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Cutaneous Microvascular Function in Hypertensive Adults is not Altered Following 16‐weeks of Pharmacological Antihypertensive Treatment
Author(s) -
Dillon Gabrielle A,
Greaney Jody L,
Stanhewicz Anna E,
Alexander Lacy M
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.696.6
Subject(s) - medicine , sodium nitroprusside , endothelial dysfunction , vasodilation , blood pressure , vasoconstriction , cardiology , endocrinology , endothelium , perfusion , agonist , nitric oxide , receptor
Hypertension is characterized by pervasive microvascular endothelial dysfunction, resulting in a shift toward a proconstrictor vascular profile and contributing to increased cardiovascular morbidity and mortality. Cross‐sectional data suggest that pharmacologically lowering blood pressure (BP) is associated with improvements in microvascular function via endothelium‐dependent mechanisms. Well controlled longitudinal studies directly assessing mechanisms underlying microvascular dysfunction in hypertensive adults before and after a pharmacological antihypertensive intervention have not been performed. We tested the hypothesis that endothelium‐dependent dilation would be improved and adrenergic‐mediated vasoconstriction would be attenuated following 16‐weeks of pharmacological treatment to lower BP. Microvascular function was assessed before and after 16‐weeks of antihypertensive treatment (diuretic or angiotensin converting enzyme inhibitor) in eleven stage II hypertensive adults (9 men, 54±3 yrs, 29±1 kg/m 2 , resting BP 143±4/93±3 mmHg). Red blood cell flux (laser Doppler flowmetry) was measured during graded intradermal microdialysis perfusion of the endothelium‐dependent agonist acetylcholine (ACh; 10 −10 –10 −1 M) and the adrenergic receptor agonist norepinephrine (NE, 10 −12 –10 −2 M). Cutaneous vascular conductance (CVC; flux/mmHg) was normalized to and expressed as a percentage of either baseline or maximal conductance (28 mM sodium nitroprusside and heat to 43°C). Resting BP was reduced following treatment (143±4/93±3 pre vs. 105±4/68±2 mmHg post; p=0.003). Neither baseline (0.19±0.03 pre vs. 0.19±0.03 post flux/mmHg; p=0.97) nor maximal CVC (2.16±0.48 pre vs. 1.44±0.24 post flux/mmHg; p=0.24) were different following treatment. There was no difference in ACh‐induced vasodilation following antihypertensive treatment (logEC 50 : −4.28±0.48 pre vs. −3.15±4.68 post; p=0.83). Further, NE‐induced vasoconstriction was not different after treatment (logEC 50 : −4.85±1.23 pre vs. −6.28±0.68 post; p=0.65). Contrary to our hypothesis, these preliminary data suggest that a 16‐week pharmacological antihypertensive treatment to reduce BP does not improve cutaneous microvascular function in middle‐aged hypertensive adults. Support or Funding Information NIH R01HL093238 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .