Resistance vessel endothelial function in healthy humans during transient postprandial hypertriglyceridemia.
A single high-fat meal transiently impairs conduit vessel endothelial function. We tested the hypothesis that transient moderate hypertriglyceridemia by consumption of a high-fat meal impairs forearm resistance vessel endothelial function. Fifteen healthy persons consumed isocaloric high- and low-fat meals (900 calories, 50 and 4 g of fat, respectively) on 2 separate days. Endothelial function in forearm resistance vessels was assessed using blood flow responses to local intra-arterial infusion of nitroprusside, acetylcholine, bradykinin, and verapamil from 1 to 3 hours after the meal. Serum triglycerides increased from 112 +/- 15 mg/dl preprandially to 165 +/- 20 mg/dl 4 hours after the high-fat meal, which was a significantly larger increase than levels after the low-fat meal (p = 0.01). Total cholesterol, high-density lipoprotein, low-density lipoprotein, and very low density lipoprotein (VLDL) cholesterol concentrations did not change. There was no difference between high- and low-fat meals in vasodilation to the endothelium-dependent agents acetylcholine (low fat, 337 +/- 47%; high fat, 356 +/- 88%; p = 0.81) and bradykinin (low fat, 312 +/- 39%; high fat, 403 +/- 111%; p = 0.28), or to the endothelium-independent vasodilators nitroprusside (low fat, 313 +/- 27%; high fat, 355 +/- 42%; p = 0.31) and verapamil (low fat, 292 +/- 48%; high fat, 299 +/- 36%; p = 0.18). Thus, transient hypertriglyceridemia due to a high-fat meal does not impair resistance vessel endothelial function. These data contrast with previous studies in conduit vessels that showed substantial endothelial dysfunction. Therefore, although high-fat intake may contribute to large artery atherosclerosis, it probably does not predispose to hypertension or ischemia through resistance vessel dysfunction. The results suggest that the mechanism by which triglyceride-rich lipoproteins impair endothelial function in conduit vessels is not operative in resistance vessels.
Gudmundsson
G S
GS
Department of Internal Medicine, General Clinical Research Center, University of Iowa Hospitals and Clinics, Iowa City 52242, USA.
Sinkey
C A
CA
Chenard
C A
CA
Stumbo
P J
PJ
Haynes
W G
WG
D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D001920:Bradykinin / Q000494:pharmacology; D018592:Cross-Over Studies; D004041:Dietary Fats / Q000008:administration & dosage*; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D005542:Forearm / Q000098:blood supply; D006801:Humans; D015228:Hypertriglyceridemia / Q000503:physiopathology*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D019518:Postprandial Period; D012016:Reference Values; D012039:Regional Blood Flow; D014280:Triglycerides / Q000097:blood; D014655:Vascular Resistance / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014700:Verapamil / Q000494:pharmacology
D004041:Dietary Fats; D014280:Triglycerides; D014665:Vasodilator Agents; D009599:Nitroprusside; D014700:Verapamil; D000109:Acetylcholine; D001920:Bradykinin