Abstract
We have determined the role of nitric oxide (NO) in the nucleus of the solitary tract (NTS) of normotensive Wistar rats. The unilateral microinjection of N(ω)-nitro-L-arginine methyl ester (10 nmol) to block the synthesis of NO into the NTS significantly decreased the medal pressure, heart rate (HR) and renal sympathetic nerve activity (RSNA) (-19 ± 2 mmHg, - 23 ± 5 beats/min, -30 ± 2%, respectively). The microinjection of carboxy- 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (Carboxy PTIO) (trapper of NO; 0.1 nmol) into the NTS also decreased arterial pressure and RSNA. Conversely, the microinjection of Et2N[N(O)NO]Na (NOC 18) (NO donor; 10 nmol) caused increases in arterial pressure, HR and RSNA (+ 14 ± 2 mmHg, + 11 ± 2 beats/min, +38 ± 7%, respectively), which was inhibited by the pre-microinjection of carboxy PTIO (0.1 nmol). On the other hand, not only L- arginine (10 nmol) but also D-arginine (10 nmol), which is inactive to produce NO, significantly decreased the medal pressure and RSNA. These results suggest that (1) NO acts at the NTS to increase the arterial pressure and RSNA, and (2) the microinjection of L-arginine as well as D-arginine led to decreases in arterial pressure and RSNA that were not mediated by the formation of NO in the NTS.
| Original language | English |
|---|---|
| Pages (from-to) | 232-238 |
| Number of pages | 7 |
| Journal | Brain Research |
| Volume | 798 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Jul 6 1998 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology
Cite this
Role of nitric oxide in the nucleus of the solitary tract of rats. / Matsumura, Kiyoshi; Tsuchihashi, Takuya; Kagiyama, Shuntaro; Abe, Isao; Fujishima, Masatoshi.
In: Brain Research, Vol. 798, No. 1-2, 06.07.1998, p. 232-238.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of nitric oxide in the nucleus of the solitary tract of rats
AU - Matsumura, Kiyoshi
AU - Tsuchihashi, Takuya
AU - Kagiyama, Shuntaro
AU - Abe, Isao
AU - Fujishima, Masatoshi
PY - 1998/7/6
Y1 - 1998/7/6
N2 - We have determined the role of nitric oxide (NO) in the nucleus of the solitary tract (NTS) of normotensive Wistar rats. The unilateral microinjection of N(ω)-nitro-L-arginine methyl ester (10 nmol) to block the synthesis of NO into the NTS significantly decreased the medal pressure, heart rate (HR) and renal sympathetic nerve activity (RSNA) (-19 ± 2 mmHg, - 23 ± 5 beats/min, -30 ± 2%, respectively). The microinjection of carboxy- 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (Carboxy PTIO) (trapper of NO; 0.1 nmol) into the NTS also decreased arterial pressure and RSNA. Conversely, the microinjection of Et2N[N(O)NO]Na (NOC 18) (NO donor; 10 nmol) caused increases in arterial pressure, HR and RSNA (+ 14 ± 2 mmHg, + 11 ± 2 beats/min, +38 ± 7%, respectively), which was inhibited by the pre-microinjection of carboxy PTIO (0.1 nmol). On the other hand, not only L- arginine (10 nmol) but also D-arginine (10 nmol), which is inactive to produce NO, significantly decreased the medal pressure and RSNA. These results suggest that (1) NO acts at the NTS to increase the arterial pressure and RSNA, and (2) the microinjection of L-arginine as well as D-arginine led to decreases in arterial pressure and RSNA that were not mediated by the formation of NO in the NTS.
AB - We have determined the role of nitric oxide (NO) in the nucleus of the solitary tract (NTS) of normotensive Wistar rats. The unilateral microinjection of N(ω)-nitro-L-arginine methyl ester (10 nmol) to block the synthesis of NO into the NTS significantly decreased the medal pressure, heart rate (HR) and renal sympathetic nerve activity (RSNA) (-19 ± 2 mmHg, - 23 ± 5 beats/min, -30 ± 2%, respectively). The microinjection of carboxy- 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (Carboxy PTIO) (trapper of NO; 0.1 nmol) into the NTS also decreased arterial pressure and RSNA. Conversely, the microinjection of Et2N[N(O)NO]Na (NOC 18) (NO donor; 10 nmol) caused increases in arterial pressure, HR and RSNA (+ 14 ± 2 mmHg, + 11 ± 2 beats/min, +38 ± 7%, respectively), which was inhibited by the pre-microinjection of carboxy PTIO (0.1 nmol). On the other hand, not only L- arginine (10 nmol) but also D-arginine (10 nmol), which is inactive to produce NO, significantly decreased the medal pressure and RSNA. These results suggest that (1) NO acts at the NTS to increase the arterial pressure and RSNA, and (2) the microinjection of L-arginine as well as D-arginine led to decreases in arterial pressure and RSNA that were not mediated by the formation of NO in the NTS.
UR - http://www.scopus.com/inward/record.url?scp=0032490601&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032490601&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(98)00420-X
DO - 10.1016/S0006-8993(98)00420-X
M3 - Article
C2 - 9666137
AN - SCOPUS:0032490601
VL - 798
SP - 232
EP - 238
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -