Specific Actions of Halothane, Isoflurane, and Desflurane on Sympathetic Activity and A [Greek small letter delta] and C Somatosympathetic Reflexes Recorded in Renal Nerves in Dogs 

1999 ◽  
Vol 91 (2) ◽  
pp. 470-478 ◽  
Author(s):  
Chen K. Pac-Soo ◽  
Daqing Ma ◽  
Chen Wang ◽  
Mihir K. Chakrabarti ◽  
James G. Whitwam
Keyword(s):  
Sympathetic Activity ◽  
Renal Nerves ◽  
Lipid Solubility ◽  
Renal Sympathetic Nerve Activity ◽  
Bipolar Electrodes ◽  
Significant Depression ◽  
Somatosympathetic Responses ◽  
Evoked Activity ◽  
Alpha Chloralose ◽  
Renal Sympathetic

Background This was a study of the relative effects on directly recorded sympathetic activity of desflurane, isoflurane, and halothane. Methods Renal sympathetic nerve activity (RSNA) was recorded with bipolar electrodes in renal nerves exposed retroperitoneally in anesthetized (alpha-chloralose), paralyzed (succinylcholine), and artificially ventilated dogs. Somatosympathetic responses were evoked by supramaximal electrical stimulation of radial nerves (0.33 Hz, 30 V, 0.5 ms). Spontaneous and evoked activity were rectified, averaged, and integrated to allow quantitative comparison of the effects of 3-12% desflurane, 0.6-2.4% isoflurane, and 0.4-1.6% halothane. Results Increasing concentrations of isoflurane progressively depressed mean RSNA, Adelta, and C reflexes by 40% (P < 0.01), 50% (P < 0.01) and 70% (P < 0.001) respectively at 2.4% concentration. Halothane depressed both reflexes equally by approximately 60% (P < 0.01) at 1.6% concentration, without significant depression of spontaneous RSNA. Desflurane increased and subsequently decreased RSNA by 37% (P < 0.02) and 65% (P < 0.001) at concentrations of 6% and 12% respectively, and although somatosympathetic reflexes remained unchanged up to 9%, both were depressed equally by 70% (P < 0.01) at 12% concentration. Conclusion After equilibration, lower concentrations of desflurane remained excitatory, but, like isoflurane, higher concentrations depressed RSNA. The effect of halothane on RSNA was insignificant. Isoflurane depressed C more than Adelta somatosympathetic reflexes, which is uncorrelated with lipid solubility because desflurane and halothane, which have the highest and lowest minimum alveolar concentration, respectively, depressed both equally.

Neural control of renal function in edema-forming states

1988 ◽  
Vol 254 (6) ◽  
pp. R1017-R1024 ◽  
Author(s):  
G. F. DiBona ◽  
P. J. Herman ◽  
L. L. Sawin
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Isotonic Saline ◽  
Experimental Models ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Duct Ligation ◽  
Renal Sympathetic

To define the role of the renal nerves in renal sodium-retaining edema-forming states, experiments were conducted in conscious chronically instrumented rats with congestive heart failure (myocardial infarction), nephrotic syndrome (adriamycin injection), and hepatic cirrhosis (common bile duct ligation). In each experimental model, renal excretion, as water or sodium, of an acutely administered oral or intravenous isotonic saline load was significantly less than that in control rats. Bilateral renal denervation of the experimental rats restored their renal excretory response to that of the control rats. In addition, in response to the acute administration of a standard intravenous isotonic saline load, the decrease in efferent renal sympathetic nerve activity was significantly less in all three experimental models compared with that of control rats. These results suggest that the impaired ability to excrete an acute isotonic saline load in these experimental models is partially dependent on an increase in basal efferent renal sympathetic nerve activity that fails to suppress normally in response to the isotonic saline load.

Increased renal sympathetic nerve activity leads to hypertension and renal dysfunction in offspring from diabetic mothers

2013 ◽  
Vol 304 (2) ◽  
pp. F189-F197 ◽  
Author(s):  
Aline Fernanda de Almeida Chaves Rodrigues ◽  
Ingrid Lauren Brites de Lima ◽  
Cássia Toledo Bergamaschi ◽  
Ruy Ribeiro Campos ◽  
Aparecida Emiko Hirata ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Dysfunction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Diabetic Mothers ◽  
Renal Sympathetic

The exposure of the fetus to a hyperglycemic environment promotes the development of hypertension and renal dysfunction in the offspring at adult age. We evaluated the role of renal nerves in the hypertension and renal changes seen in offspring of diabetic rats. Diabetes was induced in female Wistar rats (streptozotocin, 60 mg/kg ip) before mating. Male offspring from control and diabetic dams were studied at an age of 3 mo. Systolic blood pressure measured by tail cuff was increased in offspring of diabetic dams (146 ± 1.6 mmHg, n = 19, compared with 117 ± 1.4 mmHg, n = 18, in controls). Renal function, baseline renal sympathetic nerve activity (rSNA), and arterial baroreceptor control of rSNA were analyzed in anesthetized animals. Glomerular filtration rate, fractional sodium excretion, and urine flow were significantly reduced in offspring of diabetic dams. Two weeks after renal denervation, blood pressure and renal function in offspring from diabetic dams were similar to control, suggesting that renal nerves contribute to sodium retention in offspring from diabetic dams. Moreover, basal rSNA was increased in offspring from diabetic dams, and baroreceptor control of rSNA was impaired, with blunted responses to infusion of nitroprusside and phenylephrine. Thus, data from this study indicate that in offspring from diabetic mothers, renal nerves have a clear role in the etiology of hypertension; however, other factors may also contribute to this condition.

Baroreflex dysfunction in diabetes mellitus. II. Site of baroreflex impairment in diabetic rabbits

1994 ◽  
Vol 266 (1) ◽  
pp. H244-H249 ◽  
Author(s):  
T. S. McDowell ◽  
G. Hajduczok ◽  
F. M. Abboud ◽  
M. W. Chapleau
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Companion Paper ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Diabetic Rabbits ◽  
The Right ◽  
Alpha Chloralose ◽  
Induced Changes ◽  
Renal Sympathetic

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235-H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (90–100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normoglycemic (n = 8) and rabbits given saline instead of alloxan (n = 4) served as controls. Twenty-four weeks after administration of alloxan or saline, rabbits were anesthetized with alpha-chloralose. Aortic baroreceptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure. The slope of the baroreceptor pressure-activity relation was not significantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) compared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treated normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arterial pressure-RSNA relation was not significantly different in diabetic rabbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated normoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical stimulation (10 V, 2 ms, 0.5–16 Hz) of the cut peripheral end of the right cervical vagus were similar in diabetic and alloxan-treated normoglycemic rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 084: Activation Of Trpv1-expressing Renal Sensory Nerves With N-oleoyldopamine Attenuates High Fat Diet-induced Impairment In Renal Function

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Shuang-Quan Yu ◽  
Donna H Wang
Keyword(s):  
Renal Function ◽  
Renal Injury ◽  
High Fat Diet ◽  
Sympathetic Nerve Activity ◽  
Intrathecal Injection ◽  
Renal Nerves ◽  
High Fat ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

Renal injury occurs in obesity. Accumulating evidence indicates that activation of the transient receptor potential vanilloid 1 (TRPV1) protects tissues from injury albeit the mechanisms are largely unknown. We test the hypothesis that high fat diet (HFD) intake impairs afferent renal nerves expressing TRPV1 channels, leading to increased renal sympathetic nerve activity (RSNA), decreased renal function, and hypertension, and that chronic activation of TRPV1 positive afferent renal nerves attenuates HFD-induced impairment. N-oleoyldopamine (OLDA, 1 ng/kg, daily), a selective TRPV1 agonist, was administrated intrathecally (T8-L3) via a indwelled catheter to chronically activate TRPV1 positive afferent renal nerves in rats fed a HFD or normal fat diet (Con) for 8 weeks. HFD decreased renal TRPV1 expression and afferent renal nerve activity (ARNA, Con: 133±8, Con+OLDA: 127±15, HFD: 84±5, HFD+OLDA: 115±7, p<0.05) in response to intra-pelvis perfusion of capsaicin (4 μM, 3 min, 20 ml/min), a selective TRPV1 agonist, which were prevented by OLDA. HFD increased RSNA responses to intrathecal injection of muscimol (3 nmol/kg), a GABA-A receptor agonist, and urinary norepinephrine levels, which were prevented by OLDA. HFD decreased creatinine clearance and increased urinary albumin levels, which were prevented by OLDA (Creatinine clearance, Con: 0.52±0.09, Con+OLDA: 0.54±0.12, HFD: 0.24±0.04, HFD+OLDA: 0.40±0.06 ml/min/100 gbwt, p<0.05). HFD increased levels of collagen deposition, connective tissue growth factor (CTGF), and matrix metalloproteinase-2 (MMP-2) in the kidney, which were prevented by OLDA. HFD increased systolic blood pressure by the week of 6 after HFD, which was prevented by OLDA. Thus, HFD impairs TRPV1-positive afferent renal nerves, increases renal sympathetic nerve activity, and leads to renal injury and hypertension. Segment-specific intrathecal injection of OLDA protects against HFD-induced impairment in afferent renal nerves and prevents HFD-induced renal injury and hypertension. Our data illustrate that preservation of TRPV1 positive afferent renal nerves may be a therapeutic strategy in preventing obesity- or type 2 diabetes-induced renal injury and hypertension.

Role of Renal Nerves in Edema Formation

Physiology ◽  
1994 ◽  
Vol 9 (4) ◽  
pp. 183-188 ◽  
Author(s):  
GF DiBona
Keyword(s):  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Edema Formation ◽  
Renal Sympathetic Nerve Activity ◽  
Important Regulator ◽  
Renal Tubular ◽  
Renal Sympathetic

Once viewed as physiologically insignificant by no less an authority than Homer Smith, the renal nerves have emerged as a physiologically important regulator of renal tubular sodium reabsorption. Increased renal sympathetic nerve activity contributes significantly to the renal sodium retention in edema-forming states.

Neural control of renal function

1997 ◽  
Vol 77 (1) ◽  
pp. 75-197 ◽  
Author(s):  
G. F. DiBona ◽  
U. C. Kopp
Keyword(s):  
Renal Function ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Communication Link ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Functional Components ◽  
Renal Sympathetic

The renal nerves are the communication link between the central nervous system and the kidney. In response to multiple peripheral and central inputs, efferent renal sympathetic nerve activity is altered so as to convey information to the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated. At the level of each of these individual components, information transfer occurs via interaction of the neurotransmitter released at the sympathetic nerve terminal-neuroeffector junction with specific postjunctional receptors coupled to defined intracellular signaling and effector systems. In response to normal physiological stimuli, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. Afferent input from sensory receptors located in the kidney participates in this reflex control system via renorenal reflexes that enable total renal function to be self-regulated and balanced between the two kidneys. In pathophysiological conditions, abnormal regulation of efferent renal sympathetic nerve activity contributes significantly to the associated abnormalities of renal function which, in turn, are of importance in the pathogenesis of the disease.

Activation of cardiac sympathetic afferents: effects of exogenous adenosine and adenosine analogues

1993 ◽  
Vol 265 (1) ◽  
pp. H395-H400 ◽  
Author(s):  
M. E. Dibner-Dunlap ◽  
T. Kinugawa ◽  
M. D. Thames
Keyword(s):  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Receptor Subtype ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Afferent Fibers ◽  
Adenosine Uptake ◽  
Dose Dependent ◽  
Peak Increase ◽  
Renal Sympathetic

Adenosine is released during myocardial ischemia and can cause angina-like chest pain when given by intracoronary administration. We tested the hypothesis that intracoronary adenosine activates cardiac sympathetic afferent fibers and results in reflex sympathoexcitation. In dogs with sinoaortic denervation and vagotomy, we administered 2 mg of adenosine into the left anterior descending artery over 2 min. Before dipyridamole infusion, intracoronary adenosine resulted in no change in blood pressure or renal sympathetic nerve activity. After dipyridamole infusion, which blocks adenosine uptake, intracoronary adenosine resulted in a peak increase in sympathetic activity of 34 +/- 7%. We also investigated the adenosine-receptor subtype responsible for this sympathoexcitatory response. We found that the adenosine1 agonist N6-cyclopentyladenosine elicited a dose-dependent sympathoexcitatory response similar to adenosine but that the adenosine2 agonist 5'-(N-cyclopropyl)carboxamidoadenosine failed to elicit a sympathoexcitatory response. We conclude that adenosine activates cardiac sympathetic afferent fibers and leads to a sympathoexcitatory response due to activation of adenosine1 receptors.

The Effects of Epidural Morphine on Cardiac and Renal Sympathetic Nerve Activity in α-Chloralose-anesthetized Cats 

1998 ◽  
Vol 88 (6) ◽  
pp. 1558-1565 ◽  
Author(s):  
Takashi Mori ◽  
Kiyonobu Nishikawa ◽  
Takekazu Terai ◽  
Hidekazu Yukioka ◽  
Akira Asada
Keyword(s):  
Sympathetic Nerve ◽  
Epidural Morphine ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Thoracic Epidural ◽  
Morphine Administration ◽  
Intravenous Morphine ◽  
Alpha Chloralose ◽  
Renal Sympathetic

Background Epidural morphine yields postoperative pain relief and hemodynamic stability. However, the effects of epidural morphine on sympathetic tone are unclear. This study was designed to elucidate the effects of epidural morphine on cardiac (CSNA) and renal (RSNA) sympathetic nerve activity by direct measurement in anesthetized cats. Methods Thirty mongrel cats anesthetized with alpha-chloralose were randomly assigned to one of the following five groups: control (0.2 ml/kg thoracic epidural normal saline; n=5); thoracic epidural morphine (n=9); lumbar epidural morphine (n=6); vagotomized, sinoaortic denervated, thoracic epidural morphine (n=5); or intravenous morphine (n=5). Mean arterial pressure (MAP), heart rate (HR), CSNA, and RSNA were measured 0, 15, 30, 60, 90, and 120 min after saline or morphine (200 microg/kg) administration and 15 min after reversal with 200 microg naloxone given intravenously. Results In the control group, no changes in measured variables were found after either thoracic epidural saline or intravenous naloxone. Thoracic and lumbar epidural morphine both significantly reduced MAP, HR, CSNA, and RSNA 30 through 120 min after morphine administration (P &lt; 0.05). These changes were reversed by intravenous naloxone. Changes after thoracic epidural morphine administration in vagotomized, baroreceptor-denervated cats were similar to those in intact cats. Intravenous morphine produced no significant changes except for a decrease in MAP, which was reversed by intravenous naloxone. Conclusion In contrast to intravenous morphine, thoracic and lumbar epidural morphine both inhibited cardiac and renal sympathetic nerve activity and consequently reduced MAP and HR in alpha-chloralose anesthetized cats.

Inhibition of sympathetic responses at birth in sheep by lesion of the paraventricular nucleus

2002 ◽  
Vol 283 (6) ◽  
pp. R1395-R1403 ◽  
Author(s):  
Jeffrey L. Segar ◽  
Dan L. Ellsbury ◽  
Oliva M. Smith
Keyword(s):  
Paraventricular Nucleus ◽  
Sympathetic Activity ◽  
Critical Role ◽  
Physiological Adaptation ◽  
Similar Time ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Before And After ◽  
Near Term ◽  
Renal Sympathetic

Birth is characterized by a surge in sympathetic outflow, heart rate (HR), mean arterial blood pressure (MABP) and circulating catecholamines. The paraventricular nucleus (PVN) of the hypothalamus is an important central regulatory site of sympathetic activity, but its role in the regulation of sympathoexcitation at birth is unknown. To test the hypothesis that the PVN regulates sympathetic activity at birth, experiments were performed in chronically instrumented near-term (137- to 142-day gestation, term 145 days) sheep before and after delivery by cesarean section. Stereotaxic guided electrolytic lesioning of the PVN ( n= 6) or sham lesioning ( n = 6) was performed 48 h before study. At 30 min after birth, renal sympathetic nerve activity (RSNA) increased 128 ± 26% above fetal values in the sham-lesioned animals ( P < 0.05). In contrast, at a similar time point, RSNA decreased to 52 ± 12% of the fetal value in the PVN-lesioned animals. Lesioning of the PVN did not affect the usual postnatal increases in MABP and epinephrine levels although HR failed to rise above fetal values. ANG II but not arginine vasopressin or norepinephrine levels increased in PVN-lesioned animals after birth, whereas all three hormones increased ( P < 0.05) in sham-lesioned animals. Fetal and newborn HR baroreflex responses were similar in both groups. However, the usual postnatal attenuation of baroreflex-mediated inhibition of RSNA was blunted in the PVN-lesioned group. The results of this study demonstrate that ablation of the PVN abolishes sympathoexcitation with birth at near-term gestation. The PVN may play a critical role in physiological adaptation at birth.

Role of renal sympathetic nerve activity in hypertension induced by chronic nitric oxide inhibition

2007 ◽  
Vol 292 (4) ◽  
pp. R1479-R1485 ◽  
Author(s):  
Rohit Ramchandra ◽  
Carolyn J. Barrett ◽  
Sarah-Jane Guild ◽  
Fiona McBryde ◽  
Simon C. Malpas
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Baseline Levels ◽  
Renal Sympathetic

Nitric oxide levels are diminished in hypertensive patients, suggesting nitric oxide might have an important role to play in the development of hypertension. Chronic blockade of nitric oxide leads to hypertension that is sustained throughout the period of the blockade in baroreceptor-intact animals. It has been suggested that the sympathetic nervous system is involved in the chronic increase in blood pressure; however, the evidence is inconclusive. We measured renal sympathetic nerve activity and blood pressure via telemetry in rabbits over 7 days of nitric oxide blockade. Nitric oxide blockade via Nω-nitro-l-arginine methyl ester (l-NAME) in the drinking water (50 mg·kg−1·day−1) for 7 days caused a significant increase in arterial pressure (7 ± 1 mmHg above control levels; P < 0.05). While the increase in blood pressure was associated with a decrease in heart rate (from 233 ± 6 beats/min before the l-NAME to 202 ± 6 beats/min on day 7), there was no change in renal sympathetic nerve activity (94 ± 4 %baseline levels on day 2 and 96 ± 5 %baseline levels on day 7 of l-NAME; baseline nerve activity levels were normalized to the maximum 2 s of nerve activity evoked by nasopharyngeal stimulation). The lack of change in renal sympathetic nerve activity during the l-NAME-induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits.

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