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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 582/2/711    most recent jphysiol.2007.128983v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McMullan, S. Articles by Pilowsky, P. M. Search for Related Content PubMed PubMed Citation Articles by McMullan, S. Articles by Pilowsky, P. M. Related Collections Cardiovascular

¹ Hypertension & Stroke Research Laboratory, University of Sydney, NSW, Australia
² Australian School of Advanced Medicine, Macquarie University, NSW, Australia

Chronic intravenous angiotensin II (Ang II) has been widely used to establish centrally mediated hypertension in experimental animals, and disruption of Ang II activity is a frontline treatment for hypertensive disease. However, the acute central actions of circulating Ang II are poorly understood. We examined the effects of intravenous pressor doses of Ang II on autonomic activity in anaesthetized rats under neuromuscular blockade, and compared baroinhibition evoked by Ang II pressor ramps to equipressor responses evoked by phenylephrine (PE). Baroinhibition of splanchnic sympathetic nerve activity was attenuated during Ang II trials compared with PE, and rats remained sensitive to electrical stimulation of the aortic depressor nerve at higher arterial pressures during Ang II trials. This was not due to a direct effect of Ang II on aortic nerve baroreceptors. In a separate series of experiments, we provide direct evidence that bulbospinal barosensitive neurones in the rostral ventrolateral medulla are differentially sensitive to pressure ramps evoked by Ang II or PE vasoconstriction. Nineteen out of 41 units were equally sensitive to increased arterial pressure evoked by Ang II or PE. In 17 of 41 units, barosensitivity was attenuated during Ang II trials, and in five of 41 cases units that had previously been barosensitive increased their firing rate during Ang II trials. These results show, for the first time, that circulating Ang II acutely modulates central cardiovascular control mechanisms. We suggest that this results from activation by Ang II of a central pathway originating at the circumventricular organs.

(Received 23 January 2007; accepted after revision 15 March 2007; first published online 15 March 2007)
Corresponding author P. Pilowsky: c/o J. Davidson, Macquarie University Neuroscience Centre, Australian School of Advanced Medicine, 3 Innovation Road, Macquarie University, NSW 2109, Australia. Email: jane.davidson{at}mq.edu.au

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