Correlates of endothelial function and the peak systolic blood pressure response to a graded maximal exercise test

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Abstract

Purpose: An elevated systolic blood pressure (SBP) response to a graded maximal exercise stress test (GEST) may be a predictor of endothelial dysfunction and hypertension. We examined relationships among the GEST peak SBP response and indicators of endothelial function. Methods: Men (n= 48, 43.7 ± 1.4. yr) with high BP (145.1 ± 1.5/85.5 ± 1.1. mm. Hg) completed a GEST. Peak SBP was the highest SBP achieved during the GEST. Blood samples were taken for fasting glucose and insulin, nitric oxide (NO), and DNA. Endothelial nitric oxide synthase (NOS3, rs2070744) -786 T > C genotyping was determined by PCR. NOS3 genotypes were combined using a dominant model [TT (n= 24); TC/CC (n= 24)]. Brachial artery reactivity (BAR) was determined via ultrasound before, 1. min, and 3. min post occlusion and calculated as % change. Analysis of variance (ANOVA) tested changes in the peak SBP GEST response by NOS3 genotype. Multiple variable regression analyses examined relationships among the GEST peak SBP response and measures of endothelial function. Results: %BAR change at 1min (r 2=0.093, p=0.020), glucose (r 2=0.062, p=0.014), NOS3 -786 T>C (r 2=0.040, p=0.024), NO (r 2=0.037, p=0.064), and age (r 2=0.009, p=0.014) explained 24.1% of the GEST peak SBP response (p=0.043). The GEST peak SBP change from baseline was 11.1±5.0mmHg higher among those with the NOS3 C allele (92.4mmHg+3.8) than the NOS3 TT genotype (81.3mmHg+3.2) (p=0.03). Conclusion: Indicators of endothelial function appear to explain a clinically significant portion of the GEST peak SBP response. Further investigation is needed to unravel the mechanisms by which endothelial function influences the GEST peak SBP response. © 2012.

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Olson, K. M., Augeri, A. L., Seip, R. L., Tsongalis, G. J., Thompson, P. D., & Pescatello, L. S. (2012). Correlates of endothelial function and the peak systolic blood pressure response to a graded maximal exercise test. Atherosclerosis, 222(1), 202–207. https://doi.org/10.1016/j.atherosclerosis.2012.01.027

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