Visceral afferent activation-induced changes in sympathetic nerve activity and baroreflex sensitivity

1999 ◽  
Vol 276 (6) ◽  
pp. R1780-R1791 ◽  
Author(s):  
Tarek M. Saleh ◽  
Barry J. Connell ◽  
Gary V. Allen
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Parabrachial Nucleus ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Relative Contribution

The following experiments were done to determine whether changes in baroreflex sensitivity evoked by cervical vagus nerve stimulation are due to sympathoexcitation mediated by the parabrachial nucleus. The relative contribution of cardiopulmonary and general gastric afferents within the cervical vagus nerve to the depression in baroreflex sensitivity are also investigated. Male Sprague-Dawley rats anesthetized with thiobutabarbital sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate or for the continuous monitoring of renal sympathetic nerve activity. Baroreflex sensitivity was measured using bolus injections of phenylephrine. Electrical stimulation of the cervical vagus (with or without the aortic depressor nerve) or the abdominal vagus nerve produced a significant increase in renal nerve activity and a decrease in baroreflex sensitivity. Both of these effects were blocked after the microinjection of lidocaine into the parabrachial nucleus before nerve stimulation. Therefore, we conclude that an increase in the activity of cardiac, pulmonary, or general gastric afferents mediated the increased sympathetic output and decreased baroreflex sensitivity via a pathway involving the parabrachial nucleus.

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.

Age-related central and baroreceptor impairment in female Sprague-Dawley rats

1989 ◽  
Vol 256 (5) ◽  
pp. H1399-H1406 ◽  
Author(s):  
S. Tanabe ◽  
R. D. Bunag
Keyword(s):  
Heart Rate ◽  
Sodium Nitroprusside ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Reflex Responses ◽  
Sprague Dawley Rats ◽  
Old Rats

To determine whether baroreflex sensitivity changes with age, we compared drug-induced reflex responses in 2- and 9-mo-old female Sprague-Dawley rats anesthetized with urethan-chloralose. Baroreflexes were stimulated by elevating or lowering blood pressure with intravenous infusions of phenylephrine or sodium nitroprusside. Reflex responses in heart rate and sympathetic nerve activity during phenylephrine infusions were weaker in 9- than in 2-mo-old rats, as were reflex tachycardia during sodium nitroprusside infusion and decreases in heart rate and sympathetic nerve activity elicited by electrical stimulation of the left aortic depressor nerve. Afferent aortic nerve activity was also appreciably lower in 9-mo-old rats at pressures greater than 130 mmHg but did not differ between rat groups at normotensive pressures. These results suggest that baroreflex sensitivity in 9-mo-old rats can be characterized as follows: 1) impaired at pressures greater than 130 mmHg but still adequate at normotensive pressures, and 2) all reflex arc components may be impaired.

scholarly journals Non-invasive Vagus Nerve Stimulation in Healthy Humans Reduces Sympathetic Nerve Activity

2014 ◽  
Vol 7 (6) ◽  
pp. 871-877 ◽  
Author(s):  
Jennifer A. Clancy ◽  
David A. Mary ◽  
Klaus K. Witte ◽  
John P. Greenwood ◽  
Susan A. Deuchars ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Vagus Nerve Stimulation ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Non Invasive ◽  
Healthy Humans

scholarly journals Arcuate nucleus injection of an anti-insulin affibody prevents the sympathetic response to insulin

2013 ◽  
Vol 304 (11) ◽  
pp. H1538-H1546 ◽  
Author(s):  
Brittany S. Luckett ◽  
Jennifer L. Frielle ◽  
Lawrence Wolfgang ◽  
Sean D. Stocker
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arcuate Nucleus ◽  
Insulin Receptors ◽  
Ventromedial Hypothalamus ◽  
Intracerebroventricular Injection ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sympathetic Response ◽  
Sprague Dawley Rats

Accumulating evidence suggests that insulin acts within the hypothalamus to alter sympathetic nerve activity (SNA) and baroreflex function. Although insulin receptors are widely expressed across the hypothalamus, recent evidence suggests that neurons of the arcuate nucleus (ARC) play an important role in the sympathoexcitatory response to insulin. The purpose of the present study was to determine whether circulating insulin acts directly in the ARC to elevate SNA. In anesthetized male Sprague-Dawley rats (275–425 g), the action of insulin was neutralized by microinjection of an anti-insulin affibody (1 ng/40 nl). To verify the efficacy of the affibody, ARC pretreatment with injection of the anti-insulin affibody completely prevented the increase in lumbar SNA produced by ARC injection of insulin. Next, ARC pretreatment with the anti-insulin affibody attenuated the lumbar sympathoexcitatory response to intracerebroventricular injection of insulin. Third, a hyperinsulinemic-euglycemic clamp increased lumbar, but not renal, SNA in animals that received ARC injection of a control affibody. However, this sympathoexcitatory response was absent in animals pretreated with the anti-insulin affibody in the ARC. Injection of the anti-insulin affibody in the adjacent ventromedial hypothalamus did not alter the sympathoexcitatory response to insulin. The ability of the anti-insulin affibody to prevent the sympathetic effects of insulin cannot be attributed to a general inactivation or nonspecific effect on ARC neurons as the affibody did not alter the sympathoexcitatory response to ARC disinhibition by gabazine. Collectively, these findings suggest that circulating insulin acts within the ARC to increase SNA.

Is there a central nervous system component to acute baroreflex resetting in rats?

1992 ◽  
Vol 262 (2) ◽  
pp. H503-H510 ◽  
Author(s):  
C. M. Heesch ◽  
K. W. Barron
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
System Component ◽  
Nerve Activity ◽  
Linear Portion ◽  
Aortic Nerve ◽  
Maximum Inhibition

This study was designed to evaluate a possible central nervous system (CNS) component to acute baroreflex resetting. In nine arterial baroreceptor-denervated, chloralose-urethan-anesthetized rats, a control (C) aortic nerve stimulation curve (3-5 V, 1 ms, 0-64 Hz) was obtained. Next, a constant "baroreceptor" input was delivered to the CNS (left aortic nerve stimulation, 10 min, 10.2 +/- 1.5 Hz). Within the first 13 s of aortic nerve stimulation, maximum inhibition of lumbar sympathetic nerve activity (LSNA) was 60 +/- 7.8% of baseline and at 1 min it increased to 68 +/- 5.6% of baseline. At the end of the 10-min aortic nerve stimulation, LSNA was not different from the response at 1 min (68 +/- 5.6% = 74 +/- 4.1%). Immediately after the constant stimulation (within 30 s), a test or reset (RS) curve was obtained (0-64 Hz). A recovery (RC) curve was obtained 10-20 min later. The slope of the linear portion of the curve and the stimulation frequency that produced 50% maximum inhibition (ES50) were compared among the three baroreflex curves (C, RS, RC,) and no significant differences were found. Thus, although a CNS component to baroreflex adaptation was evident during the first minute of aortic nerve stimulation, a longer term acute resetting of the baroreflex curve did not occur.

Arteriolar wall Po 2 and nitric oxide release during sympathetic vasoconstriction in the rat intestine

2000 ◽  
Vol 279 (2) ◽  
pp. H484-H491 ◽  
Author(s):  
Bryan A. Sauls ◽  
Matthew A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Rat Intestine ◽  
Nerve Activity ◽  
Sympathetic Nerve Stimulation ◽  
Nitric Oxide Release ◽  
Sympathetic Vasoconstriction ◽  
Arteriolar Wall

Endothelium-derived nitric oxide (NO) attenuates arteriolar constriction in the rat small intestine during periods of increased sympathetic nerve activity. This study was undertaken to test the hypothesis that a flow-dependent fall in arteriolar wall Po 2 serves as the stimulus for endothelial NO release under these conditions. Sympathetic nerve stimulation at 3–16 Hz induced frequency-dependent arteriolar constriction, with arteriolar wall O2 tension (Po 2) falling from 67 ± 3 mmHg to as low as 41 ± 6 mmHg. Arteriolar responses to nerve stimulation were enhanced after inhibition of NO synthase with N G-monomethyl-l-arginine (l-NMMA). Under a high-O2 (20%) superfusate, the fall in wall Po 2 was significantly attenuated, arteriolar constrictions were increased by 57 ± 9 to 66 ± 12%, and these responses were no longer sensitive tol-NMMA. The high-O2 superfusate had no effect on vascular smooth muscle responsiveness to NO (as judged by arteriolar responses to sodium nitroprusside) or on arteriolar wall oxidant activity (as determined by the reduction of tetranitroblue tetrazolium dye). These results indicate that a flow-dependent fall in arteriolar wall Po 2 may serve as a stimulus for the release of endothelium-derived NO during periods of increased sympathetic nerve activity.

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