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 (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 language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 283 |
| Issue number | 1 52-1 |
| State | Published - Jul 10 2002 |
| Externally published | Yes |
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Keywords
- Bradykinin
- Cyclooxygenase
- Endothelium
- Epoxyeicosatrienoic acids
- Nitric oxide
- Superoxide
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)
Cite this
High-salt diet depresses acetylcholine reactivity proximal to NOS activation in cerebral arteries. / Sylvester, Francis A.; Stepp, David W; Frisbee, Jefferson C.; Lombard, Julian H.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 283, No. 1 52-1, 10.07.2002.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - High-salt diet depresses acetylcholine reactivity proximal to NOS activation in cerebral arteries
AU - Sylvester, Francis A.
AU - Stepp, David W
AU - Frisbee, Jefferson C.
AU - Lombard, Julian H.
PY - 2002/7/10
Y1 - 2002/7/10
N2 - 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.
AB - 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.
KW - Bradykinin
KW - Cyclooxygenase
KW - Endothelium
KW - Epoxyeicosatrienoic acids
KW - Nitric oxide
KW - Superoxide
UR - http://www.scopus.com/inward/record.url?scp=0036299748&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036299748&partnerID=8YFLogxK
M3 - Article
VL - 283
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
SN - 0363-6135
IS - 1 52-1
ER -