The renin-angiotensin-aldosterone system

Vecsei, P.; Hackenthal, E.; Ganten, Detlev

doi:10.1007/bf01477448

Cited by 127 publications

(13 citation statements)

References 157 publications

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“…That discovery also led to the appreciation of the mouse submaxillary renin [19], that in turn led to the first utilitarian transgenic model of hypertension [20]. The AT1 receptor was cloned 1 year later [21]. Thereafter, the progress is prodigious.…”

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confidence: 99%

“…The rest of the story is more or less contemporary and will unfold as part of this thematic issue of Journal of Molecular Medicine. Important parts include the cloning and characterization of the (pro)renin receptor, the discovery of ACE2, the identification of other angiotensins, already a theme in the 1978 symposium [21], and characterization of the Mas receptor. Also a fitting postlude to this introductory editorial is the long-awaited development of direct renin inhibitors.…”

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confidence: 99%

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A brief history of renin

Luft

2008

J Mol Med

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confidence: 99%

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confidence: 99%

A brief history of renin

Luft

2008

J Mol Med

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“…Angiotensin II (AII) is a product of the renin-angiotensin system which plays an important role in the regulation of blood pressure and fluid and electrolyte balance (49). However, this eight-amino-acid peptide does not exclusively control blood pressure; it has also been shown to modulate wound repair in several animal models.…”

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confidence: 99%

Angiotensin II Increases Host Resistance to Peritonitis

Rodgers

Xiong

Espinoza

et al. 2000

Clin Diagn Lab Immunol

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Studies by other laboratories have shown that angiotensin II (AII) can affect the function of cells which comprise the immune system. In the present study, the effect of AII on the function of peritoneal macrophages and peripheral blood monocytes was assessed. In vitro exposure (4 h prior to assay) of peritoneal macrophages from mice and rats to AII increased the percentage of cells that phagocytosed opsonized yeast and the number of yeast per macrophage. Furthermore, AII increased the respiratory burst capacity of peritoneal macrophages from mice and rats and peripheral blood mononuclear cells from humans. Because of these observations, the effect of AII on host resistance to bacterial infection was assessed. Intraperitoneal administration of AII was shown to increase host resistance (reduced abscess formation) in an animal model of bacterial peritonitis. Studies were then conducted to assess whether parenteral administration of AII, a clinically relevant route, could affect peritoneal host resistance in a manner similar to that observed after peritoneal administration. These studies showed that subcutaneous administration of AII throughout the postinfection interval increased the level of host resistance to bacterial peritonitis. Furthermore, in a study which compared AII and Neupogen, an agent approved for use for the reduction of febrile neutropenia after myeloablative therapy, daily subcutaneous administration of AII reduced abscess size and incidence, whereas Neupogen did not have any therapeutic benefit in this model. These data suggest that AII may be of therapeutic benefit as an immunomodulatory agent.Angiotensin II (AII) is a product of the renin-angiotensin system which plays an important role in the regulation of blood pressure and fluid and electrolyte balance (49). However, this eight-amino-acid peptide does not exclusively control blood pressure; it has also been shown to modulate wound repair in several animal models. Rodgers et al. (35) found that administration of AII accelerated the repair of full-thickness excisional wounds in healthy and impaired rats, as well as diabetic mice. Furthermore, it has been shown that administration of AII accelerated the healing of partial-thickness burns (36). More recently, AII has been shown to act as a hematopoietic factor in the acceleration of the recovery of white blood cells and survival after myeloablative therapy (K. E. Rodgers et al., unpublished data). It is conceivable that part of the survival benefit was due to increased leukocyte function and subsequent host resistance to infection. The studies described here were conducted to test this hypothesis.Prabha et al. (32) first observed that AII, when tested at physiological concentrations, can increase free-radical generation by polymorphonuclear neutrophils (PMNs). This observation was confirmed by Kumar and Das (22). Hydrogen peroxide is an important component in the respiratory burst system that can be used to measure increased activation of neutrophils and macrophages. Based on these studies and ...

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“…It is generated from an giotensin I (ANG I) by angiotensin-converting enzyme. Under physiological conditions, the RAS has many func tions, mostly related to the regulation of blood pressure, fluid and electrolyte homeostasis [10,11], An involvement o f the RAS with increased renin and ANG II plasma levels has been shown in different kinds of stress and hemorrhage [12,13], AR are stress-related situations. Therefore, know ing the importance of the RAS on cardiovascular function we were intrigued to study the role of the RAS during an AR as a counteracting stabilizing factor.…”

Section: Introductionmentioning

confidence: 99%

Increased Urinary Excretion of Angiotensin during Anaphylactoid Reactions

Rittweger

Hermann²,

Ring³

1994

Int Arch Allergy Immunol

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Immunoreactive angiotensin I (ANG I) and angiotensin II (ANG II) were measured in human urine, after purification on octadecasilyl-silica cartridges.The total daily excretion of ANG I and II in healthy volunteers was 292.2 ± 62.5 and 12.2 ± 2.5 pmol/24 h (mean ± SEM; n = 14). No differences in the concentrations of ANG I or II were detected between females and males. Although lower levels of ANG I and II were found during the nighttime, no clear-cut circadian rhythm in the excretion of the peptides was found. ANG II was not degraded in acidified urine which shows the effective inhibition of ANG-II-degegrading enzymes. Oral provocation tests (OPT) in patients with a history of anaphylactoid reactions (AR) to drugs, foods and food additives were associated with elevated ANG I and II concentrations when symptoms of anaphylaxis occurred. The excretion of ANG I increased by a factor of 7.8 ± 2.4 and the excretion of ANG II by a factor of 6.1 ± 1.6 (mean ± SEM; n = 15). In patients with negative OPT and no clinical symptoms of anaphylaxis, the levels of ANG I and II remained unchanged (n = 26). It is concluded that angiotensin peptides play a role during the events of AR. The peptides may be considered as counteracting factors which stabilize cardiovascular functions.

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The renin-angiotensin-aldosterone system

Cited by 127 publications

References 157 publications

A brief history of renin

A brief history of renin

Angiotensin II Increases Host Resistance to Peritonitis

Increased Urinary Excretion of Angiotensin during Anaphylactoid Reactions

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