Oxidative Stress Mediates the Stimulation of Sympathetic Nerve Activity in the Phenol Renal Injury Model of Hypertension

The role of nucleus of solitary tract (NTS) A2a adenosine receptors in baroreflex mechanisms is controversial. Stimulation of these receptors releases glutamate within the NTS and elicits baroreflex-like decreases in mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas inhibition of these receptors attenuates HR baroreflex responses. In contrast, stimulation of NTS A2a adenosine receptors increases preganglionic adrenal sympathetic nerve activity (pre-ASNA), and the depressor and sympathoinhibitory responses are not markedly affected by sinoaortic denervation and blockade of NTS glutamatergic transmission. To elucidate the role of NTS A2a adenosine receptors in baroreflex function, we compared full baroreflex stimulus-response curves for HR, RSNA, and pre-ASNA (intravenous nitroprusside/phenylephrine) before and after bilateral NTS microinjections of selective adenosine A2a receptor agonist (CGS-21680; 2.0, 20 pmol/50 nl), selective A2a receptor antagonist (ZM-241385; 40 pmol/100 nl), and nonselective A1 + A2a receptor antagonist (8-SPT; 1 nmol/100 nl) in urethane/α-chloralose anesthetized rats. Activation of A2a receptors decreased the range, upper plateau, and gain of baroreflex-response curves for RSNA, whereas these parameters all increased for pre-ASNA, consistent with direct effects of the agonist on regional sympathetic activity. However, no resetting of baroreflex-response curves along the MAP axis occurred despite the marked decreases in baseline MAP. The antagonists had no marked effects on baseline variables or baroreflex-response functions. We conclude that the activation of NTS A2a adenosine receptors differentially alters baroreflex control of HR, RSNA, and pre-ASNA mostly via non-baroreflex mechanism(s), and these receptors have virtually no tonic action on baroreflex control of these sympathetic outputs.

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Effects of corticospinal tract stimulation on renal sympathetic nerve activity in rats with intact and chronically lesioned spinal cords

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00044.2007 ◽

2007 ◽

Vol 293 (1) ◽

pp. R178-R184 ◽

Cited By ~ 7

Author(s):

Baohan Pan ◽

Matthew R. Zahner ◽

Ewa Kulikowicz ◽

Lawrence P. Schramm

Keyword(s):

Spinal Cord ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Corticospinal Tract ◽

Sympathetic Neurons ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic ◽

Stimulation Of

Sympathetic preganglionic neurons and interneurons are closely apposed (presumably synapsed upon) by corticospinal tract (CST) axons. Sprouting of the thoracic CST rostral to lumbar spinal cord injuries (SCI) substantially increases the incidence of these appositions. To test our hypothesis that these additional synapses would increase CST control of sympathetic activity after SCI, we measured the effects of electrical stimulation of the CST on renal sympathetic nerve activity (RSNA) and arterial pressure (AP) in α-chloralose-anesthetized rats with either chronically intact or chronically lesioned spinal cords. Stimuli were delivered to the CST at intensities between 25–150 μA and frequencies between 25 and 75 Hz. Stimulation of the CST at the midcervical level decreased RSNA and AP. These decreases were not mediated by direct projections of the CST to the thoracic spinal cord because we could still elicit them by midcervical stimulation after acute lesions of the CST at caudal cervical levels. In contrast, caudal thoracic CST stimulation increased RSNA and AP. Neither the responses to cervical nor thoracic stimulation were affected by chronic lumbar SCI. These data show that the CST mediates decreases in RSNA via a cervical spinal system but excites spinal sympathetic neurons at caudal thoracic levels. Because chronic lumber spinal cord injury affected responses evoked from neither the cervical nor thoracic CST, we conclude that lesion-induced or regeneration-induced formation of new synapses between the CST and sympathetic neurons may not affect cardiovascular regulation.

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A highly selective cardiorenal serotonergic 5-HT3-mediated reflex in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.264.6.h1871 ◽

1993 ◽

Vol 264 (6) ◽

pp. H1871-H1877 ◽

Cited By ~ 5

Author(s):

R. Veelken ◽

K. F. Hilgers ◽

M. Leonard ◽

K. Scrogin ◽

J. Ruhe ◽

...

Keyword(s):

Sympathetic Nerve ◽

Receptor Agonist ◽

Sympathetic Nerve Activity ◽

Short Term ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Prolonged Stimulation ◽

Saline Loading ◽

Renal Sympathetic ◽

Stimulation Of

To elucidate whether prolonged stimulation of cardiopulmonary serotonergic (5-HT3) receptors could play a role in the control of renal sympathetic nerve activity (RSNA), we compared 15-min intravenous infusions to bolus administrations of the 5-HT3 receptor agonist phenyl biguanide (PBG) and to a 0.9% saline load (5% body wt) in rats. Short-term and prolonged stimulation of 5-HT3-sensitive cardiopulmonary reflexes caused dose-related decreases in RSNA but not in lumbar sympathetic nerve activity (LSNA); only short-term stimulation caused decreases in blood pressure (BP) and heart rate (HR). Saline loading lowered RSNA but not LSNA, BP, or HR. Baroreceptor denervation did not influence any of these responses. Scopolamine attenuated BP and HR but not RSNA responses to bolus PBG. Pretreatment with a 5-HT3 receptor antagonist inhibited responses to PBG but not to saline. Vagotomy abolished all responses to all interventions. Thus 1) the prolonged stimulation of cardiopulmonary 5-HT3 receptors caused sustained suppression of RSNA, 2) decreased BP and HR were manifest only during short-term stimulation (3 min), and 3) blockade of 5-HT3 receptors did not influence responses to cardiopulmonary mechanoreceptor stimulation.

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Sympathetic nerve activity during natural stimulation of horizontal semicircular canals in humans

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.4.r1274 ◽

1998 ◽

Vol 275 (4) ◽

pp. R1274-R1278 ◽

Cited By ~ 28

Author(s):

Chester A. Ray ◽

Keith M. Hume ◽

Samuel L. Steele

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Semicircular Canals ◽

Head Rotation ◽

Otolith Organs ◽

Nerve Activity ◽

Natural Stimulation ◽

Vascular Beds ◽

Static Head ◽

Stimulation Of

We have shown that static head-down neck flexion elicits increases in muscle (MSNA) but not skin sympathetic nerve activity (SSNA) in humans. These findings suggest that stimulation of the otolith organs causes differential sympathetic outflow to vascular beds. The purpose of the present study was to determine whether yaw head rotation (YHR), which stimulates the horizontal semicircular canals, elicits sympathetic nerve responses. To test this question, we recorded MSNA ( n = 33) and SSNA ( n = 25) before and during 3 min of sinusoidal YHR performed at 0.1, 0.6, and 1.0 Hz. At all frequencies, YHR elicited no significant changes in heart rate and mean arterial pressure. Likewise, YHR did not significantly change either MSNA or SSNA at all frequencies. Our results indicate that stimulation of the horizontal semicircular canals by YHR does not alter SNA to either muscle or skin. Moreover, these results provide evidence to support the concept that the otolith organs but not the horizontal semicircular canals participate in the regulation of SNA in humans.

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