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Effect of Prazosin on the Peripheral Vasculature during Rest Low, Mild, and Heavy Exercise Workloads.: 878June 1 1:00 PM - 1:15 PM

Brothers, R Matthew; Ogoh, Shigehiko; Eubank, Wendy; Dawson, Ellen; Hawkins, Megan; Barnes, Quinton; O-Yurvati, Albert; Raven, Peter B. FACSM

Medicine & Science in Sports & Exercise: May 2007 - Volume 39 - Issue 5 - p S84
doi: 10.1249/01.mss.0000273237.09699.f2
F-15 Free Communication/Slide -Vascular Function: JUNE 1, 2007 1:00 PM -2:30 PM ROOM: 262

Univ. of North Texas Health Science, Forth Worth, TX. (Sponsor: Peter B. Raven, FACSM)


INTRODUCTION: Metabolic inhibition of alpha-1 mediated vasoconstriction in exercising muscles is evident in both animal and human models. A majority of the studies investigating the role of alpha-1 receptors have infused exogenous α1-receptor agonists intra-arterially to activate these receptors. However the role of physiological activation of these receptors in humans is incompletely understood.

PURPOSE: To test the hypothesis that as exercise intensity increases physiological activation of α1-receptors has a decreased role in the control of the peripheral vasculature in exercising muscles.

METHODS: We compared the vasoconstrictor responses before and after oral ingestion of the α1-receptor blocker Prazosin (1mg/20kg of body weight) in healthy humans (n=5) during rest and dynamic knee-extensor exercise at roughly 40%, 60% and 80% of workloadmax. Neck pressure (NP) stimuli were used to unload carotid baroreceptors thus leading to sympathoexcitation. Ultrasound Doppler provided direct measurements of femoral blood flow (FBF) and intra-arterially measured blood pressures were used to calculate femoral vascular conductance (FVC).

RESULTS: Prazosin resulted in significant increases FVC at rest when compared to the control protocol (+68 ± 6%). During exercise the Prazosin mediated increases in FVC decreased with increasing exercise intensities (+68 ± 4%, +39 ±4%, and +23 ± 6% respectively). In both conditions “functional sympatholyis” was occurring because the NP mediated vasoconstriction was attenuated in an exercise intensity dependent manner. During NP the % decreases in FVC were not significantly different between conditions.

CONCLUSIONS: These data demonstrate that vasoconstriction elicited by physiological activation of ?1 -receptors with circulating endogenous agonists as a result of intense dynamic exercise is reduced as exercise intensity increases. Additionally there was a reduced response to sympathetically mediated vasoconstriction as a result of functionally unloading the carotid baroreceptors with NP stimuli in both conditions, i.e. functional sympatholysis was present. Furthermore the NP mediated vasoconstriction was attenuated to a similar degree in both conditions.

Supported in part by NIH grant # HL-045547

© 2007 American College of Sports Medicine