angiotensin-iii and Kidney-Failure--Chronic

The renin-angiotensin-aldosterone system (RAAS) plays a major role in the regulation of blood pressure and homeostasis. Therefore, it is a commonly used target for pharmacotherapy of cardiovascular diseases in adults. However, the efficacy of this pharmacotherapy can only be limitedly derived into children. Comprehensive knowledge of the humoral parameters acting in the paediatric RAAS (e.g. angiotensin I, angiotensin II, angiotensin 1-7, angiotensin III, and angiotensin IV) might facilitate a more effective and rational pharmacotherapy in children. Therefore, this review aims to provide an overview of the maturing RAAS. Out of 925 identified records, 35 publications were classified as relevant. Physiological and pathophysiological concentrations of angiotensin peptides were compiled and categorised according to European Medicines Agency age groups. Age has a major impact on circulating angiotensin I, angiotensin II, and angiotensin 1-7, which is reflected in an age-dependent decrease during childhood. In contrast to data obtained in adults, no gender-related differences in angiotensin levels were identified. The observed increase in peptide concentrations regarding cardiac- and renal-diseased children is influenced by surgical repair, while evidence for a pharmacological impact is conflicting. A comprehensive set of angiotensin I, angiotensin II, and angiotensin 1-7 values from neonates up to adolescents was compiled. Indicating age as a strong effector. However, evidence about potential promising targets of the RAAS like angiotensin III and angiotensin IV is still lacking in children.

Topics: Adolescent; Age Factors; Angiotensin I; Angiotensin II; Angiotensin III; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Child; Child, Preschool; Female; Humans; Hypertension; Infant; Infant, Newborn; Kidney Failure, Chronic; Male; Peptide Fragments; Renin-Angiotensin System

ACTH and des-Asp1-angiotensin II (AIII) can raise plasma aldosterone. To assess the threshold for ACTH and AIII stimulated adrenal steroidogenesis we infused ACTH (from 0.03 to 10 ng ACTH/min) and AIII (from 0.1 to 20 ng/kg/min) to dexamethasone pretreated sodium deplete normal subjects and patients with primary aldosteronism, chronic renal failure, and end stage renal disease maintained with continuous ambulatory peritoneal dialysis. Plasma aldosterone in the primary aldosteronism group increased significantly at 0.3 ng ACTH/min compared with 1 to 3 ng ACTH/min in all other groups. The threshold dose for an ACTH stimulated rise in plasma aldosterone was as at least as low as the dose necessary to raise cortisol in all groups. The threshold dose for an AIII stimulated rise in plasma aldosterone was 4 ng/kg/min in normals and between 1 and 3 ng/kg/min in primary aldosteronism. The metabolic clearance rate (MCR) of aldosterone was determined by constant infusion of [3H]-aldosterone. The decline in MCR during AIII infusion contributed less than 15% to the rise in plasma aldosterone in normals and patients with primary aldosteronism.

Topics: Adrenocorticotropic Hormone; Aldosterone; Angiotensin II; Angiotensin III; Dexamethasone; Electrolytes; Humans; Hyperaldosteronism; Kidney Failure, Chronic; Kinetics; Metabolic Clearance Rate; Reference Values