Naturalistic activation of barosensitive afferents release substance P in the nucleus tractus solitarius of the cat

Potts, Jeffrey T.; Fuchs, I.

doi:10.1016/s0006-8993(00)03308-4

Cited by 25 publications

(21 citation statements)

References 33 publications

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“…PREVIOUS STUDIES HAVE SUGGESTED that substance P, acting at neurons that express neurokinin-1 (NK1) receptors, may participate in transmission of arterial baroreflexes at the level of the nucleus tractus solitarii (NTS) (17,23,26). In an earlier study, we injected into NTS a toxin that selectively targeted neurons with NK1 receptors (24), and we showed that the ensuing lesion attenuated baroreflex responses (24).…”

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confidence: 99%

“…This study supports the hypothesis that NTS lesions interrupting the baroreflex may induce cardiac arrhythmias and myocardial changes similar to those seen in humans with central lesions and may lead to sudden cardiac death. baroreflex; cardiac arrhythmia; heart injuries; sudden death; sympathetic nervous system PREVIOUS STUDIES HAVE SUGGESTED that substance P, acting at neurons that express neurokinin-1 (NK1) receptors, may participate in transmission of arterial baroreflexes at the level of the nucleus tractus solitarii (NTS) (17,23,26). In an earlier study, we injected into NTS a toxin that selectively targeted neurons with NK1 receptors (24), and we showed that the ensuing lesion attenuated baroreflex responses (24).…”

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confidence: 99%

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Cardiac damage after lesions of the nucleus tractus solitarii

Nayate

Moore²,

Weiss³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Nayate A, Moore SA, Weiss R, Taktakishvili OM, Lin L.-H., Talman WT. Cardiac damage after lesions of the nucleus tractus solitarii. Am J Physiol Regul Integr Comp Physiol 296: R272-R279, 2009. First published November 19, 2008 doi:10.1152/ajpregu.00080.2008.-Humans with central lesions that augment sympathetic nerve activity are predisposed to cardiac arrhythmias, myocardial lesions, and sudden death. Previously, we showed that selectively killing neurons with neurokinin-1 receptors in the nucleus tractus solitarii (NTS) of rats attenuated the baroreflex and, in some animals, led to sudden unexplained death within ϳ2 wk. Interruption of arterial baroreflexes is known to increase sympathetic activity. Here we tested the hypothesis that lesions in the NTS lead to fatal cardiac arrhythmias and myocardial lesions. We studied electrocardiograms, echocardiograms, blood pressure, and heart rate in 14 adult male rats after bilateral microinjection into the NTS of stabilized substance P conjugated to the toxin saporin and compared the variables in five sham control rats and in five animals with toxin injected outside the NTS. Only injection of toxin into the NTS led to increased lability of arterial blood pressure, a sign of baroreflex interruption. Two animals treated with toxin died suddenly. All animals engaged in normal activity until, in two, rapid development of asystole and death over 6 -8 min. Cardiac function when examined by echocardiography was normal, but pathologic examination of the heart revealed diffuse microscopic areas of acute coagulation necrosis in the myocardium in five animals, focal subacute necrosis in two animals, and both changes in one animal. This study supports the hypothesis that NTS lesions interrupting the baroreflex may induce cardiac arrhythmias and myocardial changes similar to those seen in humans with central lesions and may lead to sudden cardiac death. baroreflex; cardiac arrhythmia; heart injuries; sudden death; sympathetic nervous system PREVIOUS STUDIES HAVE SUGGESTED that substance P, acting at neurons that express neurokinin-1 (NK1) receptors, may participate in transmission of arterial baroreflexes at the level of the nucleus tractus solitarii (NTS) (17,23,26). In an earlier study, we injected into NTS a toxin that selectively targeted neurons with NK1 receptors (24), and we showed that the ensuing lesion attenuated baroreflex responses (24). The altered baroreflex transmission was associated with sudden, unexpected, death in 33% of the experimental animals. Death in these animals was reminiscent of that seen in humans who have sustained central lesions (30). While subarachnoid hemorrhage is a most common cause, other central lesions that lead to enhanced sympathetic nerve activity also predispose an individual to the fatal outcome (30). In fact, sympathetic nerve activity and excessive circulating catecholamines alone may lead to cardiac arrhythmias and death (12,33). Sudden death in humans with central lesions correlates with cardiac arrhythmias, but the lesions also may l...

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confidence: 99%

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confidence: 99%

Cardiac damage after lesions of the nucleus tractus solitarii

Nayate

Moore²,

Weiss³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…5,6 Despite the uncertain role of SP in baroreflex transmission, it became clear that the neurokinin-1 (NK1) receptors at which SP acts 7 are found in NTS 8 -11 and could mediate cardiovascular responses to SP in NTS. Recognition of those receptors, reports that SP is released in NTS on baroreflex stimulation, 12 and recognition that SP may act as a modulator of the actions of glutamate in NTS 13,14 renewed our interest in this area.…”

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Ablation of NK1 Receptors in Rat Nucleus Tractus Solitarii Blocks Baroreflexes

et al. 2002

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The neuropeptide substance P (SP) is found in vagal afferent nerves within the nucleus tractus solitarii, where it is released on stimulation of arterial baroreflexes. The neurokinin-1 receptors at which SP may act have been identified in the nucleus tractus solitarii, but there remains uncertainty if the neurons at which SP acts are critical to baroreflex transmission. By using SP conjugated with the toxin saporin, which kills the neurons at which SP may act, we sought to test the hypothesis that neurons expressing the neurokinin-1 receptor are critical to baroreflex transmission in the nucleus tractus solitarii. One and 2 weeks after injection of the toxin into the rat nucleus tractus solitarii, immunoreactivity for the neurokinin-1 receptor was lost. When the toxin had been injected bilaterally, the baroreflex gain was significantly reduced. Therefore, neurons that express SP receptors play a critical role in mediating baroreflexes through the nucleus tractus solitarii of rat.

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“…This technique is derived from the inflation of the balloon of a Swan-Ganz (Borgdorf et al 1990) or Fogarty (Kaufman, 1984;Potts & Fuchs, 2001) catheter threaded into the aorta or vena cava of larger animals to modify pre-or afterload…”

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confidence: 99%

A Simple Method for Generating a Blood Pressure‐Unit Activity Relationship for Central Cardiovascular Neurons in the Rat

Cividjian¹,

Rentero²,

McAllen³

et al. 2002

Experimental Physiology

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One way to identify central cardiovascular neurons is to consider their barosensitivity, for example by plotting changes in their single unit activity as a function of evoked changes in blood pressure. To simplify the genesis of such pressure‐activity relationships, a coronary angioplasty catheter was threaded into the aorta of anaesthetized rats and the balloon inflated to raise the blood pressure mechanically. Here, such a procedure is exemplified for cardiac vagal motoneurons in the medulla oblongata in eight rats. This simplification bypasses potentially problematic surgery and minimizes deterioration of the animal.

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Naturalistic activation of barosensitive afferents release substance P in the nucleus tractus solitarius of the cat

Cited by 25 publications

References 33 publications

Cardiac damage after lesions of the nucleus tractus solitarii

Cardiac damage after lesions of the nucleus tractus solitarii

Ablation of NK1 Receptors in Rat Nucleus Tractus Solitarii Blocks Baroreflexes

A Simple Method for Generating a Blood Pressure‐Unit Activity Relationship for Central Cardiovascular Neurons in the Rat

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