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1 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas 75231; and 2 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390
To test the hypothesis that
phenylephrine-induced elevations in blood pressure are attenuated in
heat-stressed humans, blood pressure was elevated via steady-state
infusion of three doses of phenylephrine HCl in 10 healthy subjects in
both normothermic and heat stress conditions. Whole body heating
significantly increased sublingual temperature by ~0.5°C, muscle
sympathetic nerve activity (MSNA), heart rate, and cardiac output and
decreased total peripheral vascular resistance (TPR; all
P < 0.005) but did not change mean arterial blood
pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was
significantly attenuated during the heat stress [
MAP 8.4 ± 1.2 mmHg;
TPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (
MAP 15.4 ± 1.4 mmHg,
TPR
7.13 ± 1.18 PRU; all P < 0.001). The sensitivity
of baroreflex control of MSNA and heart rate, expressed as the slope of
the relationship between MSNA and diastolic blood pressure, as well as
the slope of the relationship between heart rate and systolic blood
pressure, respectively, was similar between thermal conditions (each
P > 0.05). These data suggest that
phenylephrine-induced elevations in MAP are attenuated in heat-stressed
humans without affecting baroreflex control of MSNA or heart rate.
baroreflex sensitivity; vasoconstrictor agents; muscle sympathetic nerve activity; heart rate; whole body heating
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