Effect of Angiotensin II on the peripheral vasculature during rest low, mild, and heavy exercise workloads

Abstract

INTRODUCTION: Exercise mediated increases in sympathetic activity leads to increased production of the non-adrenergic vasoconstrictor Angiotensin II (AngII). PURPOSE: To test the hypothesis that as exercise intensity increases AngII plays a greater role in the control of the peripheral vasculature. METHODS: We compared the vasoconstrictor responses before and after blockade of the Angiotensin type 1 receptor (AT1) with Valsartan (80mg) in healthy humans (n=5) during rest and knee-extensor exercise at ~40%, 60% and 80% of workmax. Neck suction (NS) stimuli were used to partially withdraw the arterial baroreflex mediated sympathetic activity. Ultrasound Doppler provided measurements of femoral blood flow (FBF) and blood pressures were used to calculate femoral vascular conductance (FVC). RESULTS: FVC was unchanged at rest and during the 40% and 60% exercise trials with Valsartan, however during 80% exercise with Valsartan FVC was increased by 17 ± 3% with Valsartan when compared to control exercise. NS elicited significant increases in FVC during rest and all 3 exercise trials. During 80% exercise NS mediated increases in FVC was further increased by 40 ± 7% with Valsartan when compared to control exercise. CONCLUSION: These data identify that as exercise intensity and duration increases AngII plays a greater percentage role in the control of the peripheral vasculature. Supported in part by NIH grant #HL-045547