Xin Ni1, Ding-Feng Su2, WeiWang4, Ming-Juan Xu5*, and Wei-ZhongWang1,6*
1Department of Physiology, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, China; 2Department of Pharmacology, School of Pharmacy, Second Military MedicalUniversity, Shanghai 200433, China; 3Department of Neurobiology and Physiology, Ningxia Medical University, Yinchuan 750004, China; 4Department of Physiology, Nebraska MedicalCenter, Omaha 68198, USA; 5Department of Obstetrics and Gynecology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China; and 6Key Laboratory of Molecula rNeurobiology, Ministry of Education, Second Military Medical University, Shanghai 200433, China Received 18 March 2010; revised 15 August 2010; accepted 1 September 2010; online publish-ahead-of-print 9 September 2010
Cardiovascular Research (2011) 89, 473–481 doi:10.1093/cvr/cvq289
This article investigated the effects of moxonidine, an antihypertensive drug on GABA A and GABA B receptors along with GABA transmission in the RVLM. Mox activates I1R that may mediate the release of GABA. So the investigators used several techniques, a couple that we currently use in the lab. They used microinjection, western blot and microdialysis. The major findings were that the effects of mox are mediated through the GABA receptors. They also demonstrated that there is an upregulation of GABA A and GABA B receptors and this was shown by western blot. By using microdialysis, they showed that there is an increase in the amount of GABA released in the RVLM after the use of mox. These findings suggest that mox leads to an increase in GABAergic transmission in the RVLM that causes hypotension and an increase in sympathoinhibition.
Mary,
ReplyDeletewhat is I1R and where it is present? when there is an upregulation of GABA A and GABA B receptors? Did they use any inhibitors to see if the effects of mox are blocked?
- Madhan
Imidazolin 1 receptor is found in the CNS. If you are asking me whether I know if it is present in RVLM I would assume so because the action of Mox is mediate through I1R. There was upregulation of GABA A and GABA B after chronic ICV infusion of mox.They used GABA A and GABA B receptor inhibitors in order to see if the effects of mox were attenuated.
ReplyDelete