Venous capacity and compliance in hypertensive adults: influence of hypoxia and hyperoxia

Abstract

In hypertension, the cardiorespiratory responses to peripheral chemoreflex activation (hypoxia) and inactivation (hyperoxia) are reportedly augmented, but the impact on peripheral venous function is unknown. We tested the hypothesis that in hypertensives, both hypoxia and hyperoxia evoke more pronounced changes in lower limb venous capacity and compliance, than in age-matched normotensives. In 10 hypertensive [HTN: 7 women; age: 71.7±3.7 yr, mean blood pressure (BP): 101±10 mmHg, mean±SD] and 11 normotensive (NT: 6 women; age: 67.7±8.0 yr, mean BP 89±11 mmHg) participants, great saphenous vein cross-sectional area (GSV CSA; Doppler ultrasound) was measured during a standard 60 mmHg thigh cuff inflation-deflation protocol. Separate conditions of room air, hypoxia (fraction of inspired oxygen [FIO2]: 0.10) and hyperoxia (FIO2: 0.50) were tested. In HTN, GSV CSA was decreased in hypoxia (5.6±3.7 mm2, P=0.041) compared with room air (7.3±6.9 mm2), whereas no change was observed with hyperoxia (8.0±9.1 mm2, P=0.988). In NT, no differences in GSV CSA were observed between any condition ( P=0.299). Hypoxia enhanced GSV compliance in HTN (-0.0125±0.0129 vs. -0.0288±0.0090 mm2·mmHg-1, room air vs. hypoxia, respectively; P=0.004), but it was unchanged in NT (-0.0139±0.0121 vs. -0.0093±0.0066 mm2·mmHg-1, room air vs. hypoxia, respectively; P<0.541). Venous compliance was unaltered with hyperoxia in both groups ( P<0.05). In summary, compared with NT, hypoxia elicits a decrease in GSV CSA and enhanced GSV compliance in HTN, indicating enhanced venomotor responsiveness to hypoxia.

Forgotten Circulation: Reduced Mesenteric Venous Capacitance in Hypertensive Rats Is Improved by Decreasing Sympathetic Activity

“…15 A recent study in humans with hypertension reported augmented venomotor responsiveness to hypoxia. 16 A potential causative role of venous neurovascular control is suggested by studies showing that nonselective (ie, arterioles and venules) denervation of the mesenteric 17 and splanchnic 18 vascular beds ameliorated hypertension. However, the specific contribution of venoconstrictor sympathetic drive remains equivocal.…”