Key result
Hypertensive subjects have lower forearm vascular conductance during normothermia (P<0.01) but respond to passive heat stress with similar vasodilation as normotensive subjects (P>0.80).
Why the study?
Does passive heat stress elicit different cutaneous active vasodilation and thermoregulatory reflexes in unmedicated hypertensive humans compared to normotensive humans?
Does passive heat stress elicit different cutaneous active vasodilation and thermoregulatory reflexes in unmedicated hypertensive humans compared to normotensive humans?
Unmedicated hypertensive subjects have reduced baseline forearm vascular conductance but respond to passive heat stress with cutaneous vasodilation similar to normotensive subjects.
Preserved heat-induced vasodilation in unmedicated hypertension suggests no added thermoregulatory risk; leaves open effects in treated or severe disease.
During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects (P < 0.01). During heat stress, FVC rose to similar levels in both groups (P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment (P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia (P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects (P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups (P > 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.
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Kellogg et al. (1998) studied this question. Hypertensive subjects have lower forearm vascular conductance during normothermia (P<0.01) but respond to passive heat stress with similar vasodilation as normotensive subjects (P>0.80).
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