Ethnic differences in resistance artery contractility of normotensive pregnant women.
Black women are at a greater risk to develop hypertension during pregnancy, with a 4.5 times higher rate of fatal preeclampsia than white women. Therefore, it is important to identify factors that may affect this risk. Our group previously proposed that high activity of the central regulatory enzyme of energy metabolism, creatine kinase (CK), may increase ATP-buffering capacity and lead to enhanced vascular contractility and reduced nitric oxide bioavailability. Therefore, we assessed microvascular contractility characteristics in isolated resistance arteries from self-defined black and white normotensive pregnant women using a Mulvany-Halpern myograph. Additionally, morphology was assessed with electron microscopy. Resistance-sized arteries obtained from omentum donated during cesarean sections (11 black women and 20 white women, mean age: 34 yr) studied in series showed similar morphology but significantly greater maximum contractions to norepinephrine (10(-5) M) in blacks [14.0 mN (1.8 SE)] compared with whites [8.9 mN (1.4 SE), P = 0.02]. Furthermore, we found greater residual contractility after the specific CK inhibitor dinitrofluorobenzene (10(-6) M) in black women [55% (6 SE)] compared with white women [28% (4 SE), P = 0.001] and attenuated vasodilation after bradykinin (10(-7) M) in black women [103% (6 SE)] compared with white women [84% (5 SE), P = 0.023], whereas responses to sodium nitroprusside (10(-4) M) and amlodipine (10(-6) M) were similar. We conclude that compared with white women, normotensive pregnant black women display greater resistance artery contractility and evidence of higher vascular CK activity with attenuated nitric oxide synthesis. These findings in normotensives may imply that the black population is at risk for a further incline in pregnancy-related hypertensive disorders.
Depts. of Internal and Vascular Medicine, F4-222, Academic Medical Center, Meibergdreef 9, Amsterdam 1105 AZ, The Netherlands. l.m.brewster@amc.uva.nl
L M
LM
Brewster
Z
Z
Taherzadeh
S
S
Volger
J F
JF
Clark
T
T
Rolf
H
H
Wolf
E
E
Vanbavel
G A
GA
van Montfrans
D000263:Adenylate Kinase / Q000037:antagonists & inhibitors / Q000378:metabolism; D000328:Adult; D001158:Arteries / Q000502:physiology; D044383:Black People; D003402:Creatine Kinase / Q000037:antagonists & inhibitors / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D054624:Health Status Disparities; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000208:ethnology* / Q000378:metabolism / Q000503:physiopathology; D046529:Microscopy, Electron, Transmission; D009213:Myography; D009426:Netherlands; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009820:Ohio; D009852:Omentum / Q000098:blood supply*; D011247:Pregnancy; D018570:Risk Assessment; D012307:Risk Factors; D014655:Vascular Resistance; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology; D044465:White People; D001741:Black or African American
D004791:Enzyme Inhibitors; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D003402:Creatine Kinase; D000263:Adenylate Kinase