Abstract 2470: Augmented Tonic Activation Of Chemoreceptors May Contribute To Sympathetic Overactivity In Patients With Essential Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Maciej Sinski ◽  
Jacek Lewandowski ◽  
Joanna Bidiuk ◽  
Piotr Abramczyk ◽  
Anna Dobosiewicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Hemoglobin Saturation ◽  
Ambient Oxygen ◽  
Young Subjects ◽  
End Tidal ◽  
Carotid Body Chemoreceptors

Rationale : Peripheral chemoreflex contributes to regulation of arterial blood pressure and chemoreceptors respond not only to hypoxia but they are also continuously activated by normal ambient oxygen concentration. Stimulation of chemoreceptors activates sympathetic traffic and this response may be altered in subjects with essential hypertension.. Objective: The aim of our study was to investigate the effect of deactivation of carotid body chemoreceptors on sympathetic activity directly measured as MSNA (muscle sympathetic nerve activity) in young subjects with mild to moderate untreated hypertension. Methods: Twelve patients with essential hypertension (36±9 years, all men, BMI 29±4 kg/m 2 ,) and 8 controls (37±7, men BMI 27±5kg/m 2 ) participated in the study. None of the patients or controls received any medications. MSNA (burst/minute and mean burst amplitude - au), systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate (HR), ECG, hemoglobin saturation with oxygen (Sat%), end tidal CO 2 and respiratory movements were monitored and measured after 10 minute of respiration by non-rebreathing mask with 100% 0 2 or 21% O 2 applied in blinded fashion. Results: Hypertensives had higher resting MSNA (38.6 ±8.6 burst/min vs. 30.3±.7 burst/min, p<0.05), SBP (149.1± 9.9 vs. 124.1 ±11.6, p < 0.05) and DBP (92.1 ±8.6 vs. 78.1 ± 8.9, p< 0.05) than controls. Breathing with 100% oxygen caused significant decrease in MSNA in hypertensives (from 38.6 ± 8.6 burst/min to 26.3 burst/min ± 6.8 and from 100 ± 0 au to 86 ± 18 au, p< 0.05) and no change in MSNA in controls (30.3 ± 5.7 burst/min initially and 27.3 burst/min ± 6.2 after 100% 0 2 , 100 ± 0 au vs. 98 ± 11 au). Blood pressure, end tidal CO 2 , respiration frequency did not change significantly after hyperoxia while HR decreased (from 69.6 ± 9 to 64.1 ± 7 in hypertensives p<0.05 and from 67± 8 to 62.5 ± 7 in controls, p< 0.05). Sat% increased significantly in both groups to 99%. Conclusions: Increased sympathetic activity in young, untreated hypertensives may be caused by the elevated tonic chemoreflex activation.

Arterial pressure and muscle sympathetic nerve activity are increased after two hours of sustained but not cyclic hypoxia in healthy humans

2005 ◽  
Vol 98 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Renaud Tamisier ◽  
Amit Anand ◽  
Luz M. Nieto ◽  
David Cunnington ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sustained Hypoxia

Sustained and episodic hypoxic exposures lead, by two different mechanisms, to an increase in ventilation after the exposure is terminated. Our aim was to investigate whether the pattern of hypoxia, cyclic or sustained, influences sympathetic activity and hemodynamics in the postexposure period. We measured sympathetic activity (peroneal microneurography), hemodynamics [plethysmographic forearm blood flow (FBF), arterial pressure, heart rate], and peripheral chemosensitivity in normal volunteers on two occasions during and after 2 h of either exposure. By design, mean arterial oxygen saturation was lower during sustained relative to cyclic hypoxia. Baseline to recovery muscle sympathetic nerve activity and blood pressure went from 15.7 ± 1.2 to 22.6 ± 1.9 bursts/min ( P < 0.01) and from 85.6 ± 3.2 to 96.1 ± 3.3 mmHg ( P < 0.05) after sustained hypoxia, respectively, but did not exhibit significant change from 13.6 ± 1.5 to 17.3 ± 2.5 bursts/min and 84.9 ± 2.8 to 89.8 ± 2.5 mmHg after cyclic hypoxia. A significant increase in FBF occurred after sustained, but not cyclic, hypoxia, from 2.3 ± 0.2 to 3.29 ± 0.4 and from 2.2 ± 0.1 to 3.1 ± 0.5 ml·min−1·100 g of tissue−1, respectively. Neither exposure altered the ventilatory response to progressive isocapnic hypoxia. Two hours of sustained hypoxia increased not only muscle sympathetic nerve activity but also arterial blood pressure. In contrast, cyclic hypoxia produced slight but not significant changes in hemodynamics and sympathetic activity. These findings suggest the cardiovascular response to acute hypoxia may depend on the intensity, rather than the pattern, of the hypoxic exposure.

scholarly journals Sympathetic baroreflex gain in normotensive pregnant women

2015 ◽  
Vol 119 (5) ◽  
pp. 468-474 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Rachel J. Skow ◽  
Brittany A. Matenchuk ◽  
Radha S. Chari ◽  
Colleen G. Julian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Pregnant Women ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Sequence Method ◽  
Normotensive Pregnancy ◽  
Dependent Mechanism

Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting. We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls. Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m2) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m2). Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls. Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy. Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (−3.7 ± 0.5 vs. −5.4 ± 0.5 bursts·100 heart beats−1·mmHg−1, P = 0.03), as was baroreflex gain calculated with total sympathetic activity (−294 ± 24 vs. −210 ± 24 au·100 heart beats−1·mmHg−1; P = 0.03). Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2). However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women ( R = −0.7; P = 0.02). Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism.

Assessment of the Antihypertensive Effect of Atenolol with 24 H Ambulatory Monitoring of Blood Pressure

1979 ◽  
Vol 57 (s5) ◽  
pp. 387s-389s ◽  
Author(s):  
J. S. Floras ◽  
P. Fox ◽  
M. O. Hassan ◽  
J. V. Jones ◽  
P. Sleight ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Ambulatory Monitoring ◽  
Single Daily Dose ◽  
Pressure Measurements ◽  
Arterial Blood ◽  
Blood Pressure Study ◽  
Daily Dose

1. Twenty-four hour intra-arterial blood pressure measurements and electrocardiograms were obtained from 12 subjects with untreated essential hypertension. 2. The patients kept records of their activity, paying particular attention to times of retiring to bed, and times of waking in the morning. 3. All subjects were treated with a single daily dose of atenolol (50 to 200 mg) for between 2 and 9 months, and then underwent a second 24 h blood pressure study. 4. Arterial blood pressure was lowered significantly throughout the 24 h period with a single daily dose of atenolol.

Short-term intermittent hypoxia enhances sympathetic responses to continuous hypoxia in humans

2007 ◽  
Vol 103 (3) ◽  
pp. 835-842 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Cynthia S. Hogeman ◽  
Sadeq Quraishi ◽  
Latoya Linton-Frazier ◽  
Kristen S. Gray
Keyword(s):  
Blood Pressure ◽  
Sleep Apnea ◽  
Sympathetic Activity ◽  
Intermittent Hypoxia ◽  
Muscle Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Short Term ◽  
Healthy Humans ◽  
Obstructive Sleep ◽  
Normal Humans

Short-term intermittent hypoxia leads to sustained sympathetic activation and a small increase in blood pressure in healthy humans. Because obstructive sleep apnea, a condition associated with intermittent hypoxia, is accompanied by elevated sympathetic activity and enhanced sympathetic chemoreflex responses to acute hypoxia, we sought to determine whether intermittent hypoxia also enhances chemoreflex activity in healthy humans. To this end, we measured the responses of muscle sympathetic nerve activity (MSNA, peroneal microneurography) to arterial chemoreflex stimulation and deactivation before and following exposure to a paradigm of repetitive hypoxic apnea (20 s/min for 30 min; O2 saturation nadir 81.4 ± 0.9%). Compared with baseline, repetitive hypoxic apnea increased MSNA from 113 ± 11 to 159 ± 21 units/min ( P = 0.001) and mean blood pressure from 92.1 ± 2.9 to 95.5 ± 2.9 mmHg ( P = 0.01; n = 19). Furthermore, compared with before, following intermittent hypoxia the MSNA (units/min) responses to acute hypoxia [fraction of inspired O2 (FiO2) 0.1, for 5 min] were enhanced (pre- vs. post-intermittent hypoxia: +16 ± 4 vs. +49 ± 10%; P = 0.02; n = 11), whereas the responses to hyperoxia (FiO2 0.5, for 5 min) were not changed significantly ( P = NS; n = 8). Thus 30 min of intermittent hypoxia is capable of increasing sympathetic activity and sensitizing the sympathetic reflex responses to hypoxia in normal humans. Enhanced sympathetic chemoreflex activity induced by intermittent hypoxia may contribute to altered neurocirculatory control and adverse cardiovascular consequences in sleep apnea.

scholarly journals Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

2013 ◽  
Vol 304 (5) ◽  
pp. H759-H766 ◽  
Author(s):  
Seth T. Fairfax ◽  
Jaume Padilla ◽  
Lauro C. Vianna ◽  
Michael J. Davis ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Burst Size ◽  
Muscle Sympathetic Nerve Activity ◽  
Common Femoral Artery ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Arterial Blood

Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, −2.9 ± 1.1%; and multiple bursts, −11.0 ± 1.4%; both, P < 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (+3.1 ± 0.5%; P < 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.

scholarly journals THE ASSAY OF HYPERTENSIN FROM THE ARTERIAL BLOOD OF NORMOTENSIVE AND HYPERTENSIVE HUMAN BEINGS

1952 ◽  
Vol 95 (6) ◽  
pp. 523-529 ◽  
Author(s):  
Joseph R. Kahn ◽  
Leonard T. Skeggs ◽  
Norman P. Shumway ◽  
Paul E. Wisenbaugh
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Normal Blood ◽  
Moderate Degree ◽  
Human Beings ◽  
Normal Blood Pressure ◽  
Arterial Blood ◽  
The Mean ◽  
Mean Concentration ◽  
Benign Group

Hypertensin has been assayed in the blood of patients with normal blood pressure and in those with essential hypertension in both the benign and malignant phases. 250 ml. samples of arterial blood were obtained, chemically purified, and concentrated to a volume of 1 ml. These extracts were then assayed in anesthetized rats. The concentrations of hypertensin in the blood of patients with the malignant phase of essential hypertension were found to be greatly increased. The concentrations of hypertensin found in patients with benign hypertension had a moderate degree of overlapping with those found in the normotensive group, but the mean concentration of hypertensin in the former group was twice that of the controls. Although these results are statistically significant, the amounts of hypertensin recovered in the benign group are so small that no conclusions can be drawn as to its effectiveness in producing vasoconstriction in these patients.

scholarly journals Pharmacological assessment of the contribution of the arterial baroreflex to sympathetic discharge patterns in healthy humans

2018 ◽  
Vol 119 (6) ◽  
pp. 2166-2175 ◽  
Author(s):  
Jacqueline K. Limberg ◽  
Elizabeth P. Ott ◽  
Walter W. Holbein ◽  
Sarah E. Baker ◽  
Timothy B. Curry ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Activity ◽  
High Threshold ◽  
Neural Activation ◽  
Afferent Activity ◽  
Cluster Number ◽  
Arterial Blood ◽  
Rate Coding ◽  
Low Threshold

To study how changes in baroreceptor afferent activity affect patterns of sympathetic neural activation, we manipulated arterial blood pressure with intravenous nitroprusside (NTP) and phenylephrine (PE) and measured action potential (AP) patterns with wavelet-based methodology. We hypothesized that 1) baroreflex unloading (NTP) would increase firing of low-threshold axons and recruitment of latent axons and 2) baroreflex loading (PE) would decrease firing of low-threshold axons. Heart rate (HR, ECG), arterial blood pressure (BP, brachial catheter), and muscle sympathetic nerve activity (MSNA, microneurography of peroneal nerve) were measured at baseline and during steady-state systemic, intravenous NTP (0.5–1.2 µg·kg−1·min−1, n = 13) or PE (0.2–1.0 µg·kg−1·min−1, n = 9) infusion. BP decreased and HR and integrated MSNA increased with NTP ( P < 0.01). AP incidence (326 ± 66 to 579 ± 129 APs/100 heartbeats) and AP content per integrated burst (8 ± 1 to 11 ± 2 APs/burst) increased with NTP ( P < 0.05). The firing probability of low-threshold axons increased with NTP, and recruitment of high-threshold axons was observed (22 ± 3 to 24 ± 3 max cluster number, 9 ± 1 to 11 ± 1 clusters/burst; P < 0.05). BP increased and HR and integrated MSNA decreased with PE ( P < 0.05). PE decreased AP incidence (406 ± 128 to 166 ± 42 APs/100 heartbeats) and resulted in fewer unique clusters (15 ± 2 to 9 ± 1 max cluster number, P < 0.05); components of an integrated burst (APs or clusters per burst) were not altered ( P > 0.05). These data support a hierarchical pattern of sympathetic neural activation during manipulation of baroreceptor afferent activity, with rate coding of active neurons playing the predominant role and recruitment/derecruitment of higher-threshold units occurring with steady-state hypotensive stress. NEW & NOTEWORTHY To study how changes in baroreceptor afferent activity affect patterns of sympathetic neural activation, we manipulated arterial blood pressure with intravenous nitroprusside and phenylephrine and measured sympathetic outflow with wavelet-based methodology. Baroreflex unloading increased sympathetic activity by increasing firing probability of low-threshold axons (rate coding) and recruiting new populations of high-threshold axons. Baroreflex loading decreased sympathetic activity by decreasing the firing probability of larger axons (derecruitment); however, the components of an integrated burst were unaffected.

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