Blood Pressure

Lurbe

Redón

2023

Pediatric Hypertension

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Newly Discovered Components and Actions of the Renin–Angiotensin System

Cited by 59 publications

References 48 publications

Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

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

Neurohumoral and Autonomic Regulation of Blood Pressure

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