Resting and maximal forearm skin blood flows are reduced in hypertension

Abstract

To find whether the vasodilator capacity of nonacral skin is reduced in hypertension, we measured forearm blood flow by venous occlusion plethysmography in 10 seated normotensive (mean±SD mean arterial pressure, 94±5 mm Hg) and 10 hypertensive (112±9 mm Hg) men at rest for 39 minutes while the forearm was heated with water at 42°C, a maneuver known to selectively and maximally vasodilate skin. Blood pressure, measured every 5 minutes, did not change with heating. We found that in the normotensive group resting forearm blood flow was higher (3.64±1.12 versus 2.48±0.58 ml/100 ml tissue per minute, p<0.001; normotensive group versus hypertensive group) and resting forearm vascular resistance lower (30.17±10.99 versus 48.88±17.37 mm Hg · min · 100 ml tissue per minute, p<0.05; normotensive group versus hypertensive group), and maximal forearm blood flow with local heating was higher (29.32±11.99 versus 18.19±4.50 ml/100 ml tissue per minute, p<0.018; normotensive group versus hypertensive group) and vascular resistance lower (4.07±1.04 versus 6.54±1.17 mm Hg · min · 100 ml tissue per minute, p<0.005; normotensive group versus hypertensive group). To find whether this degree and duration of local warming maximally vasodilated the skin in hypertensive subjects (as it does in normotensive subjects), we measured forearm skin blood flow before and during local heating plus 10 minutes of ischemia using a laser Doppler flowmeter. Although six of 10 hypertensive subjects displayed a further increase in forearm skin blood flow when ischemia was added to local heating (mean, 65.3%; range, 53.5-81%), overall this was not a significant increase over that seen with heating alone (p>0.30). We conclude: 1) the elevated minimal vascular resistance seen in some regional circulations in hypertensive subjects is also seen in nonacral skin, probably reflecting structural changes in skin blood vessels in hypertension; 2) skin is a useful site to study vascular changes in hypertension; and 3) these changes could contribute to impaired thermoregulatory mechanisms in hypertension.