PRESSURE-HEART RATE RESPONSES TO ALPHA-ADRENERGIC STIMULATION AND HORMONAL-REGULATION IN NORMOTENSIVE PATIENTS WITH OBSTRUCTIVE SLEEP-APNEA

Citation
D. Maillard et al., PRESSURE-HEART RATE RESPONSES TO ALPHA-ADRENERGIC STIMULATION AND HORMONAL-REGULATION IN NORMOTENSIVE PATIENTS WITH OBSTRUCTIVE SLEEP-APNEA, American journal of hypertension, 10(1), 1997, pp. 24-31
Citations number
41
Categorie Soggetti
Peripheal Vascular Diseas
ISSN journal
08957061
Volume
10
Issue
1
Year of publication
1997
Pages
24 - 31
Database
ISI
SICI code
0895-7061(1997)10:1<24:PRRTAS>2.0.ZU;2-3
Abstract
Seven normotensive untreated patients with obstructive sleep apnea (OS A) and five control subjects without OSA were compared. Patients with cardiac dilation, chronic airflow limitation, liver and kidney disease , or diabetes mellitus were excluded. Change in pressure-heart rate re lation to alpha-adrenergic stimulation (P-HRR), extracellular volume ( ECV), and plasma volume (V-p) were measured during daytime. Plasma atr ial natriuretic peptide (ANP), plasma renin and aldosterone concentrat ions were obtained at 1 hour intervals during the night. A mean apnea/ hypopnea index (AHI) of 52.2 +/- 23.9/h and a mean lowest arterial oxy gen saturation (SaO(2)) of 61.2 +/- 19.3% (mean +/- SD) were determine d from polysomnographic monitoring in the patient group. Release of AN P was significantly higher during sleep in OSA patients than in contro l subjects (P < .01), with a maximum concentration between 4 and 6 AM in the former. Daytime ECV was significantly higher (P < .05) and V-p significantly lower (P < .05) in OSA patients. Night maximum concentra tion of ANP (max ANP) was negatively related to AHI (P < .05). P-HRR w as negatively related to AHI (P < .05) and positively related to max A NP (P < .05). In conclusion, OSA syndrome alters hormonal system contr ol of body fluid compartment regulation. The decreased response in nig ht max ANP secretion in the most severe OSA patients could be explaine d by the smaller V-p observed in these patients, decreasing atrial and ventricular pressure loading. Furthermore, alteration of P-HRR, corre lated to AHI and max ANP, strengthens the hypothesis that patients who develop hypertension are those in whom the protective mechanism of AN P release failed. (C) 1997 American Journal of Hypertension, Ltd.