Caitlin C Fermoyle1,2, Ryan M Broxterman1,2, D Taylor La Salle3, Stephen M Ratchford1,2, Paul N Hopkins4, Russell S Richardson1,2,3, Joel D Trinity1,2,3. 1. Geriatric Research, Education, and Clinical Center, George E. Whalen VA Medical Center. 2. Division of Geriatrics, Department of Internal Medicine. 3. Department of Nutrition and Integrative Physiology. 4. Division of Cardiovascular Genetics, Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA.
Abstract
BACKGROUND: Vascular dysfunction, an independent risk factor for cardiovascular disease, often persists in patients with hypertension, despite improvements in blood pressure control induced by antihypertensive medications. METHODS: As some of these medications may directly affect vascular function, this study sought to comprehensively examine the impact of reducing blood pressure, by a nonpharmacological approach (5 days of sodium restriction), on vascular function in 22 hypertensive individuals (14 men/8 women, 50 ± 10 years). Following a 2-week withdrawal of antihypertensive medications, two 5-day dietary phases, liberal sodium (liberal sodium, 200 mmol/day) followed by restricted sodium (restricted sodium, 10 mmol/day), were completed. Resting blood pressure was assessed and vascular function, at both the conduit and microvascular levels, was evaluated by brachial artery flow-mediated dilation (FMD), reactive hyperemia, progressive handgrip exercise, and passive leg movement (PLM). RESULTS: Despite a sodium restriction-induced fall in blood pressure (liberal sodium: 141 ± 14/85 ± 9; restricted sodium 124 ± 12/79 ± 9 mmHg, P < 0.01 for both SBP and DBP), FMD (liberal sodium: 4.6 ± 1.8%; restricted sodium: 5.1 ± 2.1%, P = 0.27), and reactive hyperemia (liberal sodium: 548 ± 201; restricted sodium: 615 ± 206 ml, P = 0.08) were not altered. Similarly, brachial artery vasodilation during handgrip exercise was not different between conditions (liberal sodium: Δ0.36 ± 0.19 mm; restricted sodium: Δ0.42 ± 0.18 mm, P = 0.16). Lastly, PLM-induced changes in peak blood flow (liberal sodium: 5.3 ± 2.5; restricted sodium: 5.8 ± 3.6 ml/min per mmHg, P = 0.30) and the total vasodilatory response [liberal sodium: 2 (0.9-2.5) vs. restricted sodium: 1.7 (1.1-2.6) ml/min per mmHg; P = 0.5] were also not different between conditions. CONCLUSION: Thus vascular dysfunction, at both the conduit and microvascular levels, persists in patients with hypertension even when blood pressure is acutely reduced by a nonpharmacological approach.
BACKGROUND: Vascular dysfunction, an independent risk factor for cardiovascular disease, often persists in patients with hypertension, despite improvements in blood pressure control induced by antihypertensive medications. METHODS: As some of these medications may directly affect vascular function, this study sought to comprehensively examine the impact of reducing blood pressure, by a nonpharmacological approach (5 days of sodium restriction), on vascular function in 22 hypertensive individuals (14 men/8 women, 50 ± 10 years). Following a 2-week withdrawal of antihypertensive medications, two 5-day dietary phases, liberal sodium (liberal sodium, 200 mmol/day) followed by restricted sodium (restricted sodium, 10 mmol/day), were completed. Resting blood pressure was assessed and vascular function, at both the conduit and microvascular levels, was evaluated by brachial artery flow-mediated dilation (FMD), reactive hyperemia, progressive handgrip exercise, and passive leg movement (PLM). RESULTS: Despite a sodium restriction-induced fall in blood pressure (liberal sodium: 141 ± 14/85 ± 9; restricted sodium 124 ± 12/79 ± 9 mmHg, P < 0.01 for both SBP and DBP), FMD (liberal sodium: 4.6 ± 1.8%; restricted sodium: 5.1 ± 2.1%, P = 0.27), and reactive hyperemia (liberal sodium: 548 ± 201; restricted sodium: 615 ± 206 ml, P = 0.08) were not altered. Similarly, brachial artery vasodilation during handgrip exercise was not different between conditions (liberal sodium: Δ0.36 ± 0.19 mm; restricted sodium: Δ0.42 ± 0.18 mm, P = 0.16). Lastly, PLM-induced changes in peak blood flow (liberal sodium: 5.3 ± 2.5; restricted sodium: 5.8 ± 3.6 ml/min per mmHg, P = 0.30) and the total vasodilatory response [liberal sodium: 2 (0.9-2.5) vs. restricted sodium: 1.7 (1.1-2.6) ml/min per mmHg; P = 0.5] were also not different between conditions. CONCLUSION: Thus vascular dysfunction, at both the conduit and microvascular levels, persists in patients with hypertension even when blood pressure is acutely reduced by a nonpharmacological approach.
Authors: Fernando Elijovich; Myron H Weinberger; Cheryl A M Anderson; Lawrence J Appel; Michael Bursztyn; Nancy R Cook; Richard A Dart; Christopher H Newton-Cheh; Frank M Sacks; Cheryl L Laffer Journal: Hypertension Date: 2016-07-21 Impact factor: 10.190
Authors: Patricia C Underwood; Bindu Chamarthi; Jonathan S Williams; Anand Vaidya; Rajesh Garg; Gail K Adler; Marissa P Grotzke; Gitana Staskus; Devendra Wadwekar; Paul N Hopkins; Claudio Ferri; Anthony McCall; Donald McClain; Gordon H Williams Journal: J Clin Endocrinol Metab Date: 2012-08-03 Impact factor: 5.958
Authors: John McDaniel; Anette S Fjeldstad; Steve Ives; Melissa Hayman; Phil Kithas; Russell S Richardson Journal: J Appl Physiol (1985) Date: 2009-11-12