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Endothelium‐dependent dilation is inversely related to hematocrit among healthy young and older adults
Author(s) -
Pierce Gary L,
Donato Anthony J,
LaRocca Thomas J,
Jablonski Kristen L,
Seals Douglas R
Publication year - 2012
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.26.1_supplement.865.13
Subject(s) - medicine , brachial artery , hematocrit , sodium nitroprusside , endothelium , young adult , endothelial dysfunction , hemoglobin , vasodilation , endocrinology , nitric oxide , cardiology , blood pressure
Hemoglobin (Hb) is a catalytic sink for endothelial‐released nitric oxide (NO) into the artery lumen. Because elevated hematocrit (Hct) within the “normal range” is related to cardiovascular (CV) events, we hypothesized that a higher normal Hct would be associated with lower endothelium‐dependent dilation (EDD) in both young and older adults. Forearm blood flow (FBF) responses to incremental brachial artery infusions of acetylcholine (EDD) and sodium nitroprusside (endothelium‐independent dilation, EID) were assessed in young (n=22; mean ± SE; age 24 ± 1 yrs) and older (n=58; 62 ± 1 yrs) healthy adults with normal Hct. EDD (peak FBF) was lower in young and older adults (Young: 15.1 ± 2.6 vs. 25.1 ± 3.7 ml/ml FAV/min; Older: 12.1 ± 1.4 vs.16.8 ± 1.8, both P<0.05) with Hct above vs. below sex‐adjusted median values, but EID was not different. EDD was inversely related to Hct (n=80, r=−0.43, P<0.01), and this remained significant after adjustment for age, sex and other clinical characteristics. In a subset (n=18), inhibition of NO (Ng‐monomethyl‐L‐arginine) reduced EDD more in adults with higher (−63%) vs. lower (−39%) Hct, abolishing group differences (P>0.05). High‐normal Hb is associated with lower EDD in both young and older healthy adults as a consequence of reduced NO bioavailability. Impaired endothelial function may contribute to the increased CV risks of high normal Hct. NIH AG013038, AG000279, UL1 RR025780