Serotonin-Mediated Cardiac Analgesia via Ah-Type Baroreceptor Activation Contributes to Silent Angina and Asymptomatic Infarction

Neuroscience ◽  
2019 ◽  
Vol 411 ◽  
pp. 150-163 ◽  
Author(s):  
Xin Wen ◽  
Xue Yu ◽  
Rong Huo ◽  
Qiu-Xin Yan ◽  
Di Wu ◽  
...  
1999 ◽  
Vol 277 (4) ◽  
pp. H1491-H1497
Author(s):  
Daniel Roach ◽  
Robert Haennel ◽  
Mary Lou Koshman ◽  
Robert Sheldon

We are developing a lexicon of specific heart period changes, or lexons, that recur frequently and whose physiological meaning can be read into ambulatory electrocardiogram (ECG). The transient, reversible “burst” of tachycardia induced by exercise initiation can also be seen on ambulatory ECG. We hypothesized that burst morphology depended on the work that preceded it and on baroreceptor activation. Ten subjects with mean age 38 yr (range 17–69 yr) underwent two protocols of semisupine cycling in which load and duration were varied. Burst duration increased with longer cycling times (median values of 18.0, 25.5, and 23.7 s with 1, 3, and 5 s of cycling, respectively; P= 0.033). Burst shape as assessed by heart period exponential decay constant and burst magnitude did not change. To assess the impact of workload, subjects cycled for 5 s at loads of 0, 25, 50, and 75 W. No significant differences were seen in burst duration, burst magnitude, or burst shape. Tachycardia preceded hypotension by 4.6 ± 2.2 s, which is inconsistent with baroreceptor involvement in the onset of burst tachycardia. Because burst morphology is a nearly quantal response to the initiation of exercise, the presence of a burst on an ambulatory ECG implies the onset of exercise.


Pain ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 853-861 ◽  
Author(s):  
Marcus A. Gray ◽  
Ludovico Minati ◽  
Giulia Paoletti ◽  
Hugo D. Critchley

2015 ◽  
pp. hpv064 ◽  
Author(s):  
Bart Spronck ◽  
Tammo Delhaas ◽  
Jos Op ‘t Roodt ◽  
Koen D. Reesink

2013 ◽  
Vol 115 (6) ◽  
pp. 819-828 ◽  
Author(s):  
Ivan T. Demchenko ◽  
Sergei Y. Zhilyaev ◽  
Alexander N. Moskvin ◽  
Alexander I. Krivchenko ◽  
Claude A. Piantadosi ◽  
...  

The cardiovascular system responds to hyperbaric hyperoxia (HBO2) with vasoconstriction, hypertension, bradycardia, and reduced cardiac output (CO). We tested the hypothesis that these responses are linked by a common mechanism—activation of the arterial baroreflex. Baroreflex function in HBO2 was assessed in anesthetized and conscious rats after deafferentation of aortic or carotid baroreceptors or both. Cardiovascular and autonomic responses to HBO2 in these animals were compared with those in intact animals at 2.5 ATA for conscious rats and at 3 ATA for anesthetized rats. During O2 compression, hypertension was greater after aortic or carotid baroreceptor deafferentation and was significantly more severe if these procedures were combined. Similarly, the hyperoxic bradycardia observed in intact animals was diminished after aortic or carotid baroreceptor deafferentation and replaced by a slight tachycardia after complete baroreceptor deafferentation. We found that hypertension, bradycardia, and reduced CO—the initial cardiovascular responses to moderate levels of HBO2—are coordinated through a baroreflex-mediated mechanism initiated by HBO2-induced vasoconstriction. Furthermore, we have shown that baroreceptor activation in HBO2 inhibits sympathetic outflow and can partially reverse an O2-dependent increase in arterial pressure.


1989 ◽  
Vol 67 (5) ◽  
pp. 2095-2100 ◽  
Author(s):  
V. K. Somers ◽  
A. L. Mark ◽  
D. C. Zavala ◽  
F. M. Abboud

The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.


1992 ◽  
Vol 263 (2) ◽  
pp. R310-R317 ◽  
Author(s):  
Y. W. Li ◽  
Z. J. Gieroba ◽  
W. W. Blessing

Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan-anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.


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