title: A low-calorie diet improves endothelium-dependent vasodilation in obese patients with essential hypertension.
abstract: BACKGROUND
  Both obesity and hypertension are associated with endothelial dysfunction. The purpose of this study was to investigate the effects of a low-calorie diet on endothelial function in obese patients with essential hypertension.
  
  
  METHODS
  We measured forearm blood flow (FBF) during intra-arterial infusion of acetylcholine (ACh; 7.5, 15, 30 microg/min), an index of endothelium-dependent vasodilation, and isosorbide dinitrate (ISDN; 0.75, 1.5, 3.0 microg/min), an index of endothelium-independent vasodilation, in obese patients with essential hypertension before and after 2 weeks on a low-calorie diet (800 kcal/d). The study included 11 obese hypertensive Japanese patients (mean body mass index, 30.8 +/- 3.6 kg/m2). Fifteen healthy Japanese normotensive individuals were recruited as a control group.
  
  
  RESULTS
  In obese patients with hypertension, the response of FBF to ACh was attenuated compared to healthy individuals (P < .001). Caloric restriction reduced body weight from 77.5 +/- 15.0 to 73.2 +/- 13.5 kg (P < .01), the mean blood pressure from 118.4 +/- 8.7 to 105.7 +/- 8.5 mm Hg (P < .01), fasting plasma insulin from 85.8 +/- 22.8 to 64.8 +/- 27.0 pmol/L (P < .05), serum total cholesterol from 5.30 +/- 0.76 to 4.67 +/- 0.58 mmol/L (P < .05), and low density lipoprotein cholesterol from 3.80 +/- 0.48 to 3.29 +/- 0.44 mmol/L (P < .05). Basal FBF was similar before and after weight reduction. Caloric restriction enhanced the response of FBF to ACh (P < .05), but did not alter the response to ISDN. The intra-arterial infusion of NG-monomethyl-L-arginine (8 micromol/min), a nitric oxide synthase inhibitor, decreased the enhanced ACh-induced blood flow response induced by caloric restriction.
  
  
  CONCLUSIONS
  The present findings suggest that the caloric restriction improves endothelial-dependent vasodilation through an increased release of nitric oxide in obese hypertensive patients.
authors: First Department of Internal Medicine, Hiroshima University, Faculty of Medicine, Japan.
authors: Shota
authors: S
authors: Sasaki
authors: Yukihito
authors: Y
authors: Higashi
authors: Keigo
authors: K
authors: Nakagawa
authors: Masashi
authors: M
authors: Kimura
authors: Kensuke
authors: K
authors: Noma
authors: Satoshi
authors: S
authors: Sasaki
authors: Keiko
authors: K
authors: Hara
authors: Hideo
authors: H
authors: Matsuura
authors: Chikara
authors: C
authors: Goto
authors: Tetsuya
authors: T
authors: Oshima
authors: Kazuaki
authors: K
authors: Chayama
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000368:Aged; D008078:Cholesterol, LDL / Q000097:blood; D004730:Endothelium, Vascular / Q000502:physiology*; D002149:Energy Intake; D005260:Female; D005542:Forearm / Q000098:blood supply; D006801:Humans; D006937:Hypercholesterolemia / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000502:physiology; D009765:Obesity / Q000503:physiopathology*; D012039:Regional Blood Flow / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D008078:Cholesterol, LDL; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D000109:Acetylcholine