Premium
Circulating adrenomedullin in obstructive sleep apnoea
Author(s) -
SCHULZ RICHARD,
FLÖTOTTO CHRISTIANE,
JAHN ANDREAS,
EISELE HANS JOACHIM,
WEISSMANN NORBERT,
SEEGER WERNER,
ROSE FRANK
Publication year - 2006
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/j.1365-2869.2006.00498.x
Subject(s) - medicine , continuous positive airway pressure , adrenomedullin , polysomnography , blood pressure , cardiology , venous blood , blood sampling , endocrinology , anesthesia , obstructive sleep apnea , gastroenterology , apnea , receptor
Summary Adrenomedullin (AM) is a potent endothelial‐derived vasodilator secreted under the influence of various stimuli such as hypoxia, shear stress and cytokines. As all of these stimuli might be active under the conditions of obstructive sleep apnoea (OSA), we hypothesized that vascular AM production is increased in these patients. The study included 41 consecutive OSA patients and 28 control subjects without sleep‐disordered breathing who were recruited from a pool of patients hospitalized for other reasons. Both groups were matched for anthropometric and comorbid factors. In all patients, i.e. OSA and controls, peripheral venous blood samples were taken at 07:00 hours after diagnostic polysomnography. In subsets of OSA patients, this was repeated after two nights of continuous positive airway pressure (CPAP) therapy ( n = 28) and after several months of constant CPAP use ( n = 11). The controls and the untreated OSA patients did not have serial blood sampling. In all blood samples, plasma AM levels were measured by an enzyme immunoassay kit. At baseline, the OSA patients had markedly elevated AM concentrations when compared to the controls. There were no differences between normo‐ and hypertensive OSA patients. After two nights of CPAP therapy, AM levels significantly decreased. Patients on long‐term CPAP treatment showed complete normalization of plasma AM concentrations. In conclusion, this pilot study suggests that circulating AM is increased in untreated OSA irrespective of coexistent arterial hypertension and declines after CPAP therapy. AM upregulation might be considered as an adaptive mechanism to counteract the emergence of OSA‐related cardiovascular disease.