Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress
AuthorChen, D; Jancovski, N; Bassi, JK; Thu-Phuc, N-H; Choong, Y-T; Palma-Rigo, K; Davern, PJ; Gurley, SB; Thomas, WG; Head, GA; ...
Source TitleThe Journal of Neuroscience
University of Melbourne Author/sBassi, Jaspreet; Allen, Andrew; Choong, Yan Ting; CHEN, DAIAN; Jancovski, Nikola
Document TypeJournal Article
CitationsChen, D., Jancovski, N., Bassi, J. K., Thu-Phuc, N. -H., Choong, Y. -T., Palma-Rigo, K., Davern, P. J., Gurley, S. B., Thomas, W. G., Head, G. A. & Allen, A. M. (2012). Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress. JOURNAL OF NEUROSCIENCE, 32 (6), pp.2051-2061. https://doi.org/10.1523/JNEUROSCI.5360-11.2012.
Access StatusAccess this item via the Open Access location
Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC6621685
C1 - Journal Articles Refereed
The rise in blood pressure during an acute aversive stress has been suggested to involve activation of angiotensin type 1A receptors (AT(1A)Rs) at various sites within the brain, including the rostral ventrolateral medulla. In this study we examine the involvement of AT(1A)Rs associated with a subclass of sympathetic premotor neurons of the rostral ventrolateral medulla, the C1 neurons. The distribution of putative AT(1A)R-expressing cells was mapped throughout the brains of three transgenic mice with a bacterial artificial chromosome-expressing green fluorescent protein under the control of the AT(1A)R promoter. The overall distribution correlated with that of the AT(1A)Rs mapped by other methods and demonstrated that the majority of C1 neurons express the AT(1A)R. Cre-recombinase expression in C1 neurons of AT(1A)R-floxed mice enabled demonstration that the pressor response to microinjection of angiotensin II into the rostral ventrolateral medulla is dependent upon expression of the AT(1A)R in these neurons. Lentiviral-induced expression of wild-type AT(1A)Rs in C1 neurons of global AT(1A)R knock-out mice, implanted with radiotelemeter devices for recording blood pressure, modulated the pressor response to aversive stress. During prolonged cage-switch stress, expression of AT(1A)Rs in C1 neurons induced a greater sustained pressor response when compared to the control viral-injected group (22 ± 4 mmHg for AT(1A)R vs 10 ± 1 mmHg for GFP; p < 0.001), which was restored toward that of the wild-type group (28 ± 2 mmHg). This study demonstrates that AT(1A)R expression by C1 neurons is essential for the pressor response to angiotensin II and that this pathway plays an important role in the pressor response to aversive stress.
KeywordsCardiology (incl. Cardiovascular Diseases); Autonomic Nervous System; Expanding Knowledge in the Medical and Health Sciences
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