Physiology - Research Publications

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    Central Angiotensin Type 1 Receptor Blockade Decreases Cardiac But Not Renal Sympathetic Nerve Activity in Heart Failure
    RAMCHANDRA, ROHIT ; Hood, Sally ; Watson, Anna ; ALLEN, ANDREW ; MAY, CLIVE ( 2012)
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    Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress
    Chen, D ; Jancovski, N ; Bassi, JK ; Thu-Phuc, N-H ; Choong, Y-T ; Palma-Rigo, K ; Davern, PJ ; Gurley, SB ; Thomas, WG ; Head, GA ; Allen, AM (SOC NEUROSCIENCE, 2012-02-08)
    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.
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    Angiotensin 1A receptors transfected into caudal ventrolateral medulla inhibit baroreflex gain and stress responses
    Palma-Rigo, Kesia ; BASSI, JASPREET ; Nguyen-Huu, Thu-Phuc ; Jackson, Kristy L. ; Davern, Pamela J. ; CHEN, DAIAN ; Elghozi, Jean-Luc ; Thomas, Walter G ; ALLEN, ANDREW ; Head, Geoffrey A. ( 2012)
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    Central angiotensin type 1 receptor blockade decreases cardiac but not renal sympathetic nerve activity in heart failure.
    RAMCHANDRA, ROHIT ; Hood, Sally ; Watson, Anna ; ALLEN, ANDREW ; MAY, CLIVE ( 2012)
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    Control of sympathetic vasomotor tone by catecholaminergic C1 neurones of the rostral ventrolateral medulla oblongata
    Marina, N ; Abdala, APL ; Korsak, A ; Simms, AE ; Allen, AM ; Paton, JFR ; Gourine, AV (OXFORD UNIV PRESS, 2011-09-01)
    AIMS: Increased sympathetic tone in obstructive sleep apnoea results from recurrent episodes of systemic hypoxia and hypercapnia and might be an important contributor to the development of cardiovascular disease. In this study, we re-evaluated the role of a specific population of sympathoexcitatory catecholaminergic C1 neurones of the rostral ventrolateral medulla oblongata in the control of sympathetic vasomotor tone, arterial blood pressure, and hypercapnia-evoked sympathetic and cardiovascular responses. METHODS AND RESULTS: In anaesthetized rats in vivo and perfused rat working heart brainstem preparations in situ, C1 neurones were acutely silenced by application of the insect peptide allatostatin following cell-specific targeting with a lentiviral vector to express the inhibitory Drosophila allatostatin receptor. In anaesthetized rats with denervated peripheral chemoreceptors, acute inhibition of 50% of the C1 neuronal population resulted in ∼50% reduction in renal sympathetic nerve activity and a profound fall in arterial blood pressure (by ∼25 mmHg). However, under these conditions systemic hypercapnia still evoked vigorous sympathetic activation and the slopes of the CO(2)-evoked sympathoexcitatory and cardiovascular responses were not affected by inhibition of C1 neurones. Inhibition of C1 neurones in situ resulted in a reversible fall in perfusion pressure and the amplitude of respiratory-related bursts of thoracic sympathetic nerve activity. CONCLUSION: These data confirm a fundamental physiological role of medullary catecholaminergic C1 neurones in maintaining resting sympathetic vasomotor tone and arterial blood pressure. However, C1 neurones do not appear to mediate sympathoexcitation evoked by central actions of CO(2).