Measurement of angiotensin II in human plasma: Technical modifications and practical experience

Kappelgaard, Anne-Marie; Nielsen, Meta Damkjær; Giese, J.

doi:10.1016/0009-8981(76)90338-7

Cited by 230 publications

(67 citation statements)

References 10 publications

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“…Blood samples for angiotensin II (AngII) levels were drawn in prechilled tubes after 30 min of supine rest and immediately centrifuged at 4°C. Plasma concentrations were measured radioimmunologically (12). Blood samples for renin concentration were taken after 30 min supine rest and measured directly by an improved immunoradiometric assay (13) …”

Section: Methodsmentioning

confidence: 99%

Additive Effect of ACE Inhibition and Angiotensin II Receptor Blockade in Type I Diabetic Patients with Diabetic Nephropathy

Jacobsen¹,

Andersen²,

Jensen³

et al. 2003

Journal of the American Society of Nephrology

194

146

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Abstract. Albuminuria and hypertension are predictors of poor renal and cardiovascular outcome in diabetic patients. This study tested whether dual blockade of the renin-angiotensin system (RAS) with both an angiotensin-converting enzyme (ACE) inhibitor (ACE-I) and an Angiotensin-II receptor blocker (ARB) is superior to either drug alone in type I diabetic patients with diabetic nephropathy (DN). A randomized double-blind crossover trial was performed with 8-wk treatment with placebo, 20 mg of benazepril once daily, 80 mg of valsartan once daily, and the combination of 20 mg of benazepril and 80 mg of valsartan. Twenty type I diabetic patients with DN were included. At the end of each treatment period, albuminuria, 24-h BP, and GFR were measured. Eighteen patients completed the study. Placebo values were: albuminuria [mean (95% CI)], 701 (490 to 1002) mg/24 h; BP [mean (SEM)], 144 (4)/79 (2) mmHg, and GFR [mean (SEM)], 82 (7) ml/min per 1.73 m 2 . Treatment with benazepril, valsartan, or dual blockade significantly reduced albuminuria and BP compared with placebo. Benazepril and valsartan were equally effective. Dual blockade induced an additional reduction in albuminuria of 43 % (29 to 54 %) compared with any type of monotherapy, and a reduction in systolic BP of 6 (0 to 13) mmHg and 7 (1 to 14) mmHg (versus benazepril and valsartan, respectively) and a reduction of 7 (4 to 10) mmHg diastolic compared with both monotherapies. GFR was reversibly reduced on dual blockade compared with monotherapy and placebo. All treatments were safe and well tolerated. In conclusion, dual blockade of the RAS may offer additional renal and cardiovascular protection in type I diabetic patients with DN.Albuminuria and hypertension are predictors of poor renal and cardiovascular outcome in patients with diabetes (1,2). Antihypertensive treatment, especially ACE-I, has been shown to reduce albuminuria, to diminish loss of kidney function, and to improve survival in type I patients with DN (1-3). Studies of diabetic and nondiabetic kidney disease suggest the initial degree of reduction in albuminuria after blockade of the reninangiotensin system (RAS) predicts an attenuated rate of decline in GFR, as reviewed by Rossing (1). As a consequence, albuminuria may serve as a surrogate end point for monitoring treatment efficacy and prognosis in DN (4).A superior effect on BP and a tendency toward a more pronounced drop in urinary albumin excretion of dual blockade of the RAS compared with single blockade has been reported in type II patients with microalbuminuria (5). We have recently shown additional drop in albuminuria and diastolic BP when adding an angiotensin receptor blocker (ARB) to angiotensinconverting enzyme inhibitor (ACE-I) treatment in type l patients with albuminuria Ͼ1 g/24 h and BP Ͼ135/85 mmHg, despite conventional antihypertensive therapy including three different agents (6). However, this subgroup is highly selected; therefore, it may differ from the patients in general with DN, especially with regard to RAS activity and ...

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Section: Methodsmentioning

confidence: 99%

Additive Effect of ACE Inhibition and Angiotensin II Receptor Blockade in Type I Diabetic Patients with Diabetic Nephropathy

Jacobsen¹,

Andersen²,

Jensen³

et al. 2003

Journal of the American Society of Nephrology

194

146

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“…Plasma angiotensinogen concentration was determined using the principle of antibody trapping 22 as modified by Millar et al 23 Plasma renin activity was determined by a double-sided immunoradiometric method, using two monoclonal antibodies against human-active renin linked to biotin and 125 I (Nichols Institute, Geneva, Switzerland). Angiotensin II (Ang II rabbit-antibody kindly provided by Professor Jan Danser, Rotterdam, Holland) 24 and aldosterone (DSL-8600 active aldosterone TM Coated-Tube Ria Kit, Diagnostics Systems Laboratories Inc., Webster, Texas, USA) were measured in plasma by radioimmunoassay. For plasma angiotensinogen, women taking anticontraceptive medication (22 subjects, 18 controls) and two outliers deviating from the mean by three (a control) and five (an EH-offspring) standard deviations were excluded from calculation.…”

Section: Protocolmentioning

confidence: 99%

Renal Haemodynamics are not Related to Genotypes in Offspring of Parents with Essential Hypertension

Skov

Madsen

Hansen

et al. 2006

J Renin Angiotensin Aldosterone Syst

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Introduction. The pathogenesis of essential hypertension (EH) has a major genetic component and is associated with renal abnormalities. Normotensive offspring of hypertensive parents are likely to develop EH and are a suitable population for identifying possible relations between genetic and renal abnormalities. Methods. We investigated if renin-angiotensin-aldosterone system associated genotypes (angiotensinogen [M235T] and ACE [I/D]) are related to blood pressure (BP), renal haemodynamics and sodium excretion in sex and age-matched (18—35 years) healthy Caucasian offspring of either two parents with EH (n=101, EH-offspring) or two normotensive parents (n=50, controls). The alpha-adducin polymorphism (G460W) was also investigated. Results. Compared to controls, BP, heart rate, renal vascular resistance (RVR) and urinary sodium excretion were, respectively, 5%, 7%, 15% and 20% higher in EH-offspring. In controls, the TT-genotype of the M235T angiotensinogen polymorphism was associated with higher BP and higher plasma angiotensinogen. By contrast, in EHoffspring the TT-genotype was associated with lower BP and unchanged plasma angiotensinogen. Plasma angiotensinogen correlated positively with BP in EH-offspring, with a similar tendency (p=0.08) in controls. The distributions of the three candidate polymorphisms were similar in EH-offspring and controls. There were no associations between any of the polymorphisms and any of the renal parameters measured. Conclusion. The markedly greater RVR, proportionally larger than the greater BP, supports a role for RVR in the pathogenesis of EH. The lack of association between the candidate polymorphisms and the investigated parameters, even in this homogenous and for hypertension strongly predisposed group, suggests that the polymorphisms investigated do not play important roles in the pathogenesis of hypertension.

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“…Blood was collected in EDTA aprotinin tubes and plasma was extracted on Sep-pak C18 prior to analysis. Active plasma renin concentrations were determined using the principle of antibody trapping 22 as modified by Millar et al 23 Plasma angiotensin II concentrations were measured according to the method of Kappelgaard et al 24 with the modification that Sep-Pac C 18 (Millipore Waters) was used for plasma extraction. Plasma aldosterone concentrations were measured using a commercial kit (DSL-8600, Diagnostic Systems Laboratories Inc., Webster, TE, USA).…”

Section: Assaysmentioning

confidence: 99%

Is inappropriate left ventricular mass related to neurohormonal factors and/or arterial changes in hypertension? a LIFE substudy

et al. 2004

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We investigated whether inappropriately high left ventricular (LV) mass, defined as observed LV mass exceeding the level of individual LV mass predicted from gender, height, and stroke work, may be associated with an imbalance between growth-promoting and growth-inhibitory factors and/or structural vascular changes. In 53 patients with hypertension and electrocardiographic LV hypertrophy, 24-h ambulatory blood pressure (BP); echocardiographic LV mass, stroke volume and stroke work; minimal forearm vascular resistance (MFVR); and intima-media cross-sectional area in common carotid arteries (IMA) were evaluated after 2 weeks of placebo treatment. Serum insulin, plasma epinephrine, norepinephrine, endothelin, angiotensin II, aldosterone, and brain natriuretic peptide (BNP) were also measured. High observed LV mass was related to high IMA (r ¼ 0.46, Po0.001), MFVR (in men: r ¼ 0.36, Po0.05), 24-h ambulatory systolic BP (r ¼ 0.30, P ¼ 0.06), and lower plasma angiotensin II (r ¼ À0.33, Po0.05), but not to other circulating growth factors. Stroke work was similarly related to IMA (r ¼ 0.42, Po0.01), MFVR (in men: r ¼ 0.41, Po0.05), and plasma angiotensin II (r ¼ À0.32, Po0.05). Inappropriate LV mass, identified by the ratio between observed LV mass and the value predicted for gender, height, and stroke work, was not significantly related to any of the arterial or neurohormonal variables. In this small series of older hypertensive patients, inappropriate LV mass was not significantly related to arterial changes or to measured circulating growth factors, although weak relations cannot be excluded. Alternatively, inappropriately high LV mass might be related to unmeasured factors such as local myocardial alterations in growth factors and/or genetic predisposition to develop excessive LV hypertrophy.

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Measurement of angiotensin II in human plasma: Technical modifications and practical experience

Cited by 230 publications

References 10 publications

Additive Effect of ACE Inhibition and Angiotensin II Receptor Blockade in Type I Diabetic Patients with Diabetic Nephropathy

Additive Effect of ACE Inhibition and Angiotensin II Receptor Blockade in Type I Diabetic Patients with Diabetic Nephropathy

Renal Haemodynamics are not Related to Genotypes in Offspring of Parents with Essential Hypertension

Is inappropriate left ventricular mass related to neurohormonal factors and/or arterial changes in hypertension? a LIFE substudy

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