Hyperpolarization contributes to endothelium-dependent relaxations to acetylcholine in femoral veins of rats

Am J Physiol. 1991 Oct;261(4 Pt 2):H1034-7. doi: 10.1152/ajpheart.1991.261.4.H1034.

Abstract

The contribution of membrane hyperpolarization to endothelium-dependent relaxations induced by acetylcholine was investigated in the femoral vein of the rat using a microelectrode technique and isometric tension recordings. Acetylcholine caused endothelium-dependent relaxations and hyperpolarization in tissues contracted with norepinephrine. The relaxation was sustained during a prolonged exposure to acetylcholine (less than or equal to 10 min). In contrast, the hyperpolarization declined with time. In the presence of nitro-L-arginine, a blocker of nitric oxide synthesis, the relaxation became smaller and transient, whereas the hyperpolarization was not affected. There was a temporal relationship between the relaxation and the hyperpolarization in the presence of nitro-L-arginine, when the two parameters were recorded simultaneously. In tissues contracted with 60 mM K+, in which hyperpolarization could not be observed, acetylcholine caused relaxations and these relaxations were abolished by nitro-L-arginine. The results suggest a contribution of both nitric oxide and membrane hyperpolarization to the endothelium-dependent relaxation induced by acetylcholine in the femoral vein of the rat.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetylcholine / pharmacology*
  • Animals
  • Arginine / analogs & derivatives
  • Arginine / pharmacology
  • Electrophysiology
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / physiology
  • Femoral Vein / drug effects*
  • Femoral Vein / physiology
  • Male
  • Nitroarginine
  • Norepinephrine / pharmacology
  • Potassium / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Vasoconstriction / drug effects
  • Vasodilation*

Substances

  • Nitroarginine
  • Arginine
  • Acetylcholine
  • Potassium
  • Norepinephrine