Nephrectomy, converting enzyme inhibition, and angiotensin peptides.

Campbell, Duncan J.; Kladis, Athena; Duncan, Ann-Maree

doi:10.1161/01.hyp.22.4.513

Cited by 161 publications

(99 citation statements)

References 35 publications

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“…When these two agents are used, the expression of ACE2 is enhanced, which shifts the angiotensin peptide balance favoring metabolism of ANG II to produce ANG-(1-7). In previous reports, the anti-proliferative responses to ANG-(1-7) are both dose-and timedependent (Campbell et al 1993). ACEI and ARB can cause a significant elevation in both tissue and circulating ANG-(1-7) (Agata et al 2006).…”

Section: Discussionmentioning

confidence: 87%

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Zhou

Zhang

Yao

et al. 2009

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 87%

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Zhou

Zhang

Yao

et al. 2009

Tohoku J. Exp. Med.

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“…15 Angiotensin peptides were acetylated before HPLC, and assay of HPLC fractions was performed with N-terminal-directed radioimmunoassay. 16 …”

Section: Extraction and Radioimmunoassay Of Angiotensin Peptides Frommentioning

confidence: 99%

“…- 16 The time delay between decapitation and homogenization of the kidney was 60 seconds; heart and lung were homogenized within 90 seconds, and aorta and brown adipose tissue were homogenized within 150 seconds.…”

mentioning

confidence: 99%

Effects of converting enzyme inhibitors on angiotensin and bradykinin peptides.

1994

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We examined the dose-related effects of angiotensin-converting enzyme inhibitors on circulating and tissue levels of angiotensin and bradykinin peptides by administering perindopril or lisinopril to rats in drinking water for 7 days. A reduction in the ratio of plasma angiotensin II (Ang II) to Ang I was seen for 0.006 mg/kg per day perindopril, with an increase in plasma renin and Ang I at 0.017 mg/kg per day. Plasma Ang II levels did not decrease until 1.4 mg/kg per day perindopril, at which dose plasma Ang I levels reached a plateau of an approximate 25-fold increase. The effects of perindopril on Ang II and Ang I levels in heart, lung, aorta, and brown adipose tissue were parallel to those observed for plasma. By contrast, renal Ang I levels did not increase, and renal Ang II levels decreased by 40% at 0.017 mg/kg per day, the same threshold seen for the increase in plasma renin. Perindopril increased circulating bradykinin-(l-9) levels approximately eightfold, with a threshold dose of 0.052 mg/kg per day, and increased bradykinin-(l-9) levels in kidney, heart,

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“…This is supported by experiments demonstrating that ANG II persists in lung of nephrectomized rats (4) and findings showing that ANG II can be elevated in the lungs in the absence of an elevated systemic RAS (5). Components of RAS have been identified in lung tissue, including aogen mRNA (6,7), and angiotensin-converting enzyme (ACE), the pulmonary endothelium being the primary source for ACE in the body (8).…”

mentioning

confidence: 93%

Mast cell renin and a local renin–angiotensin system in the airway: Role in bronchoconstriction

Veerappan¹,

Reid²,

Estephan³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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We previously reported that mast cells express renin, the ratelimiting enzyme in the renin-angiotensin cascade. We have now assessed whether mast cell renin release triggers angiotensin formation in the airway. In isolated rat bronchial rings, mast cell degranulation released enzyme with angiotensin I-forming activity blocked by the selective renin inhibitor BILA2157. Local generation of angiotensin (ANG II) from mast cell renin elicited bronchial smooth muscle contraction mediated by ANG II type 1 receptors (AT 1R). In a guinea pig model of immediate type hypersensitivity, anaphylactic mast cell degranulation in bronchial rings resulted in ANG II-mediated constriction. As in rat bronchial rings, bronchoconstriction (BC) was inhibited by a renin inhibitor, an AT 1R blocker, and a mast cell stabilizer. Anaphylactic release of renin, histamine, and ␤-hexosaminidase from mast cells was confirmed in the effluent from isolated, perfused guinea pig lung. To relate the significance of this finding to humans, mast cells were isolated from macroscopically normal human lung waste tissue specimens. Sequence analysis of human lung mast cell RNA showed 100% homology between human lung mast cell renin and kidney renin between exons 1 and 10. Furthermore, the renin protein expressed in lung mast cells was enzymatically active. Our results demonstrate the existence of an airway renin-angiotensin system triggered by release of mast-cell renin. The data show that locally produced ANG II is a critical factor governing BC, opening the possibility for novel therapeutic targets in the management of airway disease.angiotensin II ͉ angiotensin II type 1 receptors ͉ asthma ͉ hypersensitivity ͉ lung T he renin-angiotensin system (RAS) has been traditionally viewed as a circulating axis, whereby renin is released into the circulation from the kidneys in response to decreased renal perfusion pressure, decreased delivery of NaCl at the macula densa, and/or increased renal sympathetic nerve activity (1). The proteolytic cleavage of angiotensinogen (aogen) by renin constitutes the rate-limiting step of the RAS cascade.In addition to this classical view, it is believed that many tissues, including the lung, may possess the capacity to generate angiotensin (ANG II) locally (2, 3). This is supported by experiments demonstrating that ANG II persists in lung of nephrectomized rats (4) and findings showing that ANG II can be elevated in the lungs in the absence of an elevated systemic RAS (5). Components of RAS have been identified in lung tissue, including aogen mRNA (6, 7), and angiotensin-converting enzyme (ACE), the pulmonary endothelium being the primary source for ACE in the body (8). ANG II receptors are also expressed in lung tissue, with the ANG II type 1 receptor (AT 1 R) subtype found on bronchial smooth muscle cells (9) and ANG II type 2 receptor (AT 2 R) observed on the bronchial epithelial cell brush border (10). An intrapulmonary source of renin protein has not yet been identified.We previously reported that mast cells synthesize, st...

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Nephrectomy, converting enzyme inhibition, and angiotensin peptides.

Cited by 161 publications

References 35 publications

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Effects of converting enzyme inhibitors on angiotensin and bradykinin peptides.

Mast cell renin and a local renin–angiotensin system in the airway: Role in bronchoconstriction

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