Selective attenuation of sympathetic component of the baroreflex by angiotensin II in the nucleus tractus solitarii

University College London 2006 (2006) Proc Physiol Soc 3, C93

Oral Communications: Selective attenuation of sympathetic component of the baroreflex by angiotensin II in the nucleus tractus solitarii

Jaimie W Polson1, Roger AL Dampney2, Pedro Boscan3, Anthony E Pickering1, Julian FR Paton1

1. Physiology, University of Bristol, Bristol, United Kingdom. 2. Physiology, University of Sydney, Sydney, NSW, Australia. 3. Anesthesia & Critical Patient Care,Veterinary Medical Teaching Hospital, University of California, Davis, CA, USA.

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It is well established that the heart rate (HR) component of the baroreflex is depressed following exogenous application of angiotensin II (ANGII) to the nucleus tractus solitarii (NTS; Casto & Phillips, 1986). However, the effect on baroreflex modulated sympathetic nerve activity (SNA) is unclear. We sought to determine if ANGII in the NTS also depresses baroreflex-evoked sympathoinhibition in the upper-middle and lower thoracic-lumbar sympathetic chain. Experiments were performed in the rat using the in situ ‘working heart-brainstem’ (Paton, 1996) and ‘decerebrate arterially perfused rat’ preparations (Pickering & Paton, 2006). Rats were terminally anaesthetized with halothane, decerebrated precollicularly and perfused via the heart or descending aorta with modified, oxygenated Ringer solution (32°C). Perfusion pressure, HR and SNA either from the inferior cardiac nerve, upper-middle thoracic chain or lower thoracic-lumbar chain were recorded. Perfusion pressure was increased to stimulate baroreceptors and baroreflex changes in HR and SNA were measured before and after injection of ANGII (500 fmol) or the GABAA agonist isoguvacine (500 pmol) bilaterally into the NTS. Baroreflex gain was calculated as the ratio of either ΔHR or ΔSNA (expressed as % of basal)/Δperfusion pressure. Data are expressed as mean ± SE. Statistical significance was determined using a Student’s t test. ANGII in NTS reduced baroreflex gain in HR (54% reduction, control 1.9 ± 0.2 vs 0.9 ± 0.1 bpm/mmHg, n=22, p<0.01), inferior cardiac (31% reduction; control 3.5 ± 0.4 vs 2.4 ± 0.4%/mmHg; n=12, p<0.05) and upper-middle thoracic SNA (46% reduction; control 3.9 ± 0.6 vs 2.1 ± 0.5%/mmHg; n=5, p<0.05) but not in the lower thoracic-lumbar SNA (9.8% increase, control 2.9 ± 0.3 vs 3.2 ± 0.4; n=9, p=0.57). In contrast, inactivating NTS with isoguvacine inhibited both the HR (by 90%, p<0.01) and all sympathetic baroreflex components measured (by 65-75%, p<0.05). Our data indicate that ANGII in the NTS does not attenuate the baroreflex inhibition of SNA in a uniform manner, but appears to be organised depending on the spinal level of origin or target organ being innervated.



Where applicable, experiments conform with Society ethical requirements.

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