Vascular reactivity in obstructive sleep apnea syndrome

The obstructive sleep apnea syndrome (OSAS) is associated with cardiovascul ar disease and systemic hypertension. Because systemic arterial blood press ure is proportional to venodilation and venous return to the heart, we hypo thesized that altered vascular responsiveness might exist in the veins of s ubjects with OSAS. We therefore investigated venodilator responses in awake , normotensive subjects with and without OSAS, using the dorsal hand vein c ompliance technique. Dose-response curves to bradykinin and nitroglycerin w ere obtained from 12 subjects with OSAS and 12 matched control subjects. Ma ximal dilation (E-max) to bradykinin was significantly lower in the OSAS gr oup (62.1% +/- 26.1%) than in the control group (94.3% +/- 10.7%) (p < 0.00 5). Vasodilation to nitroglycerin tended to be lower in the OSAS group (78. 6% +/- 31.8%) than the control group (100.3% +/- 12.9%), but this effect di d not reach statistical significance. When six of the OSAS subjects were re tested after 60 d of treatment with nasal continuous positive airway pressu re (CPAP), E-max to bradykinin rose from 60.3% +/- 20.3% to 121.4% +/- 26.9 % (p < 0.01). Vasodilation to nitroglycerin also increased, but this effect did not reach statistical significance. These results demonstrate that a b lunted venodilatory responsiveness to bradykinin exists in OSAS. This effec t appears to be reversible with nasal CPAP therapy.