Automated method for the determination of angiotensin-converting enzyme in serum

Johansen, Kari B.; Marstein, Sverre; Aas, Per

doi:10.1080/00365518709168923

Cited by 18 publications

(12 citation statements)

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“…16 Plasma aldosterone was measured by radioimmunoassay (Coat-a-Count; Diagnostics Products, Los Angeles, CA, USA). Plasma aliskiren levels were measured by Novartis using liquid chromatography with tandem mass spectrometry detection.…”

Section: Measurement Of Plasma Ace Activity and Plasma Aldosterone Anmentioning

confidence: 99%

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Aliskiren increases bradykinin and tissue kallikrein mRNA levels in the heart

Campbell

Yuan

Kelly

et al. 2011

Clin Exp Pharma Physio

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1. Aliskiren is a renin inhibitor with an IC(50) of 0.6 nmol/L for human renin, 4.5 nmol/L for mouse renin and 80 nmol/L for rat renin. 2. In the present study, we compared the effects of aliskiren (10 mg/kg per day), the angiotensin-converting enzyme inhibitor perindopril (0.2 mg/kg per day) and their combination on angiotensin and bradykinin peptides in female heterozygous (mRen-2)27 rats, transgenic for the mouse renin gene. 3. All three treatments produced similar reductions in systolic blood pressure, heart weight and plasma aldosterone levels and reduced angiotensin II levels in lung, but only perindopril and the combination reduced angiotensin II levels in kidney of (mRen-2)27 rats. In contrast, aliskiren and the combination, but not perindopril alone, increased cardiac bradykinin levels. Aliskiren increased immunostaining for tissue kallikrein in the heart and reduced cardiac fibrosis. 4. We investigated the mechanism underlying the increase in bradykinin levels following aliskiren treatment in Sprague-Dawley rats, in which aliskiren has a lower potency for renin inhibition. Aliskiren (10 mg/kg per day) reduced renal angiotensin levels within 24 h, but treatment for > 24 h was required to increase cardiac bradykinin levels. Moreover, 3 mg/kg per day aliskiren increased cardiac bradykinin levels, but did not reduce renal angiotensin levels. Aliskiren did not potentiate the hypotensive effects of bradykinin; however, it increased tissue kallikrein, but not plasma kallikrein, mRNA levels in the heart. 5. These data demonstrate that the aliskiren-induced increase in cardiac bradykinin levels is independent of renin inhibition and changes in bradykinin metabolism, but is associated with increased tissue kallikrein gene expression.

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Section: Measurement Of Plasma Ace Activity and Plasma Aldosterone Anmentioning

confidence: 99%

“…Data are the mean ± SEM (n = 8-11). *P < 0.01 compared with vehicle (repeated measures ANOVA for Weeks[4][5][6][7][8][9][10][11][12][13][14][15][16].…”

mentioning

confidence: 99%

Aliskiren increases bradykinin and tissue kallikrein mRNA levels in the heart

Campbell

Yuan

Kelly

et al. 2011

Clin Exp Pharma Physio

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“…Plasma renin, AGT and ACE were measured using previously described methods [17]. Plasma ACE was measured by enzymatic assay using 3-(2-furylacryloyl)-L-phenylalanyl-glycyl-glycine as substrate [18].…”

Section: Genetic Modelsmentioning

confidence: 99%

Angiotensinogen and angiotensin-converting enzyme gene copy number and angiotensin and bradykinin peptide levels in mice

Alexiou

Boon

Denton

et al. 2005

Journal of Hypertension

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“…Angiotensin converting enzyme ACE was measured in serum by a spectrophotometric method using 3-(2-furylacryloyl)-L-phenylalanylglycylglycine as the substrate (Johansen et al 1987). Venous blood was drawn from a cubital vein.…”

Section: Lung Function Testingmentioning

confidence: 99%

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

et al. 2006

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Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium-oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29-48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.

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Automated method for the determination of angiotensin-converting enzyme in serum

Cited by 18 publications

References 0 publications

Aliskiren increases bradykinin and tissue kallikrein mRNA levels in the heart

Aliskiren increases bradykinin and tissue kallikrein mRNA levels in the heart

Angiotensinogen and angiotensin-converting enzyme gene copy number and angiotensin and bradykinin peptide levels in mice

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

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