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Am J Physiol Heart Circ Physiol 283: H353-H363, 2002. First published March 28, 2002; doi:10.1152/ajpheart.00127.2002
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Vol. 283, Issue 1, H353-H363, July 2002

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

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

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

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<UP><SUB>2</SUB><SUP>−</SUP></UP>) production, assessed by dihydroethidine fluorescence, and ACh responses were unaffected by O<UP><SUB>2</SUB><SUP>−</SUP></UP> 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<UP><SUB>2</SUB><SUP>−</SUP></UP> levels, and 3) alteration(s) in ACh signaling are located upstream from NO synthase.

bradykinin; cyclooxygenase; endothelium; epoxyeicosatrienoic acids; nitric oxide; superoxide


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