Title page for ETD etd-07282008-135332


Type of Document Dissertation
Author Franke, Warren D
URN etd-07282008-135332
Title Effects of α1-receptor blockade on the hemodynamic responses to exercise in young normotensives and hypertensives
Degree PhD
Department Educational Research and Evaluation
Advisory Committee
Advisor Name Title
Herbert, William G. Committee Chair
Cross, Lawrence H. Committee Member
Gwazdauskas, Francis C. Committee Member
Humphrey, Reed H. Committee Member
Kenner, W. Larry Committee Member
Southard, Douglas R. Committee Member
Keywords
  • Hypertension
Date of Defense 1991-07-05
Availability restricted
Abstract

The purpose of this study was to determine if α1- adrenergic receptor blockade alters the hemodynamic response to exercise in young (<25 yr) male adult borderline hypertensives differently than in young normotensives. Five hypertensive (HTN, MAP>105 mmHg) and 7 normotensive (NTN, MAP<95 mmHg) college-age males underwent two 30 min bouts of cycle ergometry exercise at 50% V02Pk in a warm (25°C, 50% rh) environment; one bout occurred followed α1-receptor blockade with prazosin (HTN-α, NTN-α) and the other following placebo administration (HTN-p, NTN-p). At rest, HTN-p exhibited an elevated cardiac output (Q, p=.024) and MAP (p=.007). Resting Q was similar for HTN-α and NTN-α. Resting heart rate (HR) was elevated more in HTN-α than NTNα (p=.013) and not different for placebo. Resting and exercise forearm blood flows were similar between groups and altered similarly with prazosin. Exercise resulted in greater (p=.035) Q for HTN vs NTN (HTN-u > NTN-α; HTN-p = NTN-p). HR was higher (p=.043) with prazosin for both groups. Regardless of drug treatment, MAP was stable for NTN while it declined after 10 min of exercise in HTN. Rectal temperatures rose above baseline after 10 min. since Q was similar between groups with placebo but not with α1- blockade, and FBF, MAP, and HR were similarly altered between drug trials, it was concluded that young male hypertensives have an elevated blood pressure due to an elevated Q. In this group, α1-blockade may reduce Q by reducing central venous return.

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