Effect of aging on plasma renin and aldosterone in normal man

Weidmann, P; Myttenaere-Bursztein, Sylvianne De; Maxwell, Morton H.; Lima, José de Ribamar Medeiros

doi:10.1038/ki.1975.120

Cited by 421 publications

(205 citation statements)

References 35 publications

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“…In normal subjects, levels of all 3 hormones are higher when upright than when supine (12,13,18). As expected, aldosterone and norepinephrine levels were significantly higher when the patients were sitting than when supine (P < 0.02), but epinephrine levels did not change.…”

Section: Resultsmentioning

confidence: 99%

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Abnormalities of Renal Physiology in Systemic Sclerosis

Clements

Lachenbruch

Fürst

et al. 1994

Arthritis & Rheumatism

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Objective. To evaluate the prognostic value of measurements of renal plasma flow and circulating vasoactive hormones in patients with systemic sclerosis (SSc).Methods. Renal plasma flow (para-aminohippurate [PAH] clearance) and levels of selected circulating hormones (plasma renin activity [PRA] and serum aldosterone and catecholamines) were assessed in 57 SSc patients under the following conditions: at rest, in response to cold, while in upright position, and in response to sodium depletion. Survival was assessed 10.7 years after testing (20 patients had died).Results. Both unstimulated and stimulated PRA clearance rates were frequently elevated. Resting PAH clearances were usually abnormally low. PAH clearances and levels of aldosterone and catecholamines did not change during cold stimulation. Supine PRA levels

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Section: Resultsmentioning

confidence: 99%

“…The normal range for aldosterone (mean * 2 SD) was also dependent on sodium balance and posture. Normal supine and upright aldosterone levels in the sodium-replete state are <9.9 ng/100 ml and <38.1 ng/100 ml and in the sodiumdepleted state are <35.4 ng/100 ml and <149.9 ng/100 rnl, respectively (12).…”

Section: Methodsmentioning

confidence: 98%

Abnormalities of Renal Physiology in Systemic Sclerosis

Clements

Lachenbruch

Fürst

et al. 1994

Arthritis & Rheumatism

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“…The Cmax for enalaprilat was slightly but significantly later at 4-5 h and additionally was more variable, across a range of 2-10 h. Additionally, peak plasma concentrations of enalaprilat tended to be higher in the elderly but this was not apparent with benazeprilat. At 72 h post-dose similar mean plasma levels were measured for both drugs: for benazeprilat, 3.0 and 5.0 nmol 1-1 for the young and elderly respectively and for enalaprilat, 1.7 and 4.4 nmol 1-1 for the young and elderly respectively.…”

Section: Plasma Drug Concentrationsmentioning

confidence: 61%

“…Thus, the reduced pharmacodynamic response reported in elderly patients treated with the ACE inhibitor, captopril [2] might simply reflect the age-related decline in plasma renin activity [3]. It has now become apparent that the blood pressure response to ACE inhibitors is not consistently related to the pretreatment plasma renin activity [4], irrespective of age, and ACE inhibitors have been used successfully to control blood pressure in the elderly in several large clinical trials over relatively long periods of time [5,6,7].…”

Section: Introductionmentioning

confidence: 99%

The effects of age on the pharmacokinetics and pharmacodynamics of single oral doses of benazepril and enalapril.

Macdonald

Sioufi

Howie

et al. 1993

Brit J Clinical Pharma

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1. Eighteen healthy, normotensive subjects (nine young and nine elderly) participated in a double‐blind, 3‐way, crossover study to compare aspects of the pharmacokinetics and pharmacodynamics of single oral doses of 10 mg benazepril, 10 mg enalapril and placebo. 2. The hypotensive effect was similar after both drugs but the absolute reductions were greater in the elderly who had higher initial levels of blood pressure. 3. The AUCs for both benazeprilat and enalaprilat were higher in the elderly but by a significantly greater amount for enalaprilat (+ 113% vs 40%; P < 0.01). 4. The AUCs for both drugs tended to be highest in subjects with the lowest creatinine clearance. 5. The changes in kinetics and dynamics observed in the elderly after benazepril are qualitatively similar to those with other ACE inhibitors. The clinical significance of the quantitative differences requires further investigation.

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“…Thus, the relationship between 4G/5G genotype and circulating PAI-1 antigen concentrations was attenuated under high-salt conditions, when PRA and aldosterone are suppressed, compared with under low-salt conditions. Given that renin activity decreases with age, 33 the finding that activation of the RAAS accentuates the relationship between the PAI-1 genotype and PAI-1 antigen concentrations may explain the observed association between PAI-1 4G/5G genotype and MI in young, 10 but not older, 19,20 populations. Although there was no relationship between age and PAI-1 antigen concentrations in the present study, the study population was relatively young, and all but 8 subjects had normal to high PRA.…”

Section: Discussionmentioning

confidence: 95%

Interactive Effect of PAI-1 4G/5G Genotype and Salt Intake on PAI-1 Antigen

Brown

Murphey²,

Srikuma³

et al. 2001

ATVB

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Abstract-Activation of the renin-angiotensin-aldosterone system (RAAS) is associated with increased circulating PAI-1 antigen and increased risk of thrombotic cardiovascular events. A 4G/5G polymorphism located 675 bp upstream from the transcription start site of the PAI-1 gene affects PAI-1 antigen concentrations. To test the hypothesis that PAI-1 4G/5G genotype influences the effect of activation of the RAAS on PAI-1 expression, we measured morning PAI-1 antigen concentrations in 76 subjects with essential hypertension during low (10 mmol/d) and high (200 mmol/d) salt intake. Low salt intake was associated with activation of the RAAS as measured by plasma renin activity (2.3Ϯ0.2 versus 0.5Ϯ0.0 ng angiotensin I · mL Ϫ1 · h Ϫ1 , PϽ0.001) and aldosterone (529Ϯ40 versus 145Ϯ12 pmol/L). PAI-1 antigen concentrations were 17.9Ϯ2.7, 19.2Ϯ2.5, and 27.8Ϯ4.0 ng/mL during high salt intake and 19.2Ϯ2.7, 21.6Ϯ2.9, and 38.9Ϯ7.2 ng/mL during low salt intake in the 5G/5G (nϭ14), 4G/5G (nϭ40), and 4G/4G (nϭ22) groups, respectively. There was a significant effect of both salt intake (Fϭ6.0, Pϭ0.017) and PAI-1 4G/5G genotype (Fϭ7.6, Pϭ0.001) on PAI-1 antigen. More importantly, there was a significant interactive effect (Fϭ7.8, Pϭ0.001) of salt intake and PAI-1 4G/5G genotype on PAI-1 antigen. PAI-1 4G/5G genotype influenced the relationship between serum triglycerides and PAI-1 antigen such that the relationship was significant only in 4G homozygotes during either high (R 2 ϭ0.31, Pϭ0.014) or low (R 2 ϭ0.37, Pϭ0.006) salt intake. This study identifies an important gene-by-environment interaction that may influence cardiovascular morbidity and the response to pharmacological therapies that interrupt the RAAS. Key Words: thrombosis Ⅲ genetics Ⅲ fibrinolysis Ⅲ coagulation A ctivation of the renin-angiotensin-aldosterone (RAAS) system has been associated with an increased risk of myocardial infarction (MI) and stroke in patients with essential hypertension. 1,2 Conversely, interruption of the RAAS by ACE inhibition reduces the risk of MI in patients at risk for coronary artery disease. 3 Recent studies suggest that the effects of activation and interruption of the RAAS on cardiovascular morbidity and mortality derive in part from an interaction of the RAAS and fibrinolytic systems. 4,5 Endogenous fibrinolysis plays a critical role in limiting thrombosis and depends on the balance between plasminogen activators (primarily tissue plasminogen activator, tPA) and plasminogen activator inhibitors (PAI, predominantly PAI-1). 6,7 Both of these essential fibrinolytic components are synthesized locally in the vascular wall (in endothelial and smooth muscle cells), have short half-lives, and circulate in trace concentrations in the plasma. Increased PAI-1 expression has been demonstrated in atherosclerotic lesions. 8,9 Elevated PAI-1 concentrations are seen in youthful survivors of acute MI compared with age-matched control subjects, 10 and elevated levels of PAI-1 appear to be a risk factor for recurrent MI. 11 PAI-1 antigen and activity are ...

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Effect of aging on plasma renin and aldosterone in normal man

Cited by 421 publications

References 35 publications

Abnormalities of Renal Physiology in Systemic Sclerosis

Abnormalities of Renal Physiology in Systemic Sclerosis

The effects of age on the pharmacokinetics and pharmacodynamics of single oral doses of benazepril and enalapril.

Interactive Effect of PAI-1 4G/5G Genotype and Salt Intake on PAI-1 Antigen

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