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
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.