Reactive Hyperreninemia Is a Major Determinant of Plasma Angiotensin II During ACE Inhibition

Mooser, Vincent; Nussberger, Jürg; Juillerat, Lucienne; Burnier, Michel; Waeber, Bernard; Bidiville, J.; Pauly, N. C.; Brunner, Heinrich

doi:10.1097/00005344-199002000-00015

Cited by 167 publications

(78 citation statements)

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“…This might occur, for example, during treatment with angiotensin converting enzyme inhibitors, when in the face of a plasma potassium rise, plasma angiotensin I1 returns to normal (Mooser et al, 1990) or when incomplete blockade of angiotensin I1…”

Section: Resultsmentioning

confidence: 99%

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Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

1995

Clinical Endocrinology

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Although the biosynthesis of aldosterone in the zona glomerulosa of the adrenal cortex is known to be regulated by a whole array of other agents (ACTH, serotonin, dopamine, atrial natriuretic peptide, acetylcholine) (Miiller, 1988) in this short review we will concentrate on the interplay between the two major regulators, angiotensin I1 and potassium ion ( K ' ) . For many years, specific diseases as well as pathophysiological clinical situations have taught us much about the relation between the renin-angiotensin system and potassium, which has been further explored by animal experimentation. More recently, considerable progress has been achieved in our understanding of the mode of action of both angiotensin I1 and K+ at the cellular level, putting their interplay into a new light. Clinical obsewatlonsThere are many diseases and clinical settings which are caused by abnormalities of secretion of one or other member of the renin-angiotensin system and of the mineralocorticoid family of compounds, mainly aldosterone, or in which these hormones react to or adapt to disturbances of potassium economy. The latter is easily disturbed, which is not surprising given that the total potassium available in the extracellular fluid is 65 mmol, compared with some 5 mol of intracellular potassium. This is distributed mainly in muscle (approximately 2650 mmol), with the erythrocytes, liver and bones each accounting for approximately 250-300 mmol. The turnover of body potassium reflects a daily intake of approximately 100 mmol in the diet, and equivalent excretion mainly by the kidney and to a smaller extent in the stool.In circumstances under which the renin-angiotensin system is primarily stimulated, secondary hyperaldosteronCorrespondence: Professor M.

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Section: Resultsmentioning

confidence: 99%

“…This modulatory role of potassium opposing that of the renin-angiotensin action on the zona glomerulosa can be illustrated in studies performed on healthy subjects (Miiller et al, 1968). When such subjects (Fig.…”

Section: Human Studiesmentioning

confidence: 94%

Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

1995

Clinical Endocrinology

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“…However, it has been recognised for some time that the use of agents to block the RAA system is only partially effective as they interfere with negative feedback mechanisms resulting in a reactive increase in renin activity. As tissues contain ACE-independent pathways for converting angiotensin I to angiotensin II, an "escape" phenomenon can occur [12].…”

Section: Novel Approaches To Blocking the Renin-angiotensinaldosteronmentioning

confidence: 99%

New Treatments for Diabetic Chronic Kidney Disease

MacIsaac¹

2012

10.4172/2161-0959.10001J Nephrol Therapeutic30

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Despite the availability of current therapies that target hyperglycemia, hypertension, dyslipidemia and blockade of the renin-angiotensin-aldosterone (RAA) system, many people with diabetic chronic kidney disease (CKD) still progress to end stage renal disease (ESRD). Hence, new therapies to slow the progression of this important diabetic complication are urgently needed. Disappointingly many promising interventions for diabetic CKD have not coming to fruition when tested in large clinical trials. A recent clinical trial has shown that estimated GFR increases with bardoxolone. However, this finding awaits confirmation that it reflects changes in true GFR and translation into a reduction in clinical events.Here we discuss studies that have evaluated the effects of novel approaches to inhibiting the pathways involved in the pathogenesis of diabetic CKD.

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“…The acute and chronic responses of the RAS to ACE inhibitor therapy differ considerably. Studies in normal volunteers have shown the presence of a reactive hyper-reninaemia associated with the reappearance of bioactive AII octapeptide despite 'maximal' ACE inhibition when defined by substrate techniques (Mooser et al, 1990). Such hormonal changes are of considerable importance as some authors suggest that renin and AII entirely explain the response to ACE inhibitors (Case et al, 1977) such that in hypertension, responses can be defined on the basis of renal perfusion and local renin production in the kidney (Buhler, 1988;Cody, 1984;Laragh, 1989).…”

Section: Acute Vs Chronic Ace Inhibitor Treatmentmentioning

confidence: 99%

Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs.

Lees

Reid

1991

Brit J Clinical Pharma

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1. There is a body of circumstantial and direct evidence supporting the existence and functional importance of a tissue based RAS at a variety of sites. 2. The relation between circulatory and tissue based systems is complex. The relative importance of the two in determining haemodynamic effects is unknown. 3. Despite the wide range of ACE inhibitors already available, it remains unclear whether there are genuine differences related to tissue specificity. 4. Pathological states such as chronic cardiac failure need to be explored with regard to the contribution of tissue based ACE activities in generating acute and chronic haemodynamic responses to ACE inhibitors. 5. The role of tissue vs plasma ACE activity may be clarified by study of the relation between drug concentration and haemodynamic effect, provided that the temporal dissociation is examined and linked to circulating and tissue based changes in ACE activity, angiotensin peptides and sympathetic hormones.

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Reactive Hyperreninemia Is a Major Determinant of Plasma Angiotensin II During ACE Inhibition

Cited by 167 publications

References 0 publications

Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

New Treatments for Diabetic Chronic Kidney Disease

Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs.

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