scholarly journals Low-Dose Atropine Attenuates Muscle Sympathetic Nerve Activity in Healthy Humans.

2000 ◽  
Vol 23 (3) ◽  
pp. 213-218 ◽  
Author(s):  
Toyoshi YUASA ◽  
Shigeo TAKATA ◽  
Michirou MARUYAMA ◽  
Keiichi YASUMA ◽  
Hisashi YOSHIZAWA ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Low Dose ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Healthy Humans

scholarly journals Chronic intermittent hypoxia in humans during 28 nights results in blood pressure elevation and increased muscle sympathetic nerve activity

2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Chronic Intermittent Hypoxia ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Healthy Humans

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

Age-associated arterial wall thickening is related to elevations in sympathetic activity in healthy humans

2000 ◽  
Vol 278 (4) ◽  
pp. H1205-H1210 ◽  
Author(s):  
Frank A. Dinenno ◽  
Pamela P. Jones ◽  
Douglas R. Seals ◽  
Hirofumi Tanaka
Keyword(s):  
Femoral Artery ◽  
Sympathetic Nerve ◽  
Arterial Wall ◽  
Sympathetic Nerve Activity ◽  
Disease Risk ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Disease Risk ◽  
Older Men ◽  
Nerve Activity ◽  
Healthy Humans

Arterial wall hypertrophy occurs with age in humans and is a strong predictor of cardiovascular disease risk. The responsible mechanism is unknown, but data from studies in experimental animals suggest that elevated sympathetic-adrenergic tone may be involved. To test this hypothesis in humans we studied 11 young (29 ± 1 yr; means ± SE) and 13 older (63 ± 1) healthy normotensive men under supine resting conditions. Muscle sympathetic nerve activity (MSNA) burst frequency (peroneal microneurography) was 70% higher in the older men (39 ± 1 vs. 23 ± 2 bursts/min; P < 0.001). Femoral artery intima media thickness (IMT; B-mode ultrasound) and the femoral IMT-to-lumen diameter ratio (IMT/lumen) were ∼75% greater in the older men (both P < 0.001). Femoral IMT ( r = 0.82) and the femoral IMT/lumen ( r = 0.85) were strongly and positively related to MSNA (both P < 0.001). The significant age group differences in femoral IMT and the IMT/lumen were abolished when the influence of MSNA was removed. In contrast, the relationship between MSNA and femoral wall thickness remained significant after removing the influence of age. We conclude that 1) primary aging is associated with femoral artery hypertrophy in humans and 2) this is strongly related to elevations in sympathetic nerve activity to the vasculature. These results support the hypothesis that tonic elevations in sympathetic nerve activity may be an important mechanism in the arterial remodeling that occurs with human aging.

Hemodynamics and muscle sympathetic nerve activity after 8 h of sustained hypoxia in healthy humans

2007 ◽  
Vol 293 (5) ◽  
pp. H3027-H3035 ◽  
Author(s):  
Renaud Tamisier ◽  
Brian E. Hunt ◽  
Geoffrey S. Gilmartin ◽  
Mathew Curley ◽  
Amit Anand ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Respiratory Control ◽  
Normal Subjects ◽  
Nerve Activity ◽  
Healthy Humans ◽  
End Tidal ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Hypoxia

Hemodynamics, muscle sympathetic nerve activity (MSNA), and forearm blood flow were evaluated in 12 normal subjects before, during (1 and 7 h), and after ventilatory acclimatization to hypoxia achieved with 8 h of continuous poikilocapnic hypoxia. All results are means ± SD. Subjects experienced mean oxygen saturation of 84.3 ± 2.3% during exposure. The exposure resulted in hypoxic acclimatization as suggested by end-tidal CO2 [44.7 ± 2.7 (pre) vs. 39.5 ± 2.2 mmHg (post), P < 0.001] and by ventilatory response to hypoxia [1.2 ± 0.8 (pre) vs. 2.3 ± 1.3 l·min−1·1% fall in saturation−1 (post), P < 0.05]. Subjects exhibited a significant increase in heart rate across the exposure that remained elevated even upon return to room air breathing compared with preexposure (67.3 ± 15.9 vs. 59.8 ± 12.1 beats/min, P < 0.008). Although arterial pressure exhibited a trend toward an increase across the exposure, this did not reach significance. MSNA initially increased from room air to poikilocapnic hypoxia (26.2 ± 10.3 to 32.0 ± 10.3 bursts/100 beats, not significant at 1 h of exposure); however, MSNA then decreased below the normoxic baseline despite continued poikilocapnic hypoxia (20.9 ± 8.0 bursts/100 beats, 7 h Hx vs. 1 h Hx; P < 0.008 at 7 h). MSNA decreased further after subjects returned to room air (16.6 ± 6.0 bursts/100 beats; P < 0.008 compared with baseline). Forearm conductance increased after exposure from 2.9 ± 1.5 to 4.3 ± 1.6 conductance units ( P < 0.01). These findings indicate alterations of cardiovascular and respiratory control following 8 h of sustained hypoxia producing not only acclimatization but sympathoinhibition.

scholarly journals Low‐dose ketamine affects blood pressure, but not muscle sympathetic nerve activity, during progressive central hypovolemia without altering tolerance

2020 ◽  
Vol 598 (24) ◽  
pp. 5661-5672
Author(s):  
Mu Huang ◽  
Joseph C. Watso ◽  
Gilbert Moralez ◽  
Matthew N. Cramer ◽  
Joseph M. Hendrix ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Low Dose ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity

scholarly journals Role of the carotid chemoreceptors in insulin-mediated sympathoexcitation in humans

2020 ◽  
Vol 318 (1) ◽  
pp. R173-R181 ◽  
Author(s):  
Jacqueline K. Limberg ◽  
Blair D. Johnson ◽  
Michael T. Mozer ◽  
Walter W. Holbein ◽  
Timothy B. Curry ◽  
...  
Keyword(s):  
Sympathetic Nerve Activity ◽  
Low Dose ◽  
Muscle Sympathetic Nerve Activity ◽  
Healthy Adults ◽  
Fat Free Mass ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Carotid Chemoreceptors ◽  
Healthy Humans

We examined the contribution of the carotid chemoreceptors to insulin-mediated increases in muscle sympathetic nerve activity (MSNA) in healthy humans. We hypothesized that reductions in carotid chemoreceptor activity would attenuate the sympathoexcitatory response to hyperinsulinemia. Young, healthy adults (9 male/9 female, 28 ± 1 yr, 24 ± 1 kg/m2) completed a 30-min euglycemic baseline followed by a 90-min hyperinsulinemic (1 mU·kg fat-free mass−1·min−1), euglycemic infusion. MSNA (microneurography of the peroneal nerve) was continuously measured. The role of the carotid chemoreceptors was assessed at baseline and during hyperinsulinemia via 1) acute hyperoxia, 2) low-dose dopamine (1–4 µg·kg−1·min−1), and 3) acute hyperoxia + low-dose dopamine. MSNA burst frequency increased from baseline during hyperinsulinemia ( P < 0.01). Acute hyperoxia had no effect on MSNA burst frequency at rest ( P = 0.74) or during hyperinsulinemia ( P = 0.83). The insulin-mediated increase in MSNA burst frequency ( P = 0.02) was unaffected by low-dose dopamine ( P = 0.60). When combined with low-dose dopamine, acute hyperoxia had no effect on MSNA burst frequency at rest ( P = 0.17) or during hyperinsulinemia ( P = 0.85). Carotid chemoreceptor desensitization in young, healthy men and women does not attenuate the sympathoexcitatory response to hyperinsulinemia. Our data suggest that the carotid chemoreceptors do not contribute to acute insulin-mediated increases in MSNA in young, healthy adults.

Endotoxemia causes central downregulation of sympathetic vasomotor tone in healthy humans

2008 ◽  
Vol 295 (3) ◽  
pp. R891-R898 ◽  
Author(s):  
Friedhelm Sayk ◽  
Alexander Vietheer ◽  
Bernhard Schaaf ◽  
Peter Wellhoener ◽  
Gunther Weitz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Blood Levels ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Healthy Humans ◽  
Vascular Bed

Experimental endotoxemia as a model of the initial septic response affects the autonomic nervous system with profound cardiovascular sequelae. Whether the postsynaptic sympathoneural activity to the muscle vascular bed is altered in the early septic phase remains to be determined. The present study aimed to elucidate the early effects of LPS on muscle sympathetic nerve activity (MSNA) and cardiovascular regulation in healthy humans. Young, healthy volunteers randomly received either an LPS bolus (4 ng/kg body wt, n = 11) or placebo (saline; n = 7). Experimental baroreflex assessment (baseline measurements followed by infusion of vasoactive drugs nitroprusside/phenylephrine) was done prior to and 90 min following LPS or placebo challenge. MSNA, heart rate, blood pressure, and blood levels of catecholamines, TNF-α and IL-6 were measured sequentially. Endotoxin but not placebo-induced flu-like symptoms and elevated cytokine levels. In contrast to placebo, LPS significantly suppressed MSNA burst frequency 90 min after injection [mean ± SE: 12.1 ± 2.9 vs. 27.5 ± 3.3 burst/min (post- vs. pre-LPS); P < 0.005] but increased heart rate [78.4 ± 3.1 vs. 60.6 ± 2.0 beats/min (post- vs. pre-LPS); P < 0.001]. Baseline blood pressure was not altered, but baroreflex testing demonstrated a blunted MSNA response and uncoupling of heart rate modulation to blood pressure changes in the endotoxin group. We conclude that endotoxin challenge in healthy humans has rapid suppressive effects on postsynaptic sympathetic nerve activity to the muscle vascular bed and alters baroreflex function which may contribute to the untoward cardiovascular effects of sepsis.

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