Effects of NO on baroreflex control of heart rate and renal nerve activity in conscious rabbits

1996 ◽  
Vol 270 (6) ◽  
pp. R1361-R1370 ◽  
Author(s):  
J. L. Liu ◽  
H. Murakami ◽  
I. H. Zucker
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Control Level ◽  
Relative Role ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Baroreflex Control ◽  
Synthase Inhibitor

Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.

Hyperventilation alters arterial baroreflex control of heart rate and muscle sympathetic nerve activity

2000 ◽  
Vol 279 (2) ◽  
pp. H536-H541 ◽  
Author(s):  
Philippe Van de Borne ◽  
Silvia Mezzetti ◽  
Nicola Montano ◽  
Krzysztof Narkiewicz ◽  
Jean Paul Degaute ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Normal Subjects ◽  
Arterial Baroreflex ◽  
Baroreceptor Sensitivity ◽  
Nerve Activity ◽  
Baroreflex Control

Interactions between mechanisms governing ventilation and blood pressure (BP) are not well understood. We studied in 11 resting normal subjects the effects of sustained isocapnic hyperventilation on arterial baroreceptor sensitivity, determined as the α index between oscillations in systolic BP (SBP) generated by respiration and oscillations present in R-R intervals (RR) and in peripheral sympathetic nerve traffic [muscle sympathetic nerve activity (MSNA)]. Tidal volume increased from 478 ± 24 to 1,499 ± 84 ml and raised SBP from 118 ± 2 to 125 ± 3 mmHg, whereas RR decreased from 947 ± 18 to 855 ± 11 ms (all P < 0.0001); MSNA did not change. Hyperventilation reduced arterial baroreflex sensitivity to oscillations in SBP at both cardiac (from 13 ± 1 to 9 ± 1 ms/mmHg, P < 0.001) and MSNA levels (by −37 ± 5%, P < 0.0001). Thus increased BP during hyperventilation does not elicit any reduction in either heart rate or MSNA. Baroreflex modulation of RR and MSNA in response to hyperventilation-induced BP oscillations is attenuated. Blunted baroreflex gain during hyperventilation may be a mechanism that facilitates simultaneous increases in BP, heart rate, and sympathetic activity during dynamic exercise and chemoreceptor activation.

scholarly journals Habitual cigarette smoking raises pressor responses to spontaneous bursts of muscle sympathetic nerve activity

2019 ◽  
Vol 317 (2) ◽  
pp. R280-R288 ◽  
Author(s):  
Jian Cui ◽  
Rachel C. Drew ◽  
Matthew D. Muller ◽  
Cheryl Blaha ◽  
Virginia Gonzalez ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Pressor Responses ◽  
Averaging Techniques

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.

scholarly journals Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia

2009 ◽  
Vol 106 (4) ◽  
pp. 1125-1131 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David A. Low ◽  
David M. Keller ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Whole Body Heat Stress ◽  
Body Heat

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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