Does the spinal cord generate functionally significant sympathetic activity in the awake rat?

1994 ◽  
Vol 266 (4) ◽  
pp. R1102-R1110
Author(s):  
K. A. Trostel ◽  
J. W. Osborn
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Cervical Spinal Cord ◽  
Adrenergic Blockade ◽  
Nerve Activity ◽  
Nonspecific Effects ◽  
Awake Rat ◽  
Adrenergic Antagonists

Previous studies reach conflicting conclusions regarding the presence of physiologically significant sympathetic nerve activity (SNA) in conscious rats with transection of the cervical spinal cord (CST). The objective of the current study was to determine whether either spinally generated SNA or nonspecific effects of antagonists are responsible for the natriuresis and decreased heart rate that accompany adrenergic blockade in CST rats. To test the first possibility, adrenergic antagonists (phentolamine and propranolol) were administered to three groups of CST rats: 1) renal denervated, 2) adrenalectomized or sham-adrenalectomized, and 3) rats who received the ganglionic blocker hexamethonium. Neither renal denervation, adrenalectomy, nor ganglionic blockade prevented either the three- to fivefold increase in sodium excretion or the 25-50 beats/min decrease in heart rate previously reported. We then administered combinations of different adrenergic antagonists to CST rats to test for nonspecific effects of the drugs. Whereas idazoxan+propranolol reproduced the natriuresis seen with phentolamine+propranolol, prazosin+yohimbine+propranolol did not. We conclude that there is no evidence for functionally significant spinally generated SNA in conscious CST rats and that the natriuresis observed with phentolamine administration is due to imidazoline binding.

Functional evidence for sympathetic nerve activity in conscious cervical spinal rats

1991 ◽  
Vol 261 (2) ◽  
pp. R434-R441
Author(s):  
K. A. Trostel ◽  
S. A. Katz ◽  
J. W. Osborn
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cervical Spinal Cord ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Adrenergic Blockade ◽  
Nerve Activity ◽  
Urinary Potassium ◽  
Adrenergic Antagonists ◽  
Sodium And Potassium

Experiments in anesthetized animals have demonstrated sympathetic nerve activity after cervical spinal cord transection (CST), yet little evidence exists for sympathetic nerve activity in conscious spinal animals. We determined the effect of CST on mean arterial pressure (MAP), heart rate (HR), and plasma renin activity (PRA) in conscious rats. Next, we tested for the presence of functionally significant sympathetic nerve activity 24 h after CST by measuring MAP, HR, urine flow, urinary sodium excretion (UNaV), urinary potassium excretion (UKV), and PRA before and for 2 h during administration of adrenergic antagonists (propranolol + phentolamine) or vehicle. CST resulted in significant decreases in MAP (100.0 +/- 1.6 to 75.0 +/- 1.4 mmHg), HR (353 +/- 7.5 to 315 +/- 6.6 beats/min), and PRA (2.2 +/- 0.3 to 1.2 +/- 0.2 ng angiotensin I.ml-1.h-1). Subsequent adrenergic blockade resulted in a further drop in HR (-52 +/- 21 beats/min), as well as two- to threefold increases in UNaV and UKV. We conclude that CST causes an overall decrease in sympathetic drive. However, sympathetic nerve activity to the heart and kidney remains after CST and is responsible for support of HR and retention of sodium and potassium.

Alterations in sympathetic neurovascular transduction during acute hypoxia in humans

2013 ◽  
Vol 304 (11) ◽  
pp. R959-R965 ◽  
Author(s):  
Can Ozan Tan ◽  
Yu-Chieh Tzeng ◽  
Jason W. Hamner ◽  
Renaud Tamisier ◽  
J. Andrew Taylor
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Sympathetic Outflow ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Hypoxic Exercise

Resting vascular sympathetic outflow is significantly increased during and beyond exposure to acute hypoxia without a parallel increase in either resistance or pressure. This uncoupling may indicate a reduction in the ability of sympathetic outflow to effect vascular responses (sympathetic transduction). However, the effect of hypoxia on sympathetic transduction has not been explored. We hypothesized that transduction would either remain unchanged or be reduced by isocapnic hypoxia. In 11 young healthy individuals, we measured beat-by-beat pressure, multiunit sympathetic nerve activity, and popliteal blood flow velocity at rest and during isometric handgrip exercise to fatigue, before and during isocapnic hypoxia (∼80% SpO2), and derived sympathetic transduction for each subject via a transfer function that reflects Poiseuille's law of flow. During hypoxia, heart rate and sympathetic nerve activity increased, whereas pressure and flow remained unchanged. Both normoxic and hypoxic exercise elicited significant increases in heart rate, pressure, and sympathetic activity, although sympathetic responses to hypoxic exercise were blunted. Hypoxia slightly increased the gain relation between pressure and flow (0.062 ± 0.006 vs. 0.074 ± 0.004 cm·s−1·mmHg−1; P = 0.04), but markedly increased sympathetic transduction (−0.024 ± 0.005 vs. −0.042 ± 0.007 cm·s−1·spike−1; P < 0.01). The pressor response to isometric handgrip was similar during normoxic and hypoxic exercise due to the balance of interactions among the tachycardia, sympathoexcitation, and transduction. This indicates that the ability of sympathetic activity to affect vasoconstriction is enhanced during brief exposure to isocapnic hypoxia, and this appears to offset the potent vasodilatory stimulus of hypoxia.

Increased osmolality of conscious water-deprived rats supports arterial pressure and sympathetic activity via a brain action

2005 ◽  
Vol 288 (5) ◽  
pp. R1248-R1255 ◽  
Author(s):  
Virginia L. Brooks ◽  
Yue Qi ◽  
Theresa L. O'Donaughy
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Carotid Arteries ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Fluid Infusion ◽  
Hypotonic Fluid ◽  
Control Heart ◽  
The Brain

To test the hypothesis that high osmolality acts in the brain to chronically support mean arterial pressure (MAP) and lumbar sympathetic nerve activity (LSNA), the osmolality of blood perfusing the brain was reduced in conscious water-deprived and water-replete rats by infusion of hypotonic fluid via bilateral nonoccluding intracarotid catheters. In water-deprived rats, the intracarotid hypotonic infusion, estimated to lower osmolality by ∼2%, decreased MAP by 9 ± 1 mmHg and LSNA to 86 ± 7% of control; heart increased by 25 ± 8 beats per minute (bpm) (all P < 0.05). MAP, LSNA, and heart rate did not change when the hypotonic fluid was infused intravenously. The intracarotid hypotonic fluid infusion was also ineffective in water-replete rats. Prior treatment with a V1 vasopressin antagonist did not alter the subsequent hypotensive and tachycardic effects of intracarotid hypotonic fluid infusion in water-deprived rats. In summary, acute decreases in osmolality of the carotid blood of water-deprived, but not water-replete, rats decreases MAP and LSNA and increases heart rate. These data support the hypothesis that the elevated osmolality induced by water deprivation acts via a region perfused by the carotid arteries, presumably the brain, to tonically increase MAP and LSNA and suppress heart rate.

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

2004 ◽  
Vol 287 (4) ◽  
pp. H1658-H1662 ◽  
Author(s):  
N. Charkoudian ◽  
E. A. Martin ◽  
F. A. Dinenno ◽  
J. H. Eisenach ◽  
N. M. Dietz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Healthy Humans ◽  
Rapid Changes

Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10° head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased ∼2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: −3.1 ± 0.6 and −3.3 ± 1.0 versus −5.0 ± 0.6 units·beat−1·mmHg−1 ( P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.

scholarly journals Reno-Renal and Reno-Adrenal Reflexes in the Rat

1980 ◽  
Vol 59 (s6) ◽  
pp. 323s-325s ◽  
Author(s):  
G. Recordati ◽  
S. Genovesi ◽  
D. Cerati ◽  
R. Di Cintio
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Nervous System ◽  
Renal Artery ◽  
Sympathetic Activity ◽  
Nerve Activity ◽  
Natural Stimuli ◽  
Anaesthetized Rats ◽  
Excitatory Responses

1. Experiments were carried out to investigate whether the activation of renal chemoceptive receptors by natural stimuli might induce reflex alterations of efferent postganglionic activity to the ipsilateral kidney and preganglionic activity to the ipsilateral adrenal. 2. In anaesthetized rats with intact nervous system back-flow of urine and occlusion of the renal artery were accompanied by increments in efferent sympathetic activity both to the kidney and adrenal without concomitant changes in heart rate and blood pressure. 3. Greater excitatory responses in nerve activity to the same test stimuli were observed in rats with the spinal cord cut at C1. 4. These results indicate that the natural activation of renal chemoceptive receptors might induce reno-renal and reno-adrenal excitatory reflexes which are likely to be integrated at spinal and supraspinal levels.

Modification of thermoregulatory responses to cold by hypnosis

1964 ◽  
Vol 19 (6) ◽  
pp. 1043-1050 ◽  
Author(s):  
Abbott T. Kissen ◽  
Clifford B. Reifler ◽  
Victor H. Thaler
Keyword(s):  
Heart Rate ◽  
Thermal Stress ◽  
Task Performance ◽  
Cold Exposure ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Skin Resistance ◽  
Vigilance Task ◽  
Nerve Activity ◽  
Thermoregulatory Responses

The effects of hypnosis on thermoregulatory responses were studied in nonacclimatized acutely cold-exposed men. Forty exposures (4.5 @#X2013;5.0 C) were conducted in an environmental chamber under both hypnosis and nonhypnosis conditions. Five subjects, wearing 1 clo insulation, were cold exposed for 1 hr, four times for each condition, and each subject served as his own control. Variables monitored included mean skin and rectal temperatures, heart and shivering rates, basal skin resistance, and vigilance task performance. In hypnosis, shivering was suppressed, heart rate lowered, and vigilance task performance improved. Basal skin resistance differed in terms of pattern and level, being generally higher under hypnotic conditions. Rectal temperatures were lower despite maintaining skin temperature at the same level as during nonhypnosis conditions. These findings indicate that with the thermal stress imposed and levels of trance achieved, there is a general amelioration of the psychophysiological effects of the stress. The mechanism responsible for this form of “adaptation” remains speculative but is consistent with generalized suppression of sympathetic activity. thermoregulation; cold exposure; adaptation; sympathetic nerve activity; shivering; basal skin resistance; vigilance task performance Submitted on March 12, 1964

scholarly journals Effect of hypoxia on arterial baroreflex control of heart rate and muscle sympathetic nerve activity in humans

2002 ◽  
Vol 93 (3) ◽  
pp. 857-864 ◽  
Author(s):  
John R. Halliwill ◽  
Christopher T. Minson
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Normotensive Subjects

We tested the hypothesis that acute hypoxia would alter the sensitivity of arterial baroreflex control of both heart rate and sympathetic vasoconstrictor outflow. In 16 healthy, nonsmoking, normotensive subjects (8 women, 8 men, age 20–33 yr), we assessed baroreflex control of heart rate and muscle sympathetic nerve activity by using the modified Oxford technique during both normoxia and hypoxia (12% O2). Compared with normoxia, hypoxia reduced arterial O2 saturation levels from 96.8 ± 0.3 to 80.7 ± 1.4% ( P < 0.001), increased heart rate from 59.8 ± 2.4 to 79.4 ± 2.9 beats/min ( P < 0.001), increased mean arterial pressure from 96.7 ± 2.5 to 105.0 ± 3.3 mmHg ( P = 0.002), and increased sympathetic activity 126 ± 58% ( P < 0.05). The sensitivity for baroreflex control of both heart rate and sympathetic activity was not altered by hypoxia (heart rate: −1.02 ± 0.09 vs. −1.02 ± 0.11 beats · min−1 · mmHg−1; nerve activity: −5.6 ± 0.9 vs. −6.2 ± 0.9 integrated activity · beat−1 · mmHg−1; both P > 0.05). Acute exposure to hypoxia reset baroreflex control of both heart rate and sympathetic activity to higher pressures without changes in baroreflex sensitivity.

scholarly journals Recovery of baroreflex control of renal sympathetic nerve activity after spinal lesions in the rat

2011 ◽  
Vol 301 (5) ◽  
pp. R1584-R1590 ◽  
Author(s):  
Matthew R. Zahner ◽  
Ewa Kulikowicz ◽  
Lawrence P. Schramm
Keyword(s):  
Spinal Cord ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Reflex Response ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Cord Injury ◽  
Renal Sympathetic

Spinal cord injury (SCI) has serious long-term consequences on sympathetic cardiovascular regulation. Orthostatic intolerance results from insufficient baroreflex regulation (BR) of sympathetic outflow to maintain proper blood pressure upon postural changes. Autonomic dysreflexia occurs due to insufficient inhibition of spinal sources of sympathetic activity. Both of these conditions result from the inability to control sympathetic activity caudal to SCI. It is well established that limited motor ability recovers after incomplete SCI. Therefore, the goal of this study was to determine whether recovery of BR occurs after chronic, left thoracic spinal cord hemisection at either T3 or T8. Baroreflex tests were performed in rats by measuring the reflex response of left (ipsilateral) renal sympathetic nerve activity to decreases and increases in arterial pressure produced by ramped infusions of sodium nitroprusside and phenylephrine, respectively. One week after a T3 left hemisection, BR function was modestly impaired. However, 8 wk after a T3 left hemisection, BR function was normal. One week after a T8 left hemisection, BR function was significantly impaired, and 8 wk after a T8 left hemisection, BR function was significantly improved. These results indicate that BR of renal sympathetic nerve activity in rats may partially recover after spinal cord hemisections, becoming normal by 8 wk after a T3 lesion, but not after a T8 lesion. The nature of the spinal cord and/or brain stem reorganization that mediates this recovery remains to be determined.

Interactions of plasma osmolality with arterial and central venous pressures in control of sympathetic activity and heart rate in humans

2005 ◽  
Vol 289 (6) ◽  
pp. H2456-H2460 ◽  
Author(s):  
N. Charkoudian ◽  
J. H. Eisenach ◽  
M. J. Joyner ◽  
S. K. Roberts ◽  
D. E. Wick
Keyword(s):  
Heart Rate ◽  
Hypertonic Saline ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Plasma Osmolality ◽  
Central Venous ◽  
Nerve Activity ◽  
Baroreflex Control

Plasma osmolality alters control of sympathetic activity and heart rate in animal models; however, it is unknown whether physiological increases in plasma osmolality have such influences in humans and what effect concurrent changes in central venous and/or arterial pressures may have. We tested whether physiological increases in plasma osmolality (similar to those during exercise dehydration) alter control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) in humans. We studied 17 healthy young adults (7 women, 10 men) at baseline and during arterial pressure (AP) transients induced by sequential injections of nitroprusside and phenylephrine, under three conditions: control (C), after 1 ml/kg intravenous hypertonic saline (HT1), and after 2 ml/kg hypertonic saline (HT2). We continuously measured HR, AP, central venous pressure (CVP; peripherally inserted central catheter) and MSNA (peroneal microneurography) in all conditions. Plasma osmolality increased from 287 ± 1 mosmol/kg in C to 290 ± 1 mosmol/kg in HT1 ( P < 0.05) but did not increase further in HT2 (291 ± 1 mosmol/kg; P > 0.05 vs. C). Mean AP and CVP were similar between C and HT1, but both increased slightly in HT2. HR increased slightly but significantly during both HT1 and HT2 vs. C ( P < 0.05). Sensitivity of baroreflex control of MSNA was significantly increased vs. C in HT1 [−7.59 ± 0.97 (HT1) vs. −5.85 ± 0.63 (C) arbitrary units (au)·beat−1·mmHg−1; P < 0.01] but was not different in HT2 (−6.55 ± 0.94 au·beat−1·mmHg−1). We conclude that physiological changes in plasma osmolality significantly alter control of MSNA and HR in humans, and that this influence can be modified by CVP and AP.

scholarly journals Effects of glucagon-like peptide-1, yohimbine, and nitrergic modulation on sympathetic and parasympathetic activity in humans

2008 ◽  
Vol 295 (3) ◽  
pp. R874-R880 ◽  
Author(s):  
Adil E. Bharucha ◽  
Nisha Charkoudian ◽  
Christopher N. Andrews ◽  
Michael Camilleri ◽  
David Sletten ◽  
...  
Keyword(s):  
Heart Rate ◽  
Spectral Analysis ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Catecholamines ◽  
Parasympathetic Activity ◽  
Nerve Activity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1), an incretin, which is used to treat diabetes mellitus in humans, inhibited vagal activity and activated nitrergic pathways. In rats, GLP-1 also increased sympathetic activity, heart rate, and blood pressure (BP). However, the effects of GLP-1 on sympathetic activity in humans are unknown. Our aims were to assess the effects of a GLP-1 agonist with or without α2-adrenergic or -nitrergic blockade on autonomic nervous functions in humans. In this double-blind study, 48 healthy volunteers were randomized to GLP-1-(7-36) amide, the nitric oxide synthase (NOS) inhibitor N G-monomethyl-l-arginine acetate (l-NMMA), the α2-adrenergic antagonist yohimbine, or placebo (i.e., saline), alone or in combination. Hemodynamic parameters, plasma catecholamines, and cardiac sympathetic and parasympathetic modulation were measured by spectral analysis of heart rate. Thereafter, the effects of GLP-1-(7-36) amide on muscle sympathetic nerve activity (MSNA) were assessed by microneurography in seven subjects. GLP-1 increased ( P = 0.02) MSNA but did not affect cardiac sympathetic or parasympathetic indices, as assessed by spectral analysis. Yohimbine increased plasma catecholamines and the low-frequency (LF) component of heart rate power spectrum, suggesting increased cardiac sympathetic activity. l-NMMA increased the BP and reduced the heart rate but did not affect the balance between sympathetic and parasympathetic activity. GLP-1 increases skeletal muscle sympathetic nerve activity but does not appear to affect cardiac sympathetic or parasympathetic activity in humans.

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