Postexercise hypotension in conscious SHR is attenuated  by blockade of substance P receptors in NTS

Chen, Chao-Yin; Munch, P. A.; Quail, Anthony W.; Bonham, Ann C.

doi:10.1152/ajpheart.00827.2001

Cited by 28 publications

(25 citation statements)

References 51 publications

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“…Thus we speculate that group B neurons may be inhibitory interneurons and could participate in the baroreflex depression reported after microinjection of higher doses of ANG II into this nTS region. In contrast, SP influences respiratory and gastric as well as cardiovascular function (10,24,66,72). Furthermore, the localization of our group B neurons responsive to ANG II and SP in the dorsal medial nTS region (77) is congruent with the distribution of vagal afferent projections from the esophagus and stomach (62,80).…”

Section: Perspectivesmentioning

confidence: 64%

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Barnes

DeWeese

Andresen

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Barnes, Karen L., Dannette M. DeWeese, and Michael C. Andresen. Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons. Am J Physiol Regul Integr Comp Physiol 284: R1340-R1353, 2003. First published January 16, 2003 10.1152/ajpregu.00505.2002-Femtomole doses of angiotensin (ANG) II microinjected into nucleus tractus solitarii (nTS) decrease blood pressure and heart rate, mimicking activation of the baroreflex, whereas higher doses depress this reflex. ANG II might generate cardioinhibitory responses by augmenting cardiovascular afferent synaptic transmission onto nTS neurons. Intracellular recordings were obtained from 99 dorsal medial nTS region neurons in rat medulla horizontal slices to investigate whether ANG II modulated short-latency excitatory postsynaptic potentials . ANG II appeared to selectively augment presynaptic sensory transmission in one class of nTS neurons but had only postsynaptic effects on another group of cells. Thus ANG II is likely to modulate cardiovascular function by more than one nTS neuronal pathway. cardiovascular regulation; L-glutamate; substance P, non-Nmethyl-D-aspartate receptor THE NUCLEUS TRACTUS SOLITARII (nTS) in the dorsal medulla comprises rostrocaudally oriented columns of diverse neurons and fiber tracts that lie lateral to the walls of the fourth cerebral ventricle and join above the central canal caudal to the obex (4, 73). This complex structure, with bidirectional connections to medullary and forebrain nuclei that subserve autonomic functions, plays a major role in the regulation and integration of visceral systems, including normal and impaired cardiovascular mechanisms (60,61,82). Anatomic studies (25,26,43,52,85) and in vivo recordings (91) verify that a substantial proportion of the arterial baroreceptor sensory fibers that originate from receptors in the aortic arch and carotid sinus regions course through the solitary tract (TS) into the nTS and make their first synapse on neurons in the dorsal medial region of the nucleus. Neurons in this region also receive synaptic inputs from other viscera and brain autonomic nuclei via the TS (79). The nTS is a primary central site at which angiotensin (ANG) II influences cardiovascular function. Within the brain, the anatomic distributions of ANG II and its receptors and their mRNAs correlate reasonably well with the probable functions of the peptide (2, 57). However, the cellular mechanisms responsible for the cardiovascular effects of ANG II mediated by the nTS remain unclear.Microinjection of femtomole doses of ANG II into the dorsal medial region of the nTS produces a transient fall in blood pressure and heart rate very similar to the response to activation of the cardiovascular baroreflex in anesthetized rats (41,71,78) and evokes a comparable bradycardia in an in vitro beating heart-brain stem rat preparation (75). Paradoxically, however, higher doses evoke pressor responses, creating dose-response relationships that are biphasic. ANG II injection into the nTS al...

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Section: Perspectivesmentioning

confidence: 64%

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Barnes

DeWeese

Andresen

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Apart from these chronic effects of exercise, a single bout of dynamic exercise is known to induce hypotension in the post-exercise period in hypertensive subjects (3) and spontaneously hypertensive rats (SHR) (4)(5)(6). Post-exercise hypotension (PEH) is associated with no change or a reduction of heart rate (HR) (7,8) and a reduction in cardiac (9) and peripheral sympathetic nerve activity (10,11).…”

Section: Introductionmentioning

confidence: 99%

Mechanism behind Augmentation in Baroreflex Sensitivity after Acute Exercise in Spontaneously Hypertensive Rats

et al. 2006

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“…The central neural pathways that contribute to this postexercise sympathoinhibition include barosensitive neurons within the nucleus tractus solitarius (6) and the rostral ventrolateral medulla (RVLM; see Ref. 19).…”

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confidence: 99%

Forebrain regions associated with postexercise differences in autonomic and cardiovascular function during baroreceptor unloading

Kimmerly¹,

Wong²,

Salzer³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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The cortical regions representing peripheral autonomic reactions in humans are poorly understood. This study examined whether changes in forebrain activity were associated with the altered physiological responses to lower body negative pressure (LBNP) following a single bout of dynamic exercise (POST-EX). We hypothesized that, compared with the nonexercised condition (NO-EX), POST-EX would elicit greater reductions in stroke volume (SV) and larger increases in heart rate (HR) and muscle sympathetic nerve activity (MSNA) during LBNP (5, 15, and 35 mmHg). Forebrain neural activity (n = 11) was measured using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging. HR, SV, arterial blood pressure (ABP), and MSNA were collected separately. Compared with NO-EX, baseline ABP was reduced, whereas HR and total vascular conductance (TVC) were elevated in POST-EX (P < 0.05). In both conditions, 5 mmHg LBNP did not elicit a change (from baseline) in any physiological parameter. Compared with NO-EX, 35 mmHg LBNP-mediated decreases in SV and TVC produced greater increases in HR and MSNA during POST-EX (P < 0.05). The right posterior insula and dorsal anterior cingulate cortex demonstrated a larger decrease in BOLD at 5 mmHg LBNP but greater BOLD increase at 15 and 35 mmHg LBNP POST-EX vs. NO-EX (P < 0.005). Conversely, the thalamus and ventral medial prefrontal cortex displayed the opposite BOLD activity pattern (i.e., larger increase at 5 mmHg LBNP but greater decrease at 15 and 35 mmHg LBNP POST-EX vs. NO-EX). Our findings suggest that discrete forebrain regions may be involved with the generation of baroreflex-mediated sympathetic and cardiovascular responses elicited by moderate LBNP.

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Postexercise hypotension in conscious SHR is attenuated by blockade of substance P receptors in NTS

Cited by 28 publications

References 51 publications

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Mechanism behind Augmentation in Baroreflex Sensitivity after Acute Exercise in Spontaneously Hypertensive Rats

Forebrain regions associated with postexercise differences in autonomic and cardiovascular function during baroreceptor unloading

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