Flow-induced arterial enlargement is inhibited by suppression of nitric oxide synthase activity in vivo

Surgery. 1997 Aug;122(2):273-9; discussion 279-80. doi: 10.1016/s0039-6060(97)90018-0.

Abstract

Background: Acute flow-induced arterial dilation is mediated by nitric oxide (NO). The role of NO in chronic flow-induced adaptive enlargement is unknown. We assessed the role of NO in arterial adaptation to increased blood flow (BF).

Methods: Iliac artery BF was increased in adult male rats by creating a left femoral arteriovenous fistula. Left iliac BF and diameter were measured, and wall shear stress was calculated. The effect of the NO synthase inhibitor N omega-nitro-L-arginine-methyl ester (L-NAME) was studied in arteriovenous fistula rats divided into three groups (group 1, vehicle, group 2, 0.5 mg/ml; group 3, 2 mg/ml) in drinking water. Arterial diameter, blood pressure, and medial cell density were assessed after 21 days. Left iliac cyclic guanosine monophosphate content was measured in an additional group of animals.

Results: BF and wall shear stress in the left iliac artery increased fourfold immediately after arteriovenous fistula. Arterial enlargement was evident after 7 days, and wall shear stress normalized after 42 days. Flow-induced arterial enlargement was inhibited by both low- and high-dose L-NAME compared with control (analysis of variance p < 0.05). Blood pressure was elevated only in animals treated with high-dose L-NAME. Left iliac cyclic guanosine monophosphate content was lower in rats treated with L-NAME than in the control group (p < 0.05).

Conclusions: NO suppression by L-NAME inhibits flow-induced iliac artery enlargement in rats. This finding suggests that NO plays a role in flow-induced arterial remodeling.

MeSH terms

  • Animals
  • Arteriovenous Fistula
  • Blood Flow Velocity* / drug effects
  • Blood Pressure / drug effects
  • Cyclic GMP / metabolism
  • Iliac Artery / cytology
  • Iliac Artery / drug effects
  • Iliac Artery / physiology*
  • Male
  • NG-Nitroarginine Methyl Ester / pharmacology*
  • Nitric Oxide Synthase / antagonists & inhibitors*
  • Rats
  • Rats, Sprague-Dawley
  • Reference Values
  • Stress, Mechanical
  • Time Factors
  • Tunica Media / cytology
  • Tunica Media / drug effects
  • Tunica Media / physiology*

Substances

  • Nitric Oxide Synthase
  • Cyclic GMP
  • NG-Nitroarginine Methyl Ester