Baroreflex mechanisms regulating the occurrence of neural spikes in human muscle sympathetic nerve activity

2012 ◽  
Vol 107 (12) ◽  
pp. 3409-3416 ◽  
Author(s):  
Aryan Salmanpour ◽  
J. Kevin Shoemaker

This study tested the hypothesis that the discharge patterns of action potentials (APs) within bursts of postganglionic muscle sympathetic nerve activity (MSNA) are subject to arterial baroreflex control but in a manner that varies inversely with AP size. MSNA data were collected over 5 min of supine rest in 15 young and healthy individuals (8 males; 24 ± 4 yr of age; means ± SD). The baroreflex threshold and sensitivity diagrams were constructed for both the integrated sympathetic bursts and for the AP clusters. For the integrated bursts, a strong linear relationship between burst probability and diastolic blood pressure (DBP) was observed ( P < 0.05). There was little relationship between integrated burst strength (amplitude) and DBP. On average, 12 AP clusters were observed across individuals. Larger APs tended to appear in the larger bursts. Linear regression analysis was used to study the baroreflex threshold (probability of AP cluster occurrence vs. DBP) as well as the baroreflex sensitivity (AP cluster size vs. DBP). A significant reflex threshold relationship was observed in 75–100% of AP clusters across all individuals. In contrast, significant reflex sensitivity relationships were observed in only 9 of 15 individuals and for limited APs. Overall, the slope of the AP baroreflex threshold relationship was greater for the small-medium sized AP clusters than that of the larger APs. Therefore, within each burst, the small-medium sized APs are governed by the baroreflex mechanism. However, the large APs, which tend to appear in the large integrated bursts, are weakly associated with a baroreflex control feature. The variable impact of baroreflex control over AP occurrence provides a plausible explanation for the overall weak baroreflex control over integrated burst strength, a feature that is determined by both the number and size of the AP complement.

2000 ◽  
Vol 278 (2) ◽  
pp. R445-R452 ◽  
Author(s):  
Atsunori Kamiya ◽  
Satoshi Iwase ◽  
Hiroki Kitazawa ◽  
Tadaaki Mano ◽  
Olga L. Vinogradova ◽  
...  

To examine how long-lasting microgravity simulated by 6° head-down bed rest (HDBR) induces changes in the baroreflex control of muscle sympathetic nerve activity (MSNA) at rest and changes in responses of MSNA to orthostasis, six healthy male volunteers (range 26–42 yr) participated in Valsalva maneuver and head-up tilt (HUT) tests before and after 120 days of HDBR. MSNA was measured directly using a microneurographic technique. After long-term HDBR, resting supine MSNA and heart rate were augmented. The baroreflex slopes for MSNA during Valsalva maneuver (in supine position) and during 60° HUT test, determined by least-squares linear regression analysis, were significantly steeper after than before HDBR, whereas the baroreflex slopes for R-R interval were significantly flatter after HDBR. The increase in MSNA from supine to 60° HUT was not different between before and after HDBR, but mean blood pressure decreased in 60° HUT after HDBR. In conclusion, the baroreflex control of MSNA was augmented, whereas the same reflex control of R-R interval was attenuated after 120 days of HDBR.


2018 ◽  
Vol 103 (10) ◽  
pp. 1318-1325 ◽  
Author(s):  
Lauro C. Vianna ◽  
Igor A. Fernandes ◽  
Daniel G. Martinez ◽  
André L. Teixeira ◽  
Bruno M. Silva ◽  
...  

2004 ◽  
Vol 287 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Takeshi Ogawa ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
...  

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: −15 and −35 mmHg). At −15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at −35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at −15 mmHg LBNP (vs. CON) and further shifted upward at −35 mmHg LBNP. At −15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at −35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.


2019 ◽  
Vol 317 (2) ◽  
pp. R280-R288 ◽  
Author(s):  
Jian Cui ◽  
Rachel C. Drew ◽  
Matthew D. Muller ◽  
Cheryl Blaha ◽  
Virginia Gonzalez ◽  
...  

Smoking is a risk factor for cardiovascular diseases. Prior reports showed a transient increase in blood pressure (BP) following a spontaneous burst of muscle sympathetic nerve activity (MSNA). We hypothesized that this pressor response would be accentuated in smokers. Using signal-averaging techniques, we examined the BP (Finometer) response to MSNA in 18 otherwise healthy smokers and 42 healthy nonsmokers during resting conditions. The sensitivities of baroreflex control of MSNA and heart rate were also assessed. The mean resting MSNA, heart rate, and mean arterial pressure (MAP) were higher in smokers than nonsmokers. The MAP increase following a burst of MSNA was significantly greater in smokers than nonsmokers (Δ3.4 ± 0.3 vs. Δ1.6 ± 0.1 mmHg, P < 0.001). The baroreflex sensitivity (BRS) of burst incidence, burst area, or total activity was not different between the two groups. However, cardiac BRS was lower in smokers than nonsmokers (14.6 ± 1.7 vs. 24.6 ± 1.5 ms/mmHg, P < 0.001). Moreover, the MAP increase following a burst was negatively correlated with the cardiac BRS. These observations suggest that habitual smoking in otherwise healthy individuals raises the MAP increase following spontaneous MSNA and that the attenuated cardiac BRS in the smokers was a contributing factor. We speculate that the accentuated pressor increase in response to spontaneous MSNA may contribute to the elevated resting BP in the smokers.


2009 ◽  
Vol 106 (4) ◽  
pp. 1125-1131 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David A. Low ◽  
David M. Keller ◽  
...  

Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature ∼ 0.7°C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (−4.34 ± 0.40 to −3.57 ± 0.31 units·beat−1·mmHg−1, respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating ( P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation.


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