Role of Inducible Nitric Oxide Synthase in Rostral Ventrolateral Medulla in Blood Pressure Regulation in Spontaneously Hypertensive Rats

被引:21
作者
Kimura, Yoshikuni [1 ]
Hirooka, Yoshitaka [1 ]
Kishi, Takuya [1 ]
Ito, Koji [1 ]
Sagara, Yoji [1 ]
Sunagawa, Kenji [1 ]
机构
[1] Kyushu Univ, Grad Sch Med Sci, Dept Cardiovasc Med, Higashi Ku, Fukuoka 8128582, Japan
关键词
blood pressure; heart rate; brain; nitric oxide; sympathetic nervous system; OXIDATIVE STRESS; BRAIN; EXPRESSION; OVEREXPRESSION; INFLAMMATION; CONTRIBUTES;
D O I
10.1080/10641960902822534
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Nitric oxide (NO) in the brainstem modulates blood pressure (BP). Overexpression of inducible NO synthase (iNOS) in the rostral ventrolateral medulla (RVLM) increases BP in normotensive Wistar-Kyoto rats (WKY), but its role in BP regulation in spontaneously hypertensive rats (SHR) is unknown. We examined iNOS expression and the effect of iNOS inhibitors in the RVLM on BP and heart rate in SHR and WKY. iNOS levels in the RVLM were significantly higher in SHR than in WKY. Bilateral microinjection of aminoguanidine into the RVLM dose-dependently decreased BP and heart rate in SHR, but not in WKY. These findings suggest that iNOS expression in the RVLM of SHR contributes to increase BP.
引用
收藏
页码:281 / 286
页数:6
相关论文
共 20 条
[1]   Reduced functional expression and molecular synthesis of inducible nitric oxide synthase in rostral ventrolateral medulla of spontaneously hypertensive rats [J].
Chan, JYH ;
Wang, LL ;
Wu, KLH ;
Chan, SHH .
CIRCULATION, 2001, 104 (14) :1676-1681
[2]   Differential cardiovascular responses to blockade of nNOS or iNOS in rostral ventrolateral medulla of the rat [J].
Chan, SHH ;
Wang, LL ;
Wang, SH ;
Chan, JYH .
BRITISH JOURNAL OF PHARMACOLOGY, 2001, 133 (04) :606-614
[3]   Alterations of nitric oxide synthase expression with aging and hypertension in rats [J].
Chou, TC ;
Yen, MH ;
Li, CY ;
Ding, YA .
HYPERTENSION, 1998, 31 (02) :643-648
[4]   FUNCTIONAL-ORGANIZATION OF CENTRAL PATHWAYS REGULATING THE CARDIOVASCULAR-SYSTEM [J].
DAMPNEY, RAL .
PHYSIOLOGICAL REVIEWS, 1994, 74 (02) :323-364
[5]   The sympathetic control of blood pressure [J].
Guyenet, PG .
NATURE REVIEWS NEUROSCIENCE, 2006, 7 (05) :335-346
[6]   Amlodipine-Induced reduction of oxidative stress in the brain is associated with sympatho-inhibitory effects in stroke-prone spontaneously hypertensive rats [J].
Hirooka, Y ;
Kimura, Y ;
Nozoe, M ;
Sagara, Y ;
Ito, K ;
Sunagawa, K .
HYPERTENSION RESEARCH, 2006, 29 (01) :49-56
[7]   Reduced nitric oxide synthase in the brainstem contributes to enhanced sympathetic drive in rats with heart failure [J].
Hirooka, Y ;
Shigematsu, H ;
Kishi, T ;
Kimura, Y ;
Ueta, Y ;
Takeshita, A .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2003, 42 :S111-S115
[8]   Overexpression of inducible nitric oxide synthase in rostral ventrolateral medulla causes hypertension and sympathoexcitation via an increase in oxidative stress [J].
Kimura, Y ;
Hirooka, Y ;
Sagara, Y ;
Ito, K ;
Kishi, T ;
Shimokawa, H ;
Takeshita, A ;
Sunagawa, K .
CIRCULATION RESEARCH, 2005, 96 (02) :252-260
[9]   Long-acting calcium channel blocker, azelnidipine, increases endothelial nitric oxide synthase in the brain and inhibits sympathetic nerve activity [J].
Kimura, Yoshikuni ;
Hirooka, Yoshitaka ;
Sagara, Yoji ;
Sunagawa, Kenji .
CLINICAL AND EXPERIMENTAL HYPERTENSION, 2007, 29 (01) :13-21
[10]   Cardiovascular effects of overexpression of endothelial nitric oxide synthase in the rostral ventrolateral medulla in stroke-prone spontaneously hypertensive rats [J].
Kishi, T ;
Hirooka, Y ;
Ito, K ;
Sakai, K ;
Shimokawa, H ;
Takeshita, A .
HYPERTENSION, 2002, 39 (02) :264-268