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

Francis A. Sylvester, David W. Stepp, Jefferson C. Frisbee, Julian H. Lombard

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


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 (O2-) production, assessed by dihydroethidine fluorescence, and ACh responses were unaffected by O2- 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 O2- levels, and 3) alteration(s) in ACh signaling are located upstream from NO synthase.

Original languageEnglish (US)
Pages (from-to)H353-H363
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 52-1
StatePublished - 2002
Externally publishedYes


  • Bradykinin
  • Cyclooxygenase
  • Endothelium
  • Epoxyeicosatrienoic acids
  • Nitric oxide
  • Superoxide

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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