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

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

Clinica Chimica Acta

Volume 67, Issue 3, 15 March 1976, Pages 299-306

https://doi.org/10.1016/0009-8981(76)90338-7 Get rights and content

Abstract

This paper presents our experince in measurement of plasma angiotensin II concentration according to the method described by Düsterdieck, G. and Mc-Elwee, G. (1971) Eur. J. Clin. Invest. 2, 32–38. Certain technical modifications of the procedure have been worked out. For each individual plasma sample, the recovery across extraction and elution steps is determined by addition of radioiodinated angiotensin II. A time-saving recycling elution procedure is described. Evidence for the clinical applicability of the modified method is presented.

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Angiotensin blockade and progressive loss of kidney function in hemodialysis patients: A randomized controlled trial
2014, American Journal of Kidney Diseases
Glomerular filtration rate (GFR) declines during long-term dialysis treatment. In peritoneal dialysis, blockade of the renin-angiotensin-aldosterone system reduces GFR decline. Observational studies suggest that similar treatment may preserve kidney function in hemodialysis (HD).
A multicenter, randomized, placebo-controlled, double-blinded trial, with 1-year follow-up.
Adult HD patients with urine output > 300 mL/24 h, HD vintage less than 1 year, and cardiac ejection fraction > 30%. Patients were included from 6 HD centers.
Patients were randomly assigned to placebo or the angiotensin II receptor blocker irbesartan, 300 mg daily. Target systolic blood pressure (BP) was 140 mm Hg.
Primary outcomes were change in GFR measured as the mean of creatinine and urea renal clearance together with urine volume. Secondary outcomes were change in albuminuria, renin-angiotensin II-aldosterone hormone plasma levels, and time to anuria.
Of 82 patients randomly assigned (41 patients in each group), 56 completed 1 year of treatment. The placebo and irbesartan groups were comparable at baseline in terms of sex balance (26 vs 30 men), mean age (62 vs 61 years), median HD vintage (137 vs 148 days), mean HD time (10 vs 11 h/wk), median urine volume (1.19 vs 1.26 L/d), and mean GFR (4.8 vs 5.7 mL/min/1.73 m²). The target BP level was reached in both groups and BP did not differ significantly between groups over time. Adverse-event rates were similar. GFR declined by a mean of 1.7 (95% CI, 1.2-2.3) and 1.8 (95% CI, 1.1-2.4) mL/min/1.73 m² per year in the placebo and irbesartan groups, respectively. Mean difference (baseline values minus value at 12 months) between groups was −0.0 (95% CI, −0.8 to 0.8). In each group, 4 patients became anuric.
GFR decline rates were lower than expected, reducing the power.
At equal BP levels, we found that irbesartan treatment did not affect the decline in GFR or urine volume significantly during 1 year of treatment in HD patients. Irbesartan treatment was used safely in the studied population.
Erratum: Renal and hormonal effects of systemic nitric oxide inhibition in patients with congestive heart failure and in healthy control subjects (Journal of Cardiac Failure (2013) 19 (776-785))
2014, Journal of Cardiac Failure
Renal and hormonal effects of systemic nitric oxide inhibition in patients with congestive heart failure and in healthy control subjects
2013, Journal of Cardiac Failure
The significance of basal renal nitric oxide (NO) availability in the regulation of renal perfusion and sodium excretion in human congestive heart failure (CHF) has not been described previously.
We studied the effects of acute systemic NO synthesis inhibition with N^G-monomethyl-L-arginine (L-NMMA) in 12 patients with CHF and 10 healthy control subjects (CON) in a randomized placebo-controlled study. Effect parameters were renal plasma flow (RPF), renal vascular resistance (RVR), glomerular filtration rate (GFR), urine sodium excretion and plasma levels of vasoactive hormones. L-NMMA was associated with a significant decrease in RPF (CON-LNMMA: −13 ± 3% [P = .014]; CHF-LNMMA: −17 ± 7% [P = .017]) and a profound increase in RVR in both CHF and CON (CON-LNMMA: +26 ± 6% [P = .009]; CHF-LNMMA: +37 ± 70% [P = .005]). Significant decreases in sodium excretion were found in both CHF-LNMMA and CON-LNMMA. Relative changes from baseline were not statistically different between CHF-LNMMA and CON-LNMMA. After L-NMMA, RPF values correlated inversely with plasma aldosterone in CHF-LNMMA (P = .01). L-NMMA induced an increase in A-type natriuretic peptide (ANP) only in CHF-LNMMA (+18 ± 8%; P = .035), which correlated significantly with basal ANP levels (P = .034).
There was no difference in the renal response to L-NMMA in CHF vs CON, suggesting that the impact of NO on renal perfusion and sodium excretion is maintained in stable CHF. We suggest that NO influences the release of ANP during high levels of atrial stretch in CHF.
Effect of indomethacin on desmopressin resistant nocturnal polyuria and nocturnal enuresis
2012, Journal of Urology
We evaluated the acute effect of indomethacin on renal water and solute handling in children with coexisting monosymptomatic nocturnal enuresis and desmopressin resistant nocturnal polyuria, and in healthy controls.
A total of 23 subjects were recruited, consisting of 12 children with monosymptomatic nocturnal enuresis and nocturnal polyuria with partial or no response to desmopressin, and 11 age matched controls. Children completed a 48-hour inpatient study protocol consisting of fractional urine collections and blood samples. Sodium and water intake were standardized. During the second night a dose of 50 mg indomethacin was administered orally before bedtime. Diuresis, urine osmolalities, clearances and fractional excretions were calculated for sodium, potassium, urea, osmoles and solute-free water. Renin, angiotensin II, aldosterone and atrial natriuretic peptide were measured in plasma. Prostaglandin E₂ was measured in urine.
Indomethacin markedly decreased the nocturnal sodium, urea and osmotic excretion in children with enuresis and controls. The overall effect on nocturnal urine output was inconsistent in the group with enuresis. Subjects in whom nocturnal diuresis was decreased following administration of indomethacin remained dry.
Prostaglandin inhibition leads to antidiuresis, reducing the amount of sodium, urea and osmotic excretion in children with monosymptomatic nocturnal enuresis and desmopressin resistant nocturnal polyuria. The sodium regulating hormones do not seem to mediate these processes. The overall effect in desmopressin nonresponders with nocturnal polyuria is variable. The extent to which indomethacin can be applied in the treatment of enuresis needs further evaluation.
Enhanced Sodium Retention After Acute Nitric Oxide Blockade in Mildly Sodium Loaded Patients With Essential Hypertension
2007, American Journal of Hypertension
Citation Excerpt :
Blood pressures were measured every 15 min, except after L-NMMA/placebo when pressures were measured every 5 min for 30 min. Cyclic GMP, renin, Ang II, ALDO, ANP, and BNP were measured by previously described methods.4–8 Serum and urinary concentrations of lithium were measured by atomic absorption spectrophometry (Perkin Elmer 3100, Perkin Elmer, Boston, MA).
In essential hypertension (ESS) whole body and vascular nitric oxide (NO) synthesis is generally thought to be reduced. We therefore investigated the systemic and renal responses to acute treatment with N^G-monomethyl-l-arginine (L-NMMA), a competitive NOS-inhibitor, in 12 patients with ESS and 18 healthy controls (CON) in a randomized, placebo-controlled study. Main effect parameters were renal hemodynamics (glomerular filtration rate [GFR] and renal plasma flow [RPF]), systemic blood pressure (BP), and fractional excretions of sodium (FE_Na) and lithium (FE_Li). Experiments were performed on two occasions for each subject studying the effects of either L-NMMA (3 mg/kg intravenously) or placebo. The patients with ESS were studied after at least 14 days off antihypertensive medication. Renal hemodynamics were assessed by the clearances of ¹²⁵I-hippuran (RPF) and ⁵¹Cr-EDTA (GFR). The L-NMMA induced a significant increase in systemic BP and significant reductions in RPF, FE_Na, and FE_Li in both groups. The increase in diastolic BP was significantly attenuated in ESS (ESS: 8% ± 2% v CON: 14% ± 2%, P < .05). The GFR and RPF were equally reduced by L-NMMA in both groups (RPF_ESS: −19% ± 4% v RPF_CON: −15% ± 3%, P = not significant [NS]). However, the reduction in FE_Na was enhanced in ESS (ESS: −42% ± 7% v CON: −25% ± 3%, P < .01). The FE_Li decreased equally in both groups (ESS: −17% ± 2% v CON: −17% ± 6%, P = NS). It is concluded that acute NO blockade in ESS is accompanied by a reduced systemic pressor response, an unchanged renal hemodynamic response, and an enhanced reduction in FE_Na. The results suggest that patients with essential hypertension are highly dependent on NO to maintain sodium excretion.

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

Abstract

Lancet

Lancet

Clin. Chim. Acta

Nature

J. Clin. Endocrinol. Metab.

J. Lab. Clin. Med.

J. Clin. Endocrinol. Metab.