scholarly journals Tonic aortic depressor nerve stimulation does not impede baroreflex dynamic characteristics concomitantly mediated by the stimulated nerve

2018 ◽  
Vol 314 (3) ◽  
pp. R459-R467 ◽  
Author(s):  
Toru Kawada ◽  
Michael J. Turner ◽  
Shuji Shimizu ◽  
Atsunori Kamiya ◽  
Toshiaki Shishido ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Dynamic Characteristics ◽  
Sympathetic Nerve Activity ◽  
Pressure Perturbation ◽  
Arterial Baroreflex ◽  
Short Term ◽  
Baroreflex Activation Therapy ◽  
Aortic Depressor Nerve ◽  
Activation Therapy ◽  
The Right

Although electrical activation of the carotid sinus baroreflex (baroreflex activation therapy) is being explored as a device therapy for resistant hypertension, possible effects on baroreflex dynamic characteristics of interaction between electrical stimulation and pressure inputs are not fully elucidated. To examine whether the electrical stimulation of the baroreceptor afferent nerve impedes normal short-term arterial pressure (AP) regulation mediated by the stimulated nerve, we electrically stimulated the right aortic depressor nerve (ADN) while estimating the baroreflex dynamic characteristics by imposing pressure inputs to the isolated baroreceptor region of the right ADN in nine anesthetized rats. A Gaussian white noise signal with a mean of 120 mmHg and standard deviation of 20 mmHg was used for the pressure perturbation. A tonic ADN stimulation (2 or 5 Hz, 10 V, 0.1-ms pulse width) decreased mean sympathetic nerve activity (367.0 ± 70.9 vs. 247.3 ± 47.2 arbitrary units, P < 0.01) and mean AP (98.4 ± 7.8 vs. 89.2 ± 4.5 mmHg, P < 0.01) during dynamic pressure perturbation. The ADN stimulation did not affect the slope of dynamic gain in the neural arc transfer function from pressure perturbation to sympathetic nerve activity (16.9 ± 1.0 vs. 14.7 ± 1.6 dB/decade, not significant). These results indicate that electrical stimulation of the baroreceptor afferent nerve does not significantly impede the dynamic characteristics of the arterial baroreflex concomitantly mediated by the stimulated nerve. Short-term AP regulation by the arterial baroreflex may be preserved during the baroreflex activation therapy.

Acute resetting of the carotid sinus baroreflex by aortic depressor nerve stimulation

1993 ◽  
Vol 264 (4) ◽  
pp. H1215-H1222 ◽  
Author(s):  
L. Hayward ◽  
M. Hay ◽  
R. B. Felder
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Renal Sympathetic Nerve Activity ◽  
Aortic Depressor Nerve ◽  
Central Neurons ◽  
Carotid Sinus Baroreflex ◽  
Before And After ◽  
The Right ◽  
Sinus Pressure ◽  
Renal Sympathetic

The effect of prolonged aortic depressor nerve (ADN) stimulation on carotid sinus baroreflex regulation of arterial pressure (AP) and renal sympathetic nerve activity (RSNA) was examined in anesthetized rabbits. Ramp increases in carotid sinus pressure (CSP) were repeated before and after 5 min of bilateral ADN stimulation. One minute after ADN stimulation the curve relating AP to CSP had shifted up and to the right, characterized by significant increases (P < 0.05) in the maximum (91 +/- 2 to 101 +/- 3 mmHg; mean +/- SE), midpoint (118 +/- 7 to 125 +/- 8 mmHg CSP), and minimum (45 +/- 3 to 53 +/- 4 mmHg) of the AP reflex curve. There was a parallel shift downward of the curve relating RSNA to CSP, characterized by significant decreases in the maximum [100 +/- 0 to 66 +/- 8% of maximum control RSNA value (%max)], the range (90 +/- 2 to 59 +/- 8%max), and the gain (-1.0 +/- 0.2 to -0.5 +/- 0.1%max/mmHg) of the RSNA reflex curve. Values returned to control within 10 min of cessation of ADN stimulation. These results suggest that central neurons processing baroreflex information from one set of mechanoreceptors can be reset by convergent signals arising from another baroreceptor site.

Short-term electroacupuncture at Zusanli resets the arterial baroreflex neural arc toward lower sympathetic nerve activity

2006 ◽  
Vol 291 (1) ◽  
pp. H318-H326 ◽  
Author(s):  
Daisaku Michikami ◽  
Atsunori Kamiya ◽  
Toru Kawada ◽  
Masashi Inagaki ◽  
Toshiaki Shishido ◽  
...  
Keyword(s):  
Pulse Duration ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Closed Loop ◽  
Equilibrium Diagram ◽  
Threshold Current ◽  
Operating Point ◽  
Arterial Baroreflex ◽  
Short Term ◽  
Nerve Activity

Although electroacupuncture reduces sympathetic nerve activity (SNA) and arterial pressure (AP), the effects of electroacupuncture on the arterial baroreflex remain to be systematically analyzed. We investigated the effects of electroacupuncture of Zusanli on the arterial baroreflex using an equilibrium diagram comprised of neural and peripheral arcs. In anesthetized, vagotomized, and aortic-denervated rabbits, we isolated carotid sinuses and changed intra-carotid sinus pressure (CSP) from 40 to 160 mmHg in increments of 20 mmHg/min while recording cardiac SNA and AP. Electroacupuncture of Zusanli was applied with a pulse duration of 5 ms and a frequency of 1 Hz. An electric current 10 times the minimal threshold current required for visible muscle twitches was used and was determined to be 4.8 ± 0.3 mA. Electroacupuncture for 8 min decreased SNA and AP ( n = 6). It shifted the neural arc (i.e., CSP-SNA relationship) to lower SNA but did not affect the peripheral arc (i.e., SNA-AP relationship) ( n = 8). SNA and AP at the closed-loop operating point, determined by the intersection of the neural and peripheral arcs, decreased from 100 ± 4 to 80 ± 9 arbitrary units and from 108 ± 9 to 99 ± 8 mmHg (each P < 0.005), respectively. Peroneal denervation eliminated the shift of neural arc by electroacupuncture ( n = 6). Decreasing the pulse duration to <2.5 ms eliminated the effects of SNA and AP reduction. In conclusion, short-term electroacupuncture resets the neural arc to lower SNA, which moves the operating point toward lower AP and SNA under baroreflex closed-loop conditions.

Cardiopulmonary and arterial baroreflex responses to acute volume expansion during fetal and postnatal development

1994 ◽  
Vol 267 (4) ◽  
pp. H1467-H1475 ◽  
Author(s):  
D. C. Merrill ◽  
J. L. Segar ◽  
O. J. McWeeny ◽  
B. A. Smith ◽  
J. E. Robillard
Keyword(s):  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Arterial Baroreflex ◽  
Response Curves ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
The Right ◽  
Renal Sympathetic

Recent studies demonstrated that renal denervation had no effect on the natriuretic response to volume expansion (VE) in fetal sheep, suggesting that the sensitivity of the cardiopulmonary reflex in response to VE is impaired in the fetus. To test this hypothesis, we investigated the renal sympathetic nerve activity (RSNA) and heart rate (HR) responses to 20 and 50% intravascular VE in fetal (130-135 days gestation; term 145 days) (n = 7), newborn (n = 8), and 6- to 8-wk-old sheep (n = 9). Despite similar increases in right atrial pressure (RAP) in the three groups, 20% VE had no significant effect on RSNA and HR in fetal sheep but significantly decreased RSNA in newborn (-22.8 +/- 7.3%) and 6- to 8-wk-old sheep (-32.1 +/- 11.7%). Bradycardic responses to VE were also observed in both newborn (from 237 +/- 6 to 200 +/- 12 beats/min) and 6- to 8-wk-old sheep (from 170 +/- 9 to 140 +/- 9 beats/min). A 50% VE had no significant effect on fetal RSNA and HR, whereas it increased RAP by 6.8 +/- 0.9 mmHg. In addition, we tested the hypothesis that interactions between cardiopulmonary and arterial baroreflexes in response to VE change during development. We found that 20 and 50% VE shifted the RSNA and HR arterial baroreflex response curves to the right in the fetus but had no significant effects on the gain of the arterial baroreflex curves in either fetal, newborn, or 6- to 8-wk-old sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired central mediation of the arterial baroreflex in chronic renal hypertension

1984 ◽  
Vol 246 (5) ◽  
pp. H720-H727 ◽  
Author(s):  
G. B. Guo ◽  
F. M. Abboud
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Sympathetic Nerve Activity ◽  
Renal Hypertension ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Aortic Depressor Nerve ◽  
The Central Nervous System ◽  
Selective Impairment ◽  
Stimulation Of

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

Cardiac sympathetic afferent stimulation impairs baroreflex control of renal sympathetic nerve activity in rats

2004 ◽  
Vol 286 (5) ◽  
pp. H1706-H1711 ◽  
Author(s):  
Lie Gao ◽  
Zhen Zhu ◽  
Irving H. Zucker ◽  
Wei Wang
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Maximum Slope ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Renal Sympathetic ◽  
Stimulation Of

It is well known that cardiac sympathetic afferent reflexes contribute to increases in sympathetic outflow and that sympathetic activity can antagonize arterial baroreflex function. In this study, we tested the hypothesis that in normal rats, chemical and electrical stimulation of cardiac sympathetic afferents results in a decrease in the arterial baroreflex function by increasing sympathetic nerve activity. Under α-chloralose (40 mg/kg) and urethane (800 mg/kg ip) anesthesia, renal sympathetic nerve activity, mean arterial pressure, and heart rate were recorded. The arterial baroreceptor reflex was evaluated by infusion of nitroglycerin (25 μg iv) and phenylephrine (10 μg iv). Left ventricular epicardial application of capsaicin (0.4 μg in 2 μl) blunted arterial baroreflex function by 46% (maximum slope 3.5 ± 0.3 to 1.9 ± 0.2%/mmHg, P < 0.01). When the central end of the left cardiac sympathetic nerve was electrically stimulated (7 V, 1 ms, 20 Hz), the sensitivity of the arterial baroreflex was similarly decreased by 42% (maximum slope 3.2 ± 0.3 to 1.9 ± 0.4%/mmHg; P < 0.05). Pretreatment with intracerebroventricular injection of losartan (500 nmol in 1 μl of artificial cerebrospinal fluid) completely prevented the impairment of arterial baroreflex function induced by electrical stimulation of the central end of the left cardiac sympathetic nerve (maximum slope 3.6 ± 0.4 to 3.1 ± 0.5%/mmHg). These results suggest that the both chemical and electrical stimulation of the cardiac sympathetic afferents reduces arterial baroreflex sensitivity and the impairment of arterial baroreflex function induced by cardiac sympathetic afferent stimulation is mediated by central angiotensin type 1 receptors.

Wavelet-Based System Identification of Short-Term Dynamic Characteristics of Arterial Baroreflex

2008 ◽  
Vol 37 (1) ◽  
pp. 112-128 ◽  
Author(s):  
Koji Kashihara ◽  
Toru Kawada ◽  
Masaru Sugimachi ◽  
Kenji Sunagawa
Keyword(s):  
System Identification ◽  
Dynamic Characteristics ◽  
Arterial Baroreflex ◽  
Short Term

Systemic vascular effects of acute electrical baroreflex stimulation

2014 ◽  
Vol 307 (2) ◽  
pp. H236-H241 ◽  
Author(s):  
Steven Burgoyne ◽  
Dimitrios Georgakopoulos ◽  
Israel Belenkie ◽  
John V. Tyberg
Keyword(s):  
Aortic Pressure ◽  
Left Ventricular ◽  
Ang Ii ◽  
Vascular Effects ◽  
Venous Capacitance ◽  
Baroreflex Activation Therapy ◽  
Anesthetized Dogs ◽  
Activation Therapy ◽  
Baroreflex Stimulation ◽  
The Right

We intended to determine if acute baroreflex activation therapy (BAT) increases venous capacitance and aortic conductance. BAT is effective in resistant hypertension, but its effect on the systemic vasculature is poorly understood. Left ventricular (LV) and aortic pressures and subdiaphragmatic aortic and caval flows (ultrasonic) were measured in six anesthetized dogs. Changes in abdominal blood volume (Vabdominal) were estimated as the integrated difference in abdominal aortic inflow and caval outflow. An electrode was implanted on the right carotid sinus. Data were measured during control and BAT. Next, sodium nitroprusside (SNP) was infused and BAT was subsequently added. Finally, angiotensin II (ANG II) was infused, and three increased BAT currents were added. We found that BAT decreased mean aortic pressure (PAo) by 22.5 ± 1.3 mmHg ( P < 0.001) and increased aortic conductance by 16.2 ± 4.9% ( P < 0.01) and Vabdominal at a rate of 2.2 ± 0.6 ml·kg−1·min−1 ( P < 0.01). SNP decreased PAo by 17.4 ± 0.7 mmHg ( P < 0.001) and increased Vabdominal at a rate of 2.2 ± 0.7 ml·kg−1·min−1 ( P < 0.05). During the SNP infusion, BAT decreased PAo further, by 26.0 ± 2.1 mmHg ( P < 0.001). ANG II increased PAo by 40.4 ± 3.5 mmHg ( P = 0.001). When an increased BAT current was added, PAo decreased to baseline ( P < 0.01) while aortic conductance increased from 62.3 ± 5.2% to 80.2 ± 3.3% ( P < 0.05) of control. Vabdominal increased at a rate of 1.8 ± 0.9 ml·kg−1·min−1 ( P < 0.01), reversing the ANG II effects. In conclusion, BAT increases arterial conductance, decreases PAo, and increases venous capacitance even in the presence of powerful vasoactive drugs. Increasing venous capacitance may be an important effect of BAT in hypertension.

scholarly journals Aortic depressor nerve stimulation does not impede the dynamic characteristics of the carotid sinus baroreflex in normotensive or spontaneously hypertensive rats

2017 ◽  
Vol 312 (5) ◽  
pp. R787-R796 ◽  
Author(s):  
Toru Kawada ◽  
Michael J. Turner ◽  
Shuji Shimizu ◽  
Masafumi Fukumitsu ◽  
Atsunori Kamiya ◽  
...  
Keyword(s):  
Dynamic Characteristics ◽  
Sympathetic Nerve ◽  
Spontaneously Hypertensive Rats ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Aortic Depressor Nerve ◽  
Carotid Sinus Baroreflex

Recent clinical trials in patients with drug-resistant hypertension indicate that electrical activation of the carotid sinus baroreflex can reduce arterial pressure (AP) for more than a year. To examine whether the electrical stimulation from one baroreflex system impedes normal short-term AP regulation via another unstimulated baroreflex system, we electrically stimulated the left aortic depressor nerve (ADN) while estimating the dynamic characteristics of the carotid sinus baroreflex in anesthetized normotensive Wistar-Kyoto (WKY; n = 8) rats and spontaneously hypertensive rats (SHR; n = 7). Isolated carotid sinus regions were perturbed for 20 min using a Gaussian white noise signal with a mean of 120 mmHg for WKY and 160 mmHg for SHR. Tonic ADN stimulation (2 Hz, 10 V, and 0.1-ms pulse width) decreased mean sympathetic nerve activity (73.4 ± 14.0 vs. 51.6 ± 11.3 arbitrary units in WKY, P = 0.012; and 248.7 ± 33.9 vs. 181.1 ± 16.6 arbitrary units in SHR, P = 0.018) and mean AP (90.8 ± 6.6 vs. 81.2 ± 5.4 mmHg in WKY, P = 0.004; and 128.6 ± 9.8 vs. 114.7 ± 10.3 mmHg in SHR, P = 0.009). The slope of dynamic gain in the neural arc transfer function from carotid sinus pressure to sympathetic nerve activity was not different between trials with and without the ADN stimulation (12.55 ± 0.93 vs. 13.03 ± 1.28 dB/decade in WKY, P = 0.542; and 17.37 ± 1.01 vs. 17.47 ± 1.64 dB/decade in SHR, P = 0.946). These results indicate that the tonic ADN stimulation does not significantly modify the dynamic characteristics of the carotid sinus baroreflex.

New Hope for Resistant Hypertention

2012 ◽  
Vol 5 (1) ◽  
pp. 81-91
Author(s):  
Z Rahman ◽  
KK Karmaker ◽  
M Ahmed ◽  
M Aziz ◽  
S Chowdhury ◽  
...  
Keyword(s):  
Resistant Hypertension ◽  
Patient Adherence ◽  
Public Health Problem ◽  
Drug Regimen ◽  
Renal Sympathetic Denervation ◽  
Major Public Health Problem ◽  
Antihypertensive Medications ◽  
Baroreflex Activation Therapy ◽  
Activation Therapy ◽  
Increasing Trends

Hypertension is a major public health problem. Despite the increasing awareness of hypertension and its implications among patients and treating physicians, the prevalence of resistant hypertension    remains high.Resistant hypertension define as blood pressure that remains elevated above treatment goals despite administration of an optimal three drug regimen that include a diuretic1 The prevalence of resistant    hypertension is projected to increase, owing to the aging population and increasing trends in obesity, sleep apnea, and chronic kidney disease. It is estimated that at least 10% of all patients with hypertension are resistant to existing drugs. Management of resistant hypertension must begin with  a careful evaluation of the patient to confirm the diagnosis and exclude factors associated with “pseudo-resistance,” such as improper BP measurement technique, the white-coat effect, and poor patient adherence to life-style and/or antihypertensive medications. Despite the use of the appropriate dose and type of diuretic to overcome the management of resistant hypertension, we can’t achieve our goal. But there is at least two devices namely Baroreflex Activation Therapy and Catheter-based  renal sympathetic denervation make the new hope for the patient with resistant hypertension DOI: http://dx.doi.org/10.3329/cardio.v5i1.12278 Cardiovasc. j. 2012; 5(1): 81-91

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