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Am J Physiol Heart Circ Physiol (March 28, 2002). doi:10.1152/ajpheart.00127.2002
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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00127.2002
Submitted on February 21, 2002
Accepted on March 25, 2002

HIGH SALT DIET DEPRESSES ACETYLCHOLINE REACTIVITY PROXIMAL TO NOS ACTIVATION IN CEREBRAL ARTERIES

Francis A Sylvester1, David W Stepp1, Jefferson C Frisbee1, and Julian H Lombard1*

1 Physiology, Medical College of Wisconsin, Milwaukee, WI, USA

* To whom correspondence should be addressed. E-mail: jlombard{at}mcw.edu.

Rats were fed low salt (0.4% NaCl; LS) or high salt (4.0% NaCl; HS) diet for 3 days and responses of isolated cerebral arteries to acetylcholine (ACh), the NO-dependent dilator bradykinin, and the NO donor 6-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-hexanamine (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 HS diet. Inhibition of cyclooxygenase, cytochrome P450 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 diet 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) 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 nitric oxide synthase (NOS).




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