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.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Neurology
- Developmental Biology