Optimization of a direct radioimmunoassay for plasma aldosterone

Al-Dujaili, Emad A S; Edwards, C. R. W.

doi:10.1016/0022-4731(81)90360-5

Cited by 20 publications

(3 citation statements)

References 25 publications

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“…1-~ final plasma concentrations respectively) for the determination of angiotensin II by RIA [17]. Blood was collected into standard lithium heparin tubes for the aldosterone radioimmunoassay [18].…”

Section: Methodsmentioning

confidence: 99%

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

Gow

Dockrell

Edwards

et al. 1992

Eur J Clin Pharmacol

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We have investigated the effect of varying sodium intake on the renin-angiotensin system, ADP-induced platelet aggregation in vitro, and blood 5-HT concentrations in 9 male volunteers. Systolic blood pressure was slightly reduced during a low sodium diet, whereas the diastolic pressure remained unchanged. Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin II concentration also fell, but not significantly. There was a significant fall in haematocrit after an increased sodium intake, but there was no change in the whole-blood platelet count after correcting for this. There were no significant changes in either total (i.e. PRP) or platelet 5-HT concentrations. The extent of platelet aggregation induced by 5 and 20 mumol.l-1 of ADP increased significantly when dietary sodium intake was increased. When compared with low or normal sodium intakes, lower concentrations of ADP were required to produce 50% of maximum aggregation after a high sodium intake. The 5-HT2 receptor antagonist ketanserin (1 mumol.l-1 in vitro) reduced the extent of aggregation induced by 5 mumol.l-1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin II receptor antagonist saralasin (1 nmol.l-1) increased the rate of aggregation after the low sodium diet. Thus, during a high sodium intake, human platelets become more sensitive to the aggregating agent ADP. It is possible that this effect is mediated via platelet 5-HT2 receptors, since ketanserin abolished the increase in salt-induced aggregation seen with 5 mumol.l-1 ADP.

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Section: Methodsmentioning

confidence: 99%

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

Gow

Dockrell

Edwards

et al. 1992

Eur J Clin Pharmacol

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“…ume within one hour, thus in a time range in which Since the mentioned EC 50 of approximately 0.1 nmol/L genomic actions cannot be ruled out. Half-maximal efis similar to the concentration of free aldosterone in fects were demonstrated at approximately 0.1 nmol/L human serum [25], a physiological role of the rapid aldoaldosterone [13,15,16]. However, very rapid aldosterone sterone-induced effects may be hypothesized, as they effects have also been shown in these cells.…”

Section: In Vitro Effects Of Aldosteronementioning

confidence: 96%

Specific nongenomic actions of aldosterone

Falkenstein

Christ

Feuring

et al. 2000

Kidney International

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“…The effect of Mithramycin (2,umole/litre) and Cordycepin (8,umole/litre) (Sigma) on corticotropin-induced corticosterone and aldosterone production was studied in an identical manner. Aldosterone and to 40 0 u corticosterone outputs were measured by highly specific direct radioimmunoassays (Al-Dujaili & Edwards, 1981;Al-Dujaili et al, 198 ib). Responses were calculated as peak above basal output produced by a 10min pulse of corticotropin.…”

Section: Methodsmentioning

confidence: 99%

Human γ-melanotropin precursor potentiates corticotropin-induced adrenal steroidogenesis by stimulating mRNA synthesis

Al-Dujaili¹,

Williams²,

Edwards³

et al. 1982

Biochemical Journal

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Circulating human gamma-melanotropin precursor (76 amino acids) [N-POC(1-76) enhances the corticosterone and aldosterone response to corticotropin by isolated perfused rat adrenal cells [Al-Dujaili, Hope, Estivariz, Lowry & Edwards (1981) Nature (London) 291, 156-159]. Actinomycin D (4 x 10(-6) mol/litre) did not significantly affect corticotropin-induced corticosterone or aldosterone outputs, but completely inhibited the potentiating action of gamma-melanotropin precursor on rat adrenal cells. This suggests that the precursor enhances corticotropin-induced steroidogenesis via an increase in available mRNA produced from DNA transcription.

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Optimization of a direct radioimmunoassay for plasma aldosterone

Cited by 20 publications

References 25 publications

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

The sensitivity of human blood platelets to the aggregating agent ADP during different dietary sodium intakes in healthy men

Specific nongenomic actions of aldosterone

Human γ-melanotropin precursor potentiates corticotropin-induced adrenal steroidogenesis by stimulating mRNA synthesis

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