High-salt diet depresses acetylcholine reactivity proximal to NOS activation in cerebral arteries

Am J Physiol Heart Circ Physiol. 2002 Jul;283(1):H353-63. doi: 10.1152/ajpheart.00127.2002.

Abstract

Rats were fed a low-salt (LS; 0.4% NaCl) or high-salt (HS; 4.0% NaCl) diet for 3 days, and the responses of isolated cerebral arteries to acetylcholine (ACh), the nitric oxide (NO)-dependent dilator bradykinin, and the NO donor 6-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-hex-anamine (NOC-9) were determined. ACh-induced vasodilation and NO release, assessed with the fluorescent NO indicator 4,5-diaminofluorescein (DAF-2) diacetate, were eliminated with the HS diet. Inhibition of cyclooxygenase, cytochrome P-450 epoxygenase, and acetylcholinesterase did not alter ACh responses. Bradykinin and NOC-9 caused a similar dilation in cerebral arteries of all groups. Arteries from animals on LS or HS diets exhibited similar levels of basal superoxide (O(2)(-)) production, assessed by dihydroethidine fluorescence, and ACh responses were unaffected by O(2)(-) scavengers. Muscarinic type 3 receptor expression was unaffected by dietary salt intake. These results indicate that 1) a HS diet attenuates ACh reactivity in cerebral arteries by inhibiting NO release, 2) this attenuation is not due to production of a cyclooxygenase-derived vasoconstrictor or elevated O(2)(-) levels, and 3) alteration(s) in ACh signaling are located upstream from NO synthase.

Publication types

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

MeSH terms

  • Acetylcholine / pharmacology*
  • Animals
  • Bradykinin / pharmacology
  • Cerebral Arteries / drug effects*
  • Cerebral Arteries / physiology
  • Cholinesterase Inhibitors / pharmacology
  • Cytochrome P-450 CYP2J2
  • Cytochrome P-450 Enzyme Inhibitors
  • Cytochrome P-450 Enzyme System
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / pharmacology
  • Fluorescent Dyes
  • Free Radical Scavengers / pharmacology
  • In Vitro Techniques
  • Male
  • Nitric Oxide Donors / pharmacology
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitric Oxide Synthase / metabolism*
  • Oxygenases / antagonists & inhibitors
  • Prostaglandin-Endoperoxide Synthases / drug effects
  • Rats
  • Receptor, Muscarinic M3
  • Receptors, Muscarinic / biosynthesis
  • Sodium Chloride, Dietary / pharmacology*
  • Superoxides / metabolism
  • Triazenes / pharmacology
  • Vasodilation / drug effects
  • Vasodilation / physiology
  • Vasodilator Agents / pharmacology*

Substances

  • Cholinesterase Inhibitors
  • Cytochrome P-450 Enzyme Inhibitors
  • Enzyme Inhibitors
  • Fluorescent Dyes
  • Free Radical Scavengers
  • Nitric Oxide Donors
  • Receptor, Muscarinic M3
  • Receptors, Muscarinic
  • Sodium Chloride, Dietary
  • Triazenes
  • Vasodilator Agents
  • Superoxides
  • NOC 9
  • Cytochrome P-450 Enzyme System
  • Oxygenases
  • Nitric Oxide Synthase
  • Cytochrome P-450 CYP2J2
  • Prostaglandin-Endoperoxide Synthases
  • Acetylcholine
  • Bradykinin