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Articles in PresS, published online ahead of print January 11, 2002
J Appl Physiol, 10.1152/jap.00261.2001
Submitted on March 23, 2001
Accepted on December 28, 2001
1 Department of Physiology, Medical Center of Fudan University, Shanghai, Shanghai, China
2 Department of Electromicroscopy, Medical Center of Fudan University, Shanghai, Shanghai, China
3 Department of Pharmacology, School of Pharmacy, Universitry of Missouri-Kansas City, Kansas, MO, USA
4 Department of Physiology, College of Medicine, University of Florida, Gainesville, FL, USA
5 Department of Physiology, Medical Center of Fudan University, Shanghai, Shanghai, China; Department of National Key Laboratory of Medical Neurobiology, Medical Center of Fudan University, Shanghai, Shanghai, China
* To whom correspondence should be addressed. E-mail: qhu32{at}yahoo.com.
In the present study, the amino acids release in the spinal cord immediately following the application of angiotensin II (ANG II) in the rostral ventrolateral medulla (RVLM), and the distribution of ANG receptors on neurons of the RVLM were investigated. Microdialysis experiment showed that microinjection of angiotensin II (ANG II) into the RVLM significantly (p<0.01) increased the release of aspartate and glutamate in the intermediolateral column of the spinal cord (IML). Immunofluorescence technique combined with confocal microscopy demonstrated that most of the glutamatergic and GABAergic neurons in the RVLM of both Wistar and spontaneously hypertensive rats (SHR) were double-labeled with ANG type 1 (AT1) receptor. Immunocytochemical studies demonstrated that the mean optic density (MOD) of AT1 receptor of on the cell surface as well as the whole cell was higher (p<0.05) in SHR than that in Wistar rats, indicating that the higher expression of AT1 receptors in the RVLM may contribute to the higher responsiveness of SHR to ANG II stimulation. Immunogold staining and electronmicroscopic study demonstrated that AT1 receptor in the RVLM was distributed on the rough endoplasmic reticulum (RER), cell membrane and nerve processes. The results suggest that effects evoked by ANG II in the RVLM are closely related with glutamatergic and GABAergic pathways. These results indirectly support the hypothesis that ANG II in the RVLM may activate vasomotor sympathetic glutamatergic neurons, leading to an increase in sympathetic nerve activity and arterial blood pressure.
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