Relevant bibliographies by topics / Renal sympathetic nerve

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Renal sympathetic nerve'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Renal sympathetic nerve"

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Noh, Mi, Hee-Seong Jang, Jinu Kim, and Babu Padanilam. "Renal Sympathetic Nerve-Derived Signaling in Acute and Chronic Kidney Diseases." International Journal of Molecular Sciences 21, no. 5 (February 28, 2020): 1647. http://dx.doi.org/10.3390/ijms21051647.

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The kidney is innervated by afferent sensory and efferent sympathetic nerve fibers. Norepinephrine (NE) is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves, and its signaling, regulated through adrenergic receptors (AR), modulates renal function and pathophysiology under disease conditions. Renal sympathetic overactivity and increased NE level are commonly seen in chronic kidney disease (CKD) and are critical factors in the progression of renal disease. Blockade of sympathetic nerve-derived signaling by renal denervation or AR blockade in clinical and experimental studies demonstrates that renal nerves and its downstream signaling contribute to progression of acute kidney injury (AKI) to CKD and fibrogenesis. This review summarizes our current knowledge of the role of renal sympathetic nerve and adrenergic receptors in AKI, AKI to CKD transition and CKDand provides new insights into the therapeutic potential of intervening in its signaling pathways.
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Kenney, Michael J., Dale E. Claassen, Richard J. Fels, and Cristina S. Saindon. "Cold stress alters characteristics of sympathetic nerve discharge bursts." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 732–42. http://dx.doi.org/10.1152/jappl.1999.87.2.732.

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Frequency-domain analyses were used to determine the effect of cold stress on the relationships between the discharge bursts of sympathetic nerve pairs, sympathetic and aortic depressor nerve pairs, and sympathetic and phrenic nerve pairs in chloralose-anesthetized, baroreceptor-innervated rats. Sympathetic nerve discharge (SND) was recorded from the renal, lumbar, splanchnic, and adrenal nerves during decreases in core body temperature from 38 to 30°C. The following observations were made. 1) Hypothermia produced nonuniform changes in the level of activity in regionally selective sympathetic nerves. Specifically, cold stress increased lumbar and decreased renal SND but did not significantly change the level of activity in splanchnic and adrenal nerves. 2) The cardiac-related pattern of renal, lumbar, and splanchnic SND bursts was transformed to a low-frequency (0–2 Hz) pattern during cooling, despite the presence of pulse-synchronous activity in arterial baroreceptor afferents. 3) Peak coherence values relating the discharges between sympathetic nerve pairs decreased at the cardiac frequency but were unchanged at low frequencies (0–2 Hz), indicating that the sources of low-frequency SND bursts remain prominently coupled during progressive reductions in core body temperature. 4) Coherence of discharge bursts in phrenic and renal sympathetic nerve pairs in the 0- to 2-Hz frequency band increased during mild hypothermia (36°C) but decreased during deep hypothermia (30°C). We conclude that hypothermia profoundly alters the organization of neural circuits involved in regulation of sympathetic nerve outflow to selected regional circulations.
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Taylor, R. F., and L. P. Schramm. "Spinally mediated inhibition of abdominal and lumbar sympathetic activities." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 4 (April 1, 1988): R655—R658. http://dx.doi.org/10.1152/ajpregu.1988.254.4.r655.

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Renal, splenic, and lumbar sympathetic nerve activities were recorded in the paralyzed, anesthetized, artificially ventilated, and spinally transected rat. Electrical stimulation of the dorsolateral funiculus caudal to the spinal transection was used to generate stimulus-response curves for changes in sympathetic activity in each of the three sympathetic nerves using five stimulus frequencies. In all rats, spinal stimulation inhibited sympathetic activity in renal and splenogastric nerves by approximately 50%. In grouped data, threshold frequency for inhibition of renal and splenogastric sympathetic nerve activity was 5 Hz, and inhibitions were maximal (50-60%) at 10 Hz. In contrast, activity in the lumbar sympathetic chain was inhibited in only two of five rats, and grouped data did not exhibit any statistically significant inhibitions. We conclude that lumbar sympathetic activity which remains after spinal transection can be inhibited only marginally by spinal stimulation, which substantially reduces renal and splenogastric sympathetic activity.
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Taylor, R. B., and L. C. Weaver. "Dorsal root afferent influences on tonic firing of renal and mesenteric sympathetic nerves in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 6 (June 1, 1993): R1193—R1199. http://dx.doi.org/10.1152/ajpregu.1993.264.6.r1193.

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After spinal cord transection in cats and rats, the activity of many sympathetic nerves is not entirely lost, and firing of other nerves continues unabated or is increased. This study was done to evaluate the importance of dorsal root afferent discharge on the generation of tonic sympathetic activity in renal and mesenteric postganglionic nerves in spinal rats and in rats with intact neuraxes. Sympathetic discharge was recorded in anesthetized rats, and peripheral afferent influences were eliminated by dorsal rhizotomy from T4 to L2. Activity of renal and mesenteric nerves was well maintained after high cervical and thoracic (T4) cord transections. Rhizotomy had no effect on sympathetic discharge in rats with intact neuraxes but decreased renal nerve activity significantly (-25%) in spinal rats. Because rhizotomy decreased mesenteric discharge in only three of six spinal rats, mean mesenteric nerve discharge was not decreased significantly. The decreased renal nerve discharge after dorsal rhizotomy could not be attributed to input from any specific spinal segment, and ipsilateral input was no greater than contralateral input. After rhizotomy, both renal and mesenteric nerves had substantial excitatory drive from the transected, deafferented spinal cord. These findings demonstrate that dorsal root afferent influences on spinal neurons can contribute to the generation of tonic discharge in some sympathetic nerves in spinal animals.
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Sripairojthikoon, W., and J. M. Wyss. "Cells of origin of the sympathetic renal innervation in rat." American Journal of Physiology-Renal Physiology 252, no. 6 (June 1, 1987): F957—F963. http://dx.doi.org/10.1152/ajprenal.1987.252.6.f957.

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Physiological studies are rapidly elucidating the function of the renal nerves; however, the anatomical location of the postganglionic cell bodies that supply the rat kidney has not been fully clarified. The origin of the sympathetic projection to the rat kidney was investigated in the present study by use of the fluorescent dye retrograde transport technique. Application of the dye to the renal nerves resulted in the fluorescent labeling of sympathetic cell bodies in paravertebral [thoracic (T) segment 6 through lumbar (L) segment 4] and prevertebral (renal, greater splanchnic, and celiac) ganglia and along the greater splanchnic nerve. Sympathetic neurons in all of these locations were round to fusiform in shape, 16-40 micron in diameter. They were dispersed uniformly throughout the paravertebral ganglia and splanchnic nerve, but in the celiac and greater splanchnic ganglia, cells projecting to the kidney were clustered near the origin of the renal nerve. In contrast to the cat, in which greater than 50% of the renal sympathetic innervation arises from the prevertebral ganglia, in the rat the majority (greater than 70%) of labeled renal sympathetic neurons were in the paravertebral ganglia, especially T12-L1. The distribution of renal sympathetic neurons in the paravertebral ganglia closely approximates the rostrocaudal distribution of renal afferent cell bodies in the dorsal root ganglia.
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Kannan, H., Y. Hayashida, and H. Yamashita. "Increase in sympathetic outflow by paraventricular nucleus stimulation in awake rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 6 (June 1, 1989): R1325—R1330. http://dx.doi.org/10.1152/ajpregu.1989.256.6.r1325.

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Our previous studies demonstrated that stimulation of the hypothalamic paraventricular nucleus (PVN) in anesthetized rats evoked a depressor response accompanied with a decrease in sympathetic outflow (H. Kannan, A. Niijima, and H. Yamashita, J. Auton. Nerv. Syst. 19: 83-86, 1987; H. Yamashita, H. Kannan, M. Kasai, and T. Osaka, J. Auton. Nerv. Syst. 19: 229-234, 1987). Because anesthesia may alter cardiovascular responses, we examined in conscious rats the effects of PVN stimulation on arterial pressure, heart rate, and renal sympathetic nerve activity. Electrical stimulation through chronically implanted electrodes evoked increases in arterial pressure and renal sympathetic nerve activity with a slight decrease in heart rate. The magnitude of responses was dependent on the frequency and the intensity of the stimulus. Latency of the excitatory response of the renal sympathetic nerve activity was approximately 70 ms. Microinjection of L-glutamate (0.5 M, 200 nl) into the PVN area also elicited increases in blood pressure and renal sympathetic nerve activity. These results suggest that activation of PVN neurons in conscious rats produces pressor responses due to an increase in the sympathetic outflow. These findings contrast with those obtained previously in anesthetized rats.
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DiBona, G. F., and U. C. Kopp. "Neural control of renal function." Physiological Reviews 77, no. 1 (January 1, 1997): 75–197. http://dx.doi.org/10.1152/physrev.1997.77.1.75.

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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.
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Kopp, Ulla C. "Role of renal sensory nerves in physiological and pathophysiological conditions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 2 (January 15, 2015): R79—R95. http://dx.doi.org/10.1152/ajpregu.00351.2014.

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Whether activation of afferent renal nerves contributes to the regulation of arterial pressure and sodium balance has been long overlooked. In normotensive rats, activating renal mechanosensory nerves decrease efferent renal sympathetic nerve activity (ERSNA) and increase urinary sodium excretion, an inhibitory renorenal reflex. There is an interaction between efferent and afferent renal nerves, whereby increases in ERSNA increase afferent renal nerve activity (ARNA), leading to decreases in ERSNA by activation of the renorenal reflexes to maintain low ERSNA to minimize sodium retention. High-sodium diet enhances the responsiveness of the renal sensory nerves, while low dietary sodium reduces the responsiveness of the renal sensory nerves, thus producing physiologically appropriate responses to maintain sodium balance. Increased renal ANG II reduces the responsiveness of the renal sensory nerves in physiological and pathophysiological conditions, including hypertension, congestive heart failure, and ischemia-induced acute renal failure. Impairment of inhibitory renorenal reflexes in these pathological states would contribute to the hypertension and sodium retention. When the inhibitory renorenal reflexes are suppressed, excitatory reflexes may prevail. Renal denervation reduces arterial pressure in experimental hypertension and in treatment-resistant hypertensive patients. The fall in arterial pressure is associated with a fall in muscle sympathetic nerve activity, suggesting that increased ARNA contributes to increased arterial pressure in these patients. Although removal of both renal sympathetic and afferent renal sensory nerves most likely contributes to the arterial pressure reduction initially, additional mechanisms may be involved in long-term arterial pressure reduction since sympathetic and sensory nerves reinnervate renal tissue in a similar time-dependent fashion following renal denervation.
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Bandali, Karim S., and Uwe Ackermann. "Are prostaglandins involved in atrial natriuretic peptide mechanisms of cardiovascular control?" Canadian Journal of Physiology and Pharmacology 77, no. 3 (March 1, 1999): 211–15. http://dx.doi.org/10.1139/y99-004.

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Atrial natriuretic peptide (ANP) can excite cardiac nerve endings and invoke a decrease in arterial blood pressure and a reduction in renal sympathetic nerve activity. Our laboratory has previously demonstrated that this renal depressor reflex was invoked by systemic injection of ANP and not by the direct application of ANP to the epicardium, a major locus for vagal afferents. We now examine whether inhibition of prostaglandin synthesis impairs reflex responses that are normally associated with ANP injections. Renal sympathetic nerve activity, arterial blood pressure, and heart rate were recorded in anesthetized rats. Indomethacin was used to inhibit prostaglandin synthesis through the cyclooxygenase pathway. The ANP-mediated decrease in arterial blood pressure and renal sympathetic nerve activity, observed when prostaglandin synthesis was inhibited, did not differ significantly from the decreases observed in these parameters when prostaglandin synthesis was not inhibited. Heart rate remained unchanged. Our results suggest that the sympatho-inhibitory effects of ANP do not require prostaglandins as intermediary compounds.Key words: sympathetic nervous system, renal nerves, prostaglandins.
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MacNeil, B. J., A. H. Jansen, A. H. Greenberg, and D. M. Nance. "Effect of acute adrenalectomy on sympathetic responses to peripheral lipopolysaccharide or central PGE2." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 5 (May 1, 2000): R1321—R1328. http://dx.doi.org/10.1152/ajpregu.2000.278.5.r1321.

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The impact of plasma corticosterone levels on the sympathetic nervous system (SNS) response to intravenous lipopolysaccharide (LPS) or intracerebroventricular injections of PG was studied in anesthetized (urethan-chloralose) male Sprague-Dawley rats. For this, electrophysiological recordings of splenic and renal nerves were completed in control or adrenalectomized (ADX) rats. LPS (10 μg iv) similarly increased splenic and renal nerve activity in control rats with a shorter onset latency for the splenic nerve. Acute ADX enhanced the response of both nerves to LPS ( P < 0.005) and reduced the onset latency of the renal nerve ( P < 0.05). PGE2 (2 μg icv) rapidly increased the activity of both nerves but preferentially (magnitude and onset latency) stimulated the renal nerve ( P < 0.05). The magnitude of the splenic nerve response to PGE2 was unaffected by ADX. Unexpectedly, PGE2 was less effective at stimulating renal nerve activity in ADX animals relative to intact controls ( P < 0.05). Pretreatment of ADX rats with a CRF antagonist {[d-Phe12, Nle21,38, Cα-MeLeu37]CRF-(12—41)} reversed this effect such that the renal nerve responded to central PGE2 to a greater extent than the splenic nerve ( P< 0.05), as was the case in non-ADX rats. These data indicate that enhanced sensitivity of central sympathetic pathways does not account for the enhanced SNS responses to LPS in ADX rats. Also, a CRF-related process appears to diminish renal sympathetic outflow in ADX rats.
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Dissertations / Theses on the topic "Renal sympathetic nerve"

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Pac-Soo, Chen Knien. "Effects of inhalational anaesthetics on spontaneous sympathetic activity and somatosympathetic reflexes." Thesis, University of Aberdeen, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322526.

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Yamamoto, Hiromi. "Electroacupuncture changes the relationship between cardiac and renal sympathetic nerve activities in anesthetized cats." Kyoto University, 2009. http://hdl.handle.net/2433/126434.

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Carmichael, II Samuel Paterson. "HYPOTHALAMIC MEDIATION OF ACUTE INCREASES IN ARTERIAL BLOOD PRESSURE AND RENAL SYMPATHETIC NERVE ACTIVITY DURING ELECTRICAL STIMULATION OF THE LAMINA TEMRINALIS." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_theses/513.

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Discrete electrical stimulation of the organum vasculosum of the lamina terminalis (OVLT) produces sympathetically-mediated increases in peripheral resistance and arterial blood pressure (ABP). Since efferent fibers from the lamina terminalis innervate the kidney through polysynaptic connections, the present study determined whether electrical stimulation of the OVLT increased sympathetic outflow to the kidney. In anesthetized male, Sprague-Dawley rats (n=5) electrical stimulation of OVLT neurons produced frequency and current intensity dependent increases in renal sympathetic nerve activity (RSNA) and ABP that were abolished by ganglionic blockade with the nicotinic antagonist chlorisondamine (5mg/kg,i.v.). Since neurons from the OVLT terminate within the hypothalamic paraventricular nucleus (PVH), the present study also determined whether these connections mediate a portion of sympathetic and pressor responses to electrical stimulation of the OVLT. Bilateral inhibition of the PVH with the GABAA agonist muscimol (5mM/100nl) significantly attenuated the increase in ABP at all frequencies and current intensities. Spike-triggered averaging of RSNA revealed that PVH inhibition significantly blunted the RSNA responses to OVLT stimulation at 100, 200, but not 400andamp;igrave;A. The present findings indicate that electrical stimulation of the OVLT increases RSNA and ABP and that these responses are partially mediated by the tonic activity of PVH neurons.
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Carmichael, Samuel Paterson. "Hypothalamic mediation of acute increases in arterial blood pressure and renal sympathetic nerve activity during electrical stimulation of the lamina temrinalis [sic]." Lexington, Ky. : [University of Kentucky Libraries], 2008. http://hdl.handle.net/10225/793.

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Thesis (M.S.)--University of Kentucky, 2008.
Title from document title page (viewed on August 21, 2008). Document formatted into pages; contains: vi, 51 p. : ill. Includes abstract and vita. Includes bibliographical references (p. 43-49).
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Shweta, Amany 1971. "The renal sympathetic nerves : implications for vascular remodelling in the SHR kidney." Monash University, Dept. of Physiology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8351.

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Pirnat, Deni. "The importance of the renal sympathetic nerves in the natriuretic response to imidazoline receptor agonists." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62822.pdf.

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Wang, Hung-Wen, and 王鴻文. "Effects of Electroacupuncture on Renal Sympathetic Nerve Activities, Blood Pressure and Urine Excretion in the Rat." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/50284226360403764520.

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碩士
國立臺灣大學
生理學研究所
84
Experiments were carried out in female Wistar rats which were divided into two groups with different site (acupoint) of stimulation:(1)Ho-Ku, and (2) Hsing-Chien. Electroacupuncture (EA)was performed with various stimulation parameters, i.e., a combination of three different frequencies, 10, 50, &100 Hz, with three different intensities, 5*, 10*,& 20*T, (T is threshold for minimal muscle contraction). The renal sympathetic nerve activity (RSNA), blood pressure (BP)and urine excretion (UE) were continuously recorded.The results are as follows:(1) Ho-Ku:RSNA was significantly increased following EA with a frequency of 10 Hz and an intensity of 10*T or 20*T, other stimulation parameters seemed to be ineffective. As to the effect on BP, EA with 10 Hz and 10*T or 20*T,BP was elevated slowly and took a few minutes to reach the maximum level, then maintained at a higher than control level even 10 min after cessation of stimulation. However, with a frequency of 50 or 100Hz,the elevation of BP was rapid and reached the peak in 10s, but was back to control level within 20s after EA was started. On the other hand, UE was increased only when EA with a frequency of 100 Hz plus 10* or 20*T.(2) Hsing-Chien: RSNA was enhaced significantly only when EA with 50 Hz and 5*T, other frequency or intensity did not cause any change in RSNA. As to the BP, none of the stimulation parameters stated above was effective when EA was tested at the Hsing-Chien. On the contrary, UE was increased significantly by EA with 20*T plus any one of the above three frequencies. All these results indicate that EA with different stimulation parameters at different acupoint, Ho-Ku or Hsing-Chien may induce different effects on RSNA, BP and UE.
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Chu, Tai-Min, and 朱泰民. "Developing an Integrated System for Noninvasive Assessment of Real-time Sympathetic Nerve Activities." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/w57tb5.

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碩士
國立中央大學
生物醫學工程研究所
106
Traditionally, sympathetic nervous system can be measured in two ways. The gold standard is highly invasive, which is well-known as Microneurography, utilizing the tungsten microelectrode to insert percutaneously into a sympathetic nerve to detect its electric activity. Since it will cause certain pain to the subject, it is not commonly applied for clinical diagnostic. On the other hand, the analysis of Heart Rate Variability (HRV), which measures the variation of the heart beat intervals, is more commonly used. However, it requires electrocardiograph (ECG) records of a long period of time, and the indexes are less related with sympathetic activities. Previous studies have proposed a technique for simultaneous and non-invasive measurement of sympathetic activity. By measuring the electrocardiogram (ECG) on the body surface, the sympathetic nerve activity can be obtained by filtering ECG through a high-pass filter, which is called Skin Sympathetic Nerve Activity (SKNA). The thesis proposes a novel nonstationary approach to SKNA signal investigation, referred to as Multi Scale Fluctuation Analysis (MSFA). This method, based on the Multi Dynamic Trend Analysis (MDTA), can be applied by means of analyzing the fluctuation of SKNA signal under different scales. By using the Matlab mathematical software, MSFA validates the differences in sympathetic nerve regulation of postoperative patients. On the other hand, this thesis also attempted to use different instrument to measure ECG signal in order to detect SKNA signal, other than previous studies.
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Frame, Alissa. "Integrated renal and neural mechanisms contributing to sodium homeostasis and blood pressure regulation." Thesis, 2019. https://hdl.handle.net/2144/38526.

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Hypertension affects one in two adults in the United States and contributes to more than 10% of deaths worldwide. The salt sensitivity of blood pressure, a clinical phenomenon present in one half of hypertensive patients and one quarter of normotensive individuals, predicts the development of hypertension. The prevalence of hypertension rises with age, and age-related increases in salt sensitivity and sympathetic nervous system activity, which promotes renal sodium reabsorption and plays a pathophysiological role in salt sensitivity and hypertension, have been documented. Increased mechanistic insight into the integrated renal and neural mechanisms influencing sodium homeostasis and blood pressure, particularly in aging, could yield valuable information for the phenotypically targeted treatment of hypertension. The renal nerves, comprised of the sensory afferent renal nerves (ARN) and the efferent renal sympathetic nerves, influence sodium homeostasis and blood pressure. The ARN, which include mechanosensitive and chemosensitive fibers, mediate a sympathoinhibitory reno-renal reflex that suppresses renal sympathetic nerve activity. The renal sympathetic nerves release norepinephrine, which can promote salt-sensitive hypertension in part by activating the sodium chloride cotransporter (NCC). In this thesis, Sprague Dawley rats were used as a model of normal aging to demonstrate that 1) the ARN are critical to the sympathoinhibitory and natriuretic responses to alterations in sodium homeostasis and protect against salt sensitivity of blood pressure, 2) the paraventricular nucleus of the hypothalamus may be a site of central integration of the mechanosensitive sympathoinhibitory reno-renal reflex, 3) norepinephrine promotes NCC activity through an α1-adrenoceptor-gated WNK1-OxSR1-dependent signaling pathway, driving salt-sensitive hypertension, and 4) impairments in the sympathoinhibitory reno-renal reflex may promote sympathoexcitation and NCC-mediated sodium retention, driving salt-sensitive hypertension in aging rats. Finally, data from the Genetic Epidemiology of Salt Sensitivity study were used to demonstrate that variance in the gene encoding Gαi2 proteins, which are upregulated in the paraventricular nucleus during high salt intake in salt-resistant animal models and are required for dietary sodium-evoked suppression of renal sympathetic outflow, may be a biomarker for the salt sensitivity of blood pressure in humans. Together, these findings highlight the integrated renal and neural mechanisms contributing to salt sensitivity and age-related hypertension.
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Books on the topic "Renal sympathetic nerve"

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Wang, Yutang, Kyungjoon Lim, and Kate M. Denton, eds. Function of Renal Sympathetic Nerves. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-295-8.

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Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.

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Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.
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Book chapters on the topic "Renal sympathetic nerve"

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Li, Dong, Yingxiong Jin, Zhuo Yang, and Tao Zhang. "Analysis of Multifibre Renal Sympathetic Nerve Recordings." In Advances in Neural Networks - ISNN 2006, 734–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11760191_108.

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Kumagai, H., T. Onami, K. Iigaya, C. Takimoto, M. Imai, T. Matsuura, K. Sakata, N. Oshima, K. Hayashi, and T. Saruta. "Involvement of Renal Sympathetic Nerve in Pathogenesis of Hypertension." In Contributions to Nephrology, 32–45. Basel: KARGER, 2004. http://dx.doi.org/10.1159/000078710.

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Kopp, Ulla C. "Endothelin in the Control of Renal Sympathetic Nerve Activity." In Contributions to Nephrology, 107–19. Basel: KARGER, 2011. http://dx.doi.org/10.1159/000328688.

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Schlaich, Markus P. "Heart/kidney interactions." In ESC CardioMed, edited by Guido Grassi, 134–38. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0025.

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The interactions between the heart and the kidney are manifold but relate predominantly to haemodynamic and regulatory functions. The kidneys are intricately involved in electrolyte balance, volume homeostasis, and blood pressure regulation through modifying effects on regional haemodynamics and hormonal regulation affecting the heart and other organs. Alterations in cardiac output induced by a variety of clinical conditions can have a profound impact on perfusion of vital organs, including the kidneys, potentially resulting in a vicious cycle referred to as cardiorenal syndrome with high mortality if not treated appropriately. Communication between the kidney and the heart occurs at multiple levels including the sympathetic nervous system, the renin–angiotensin–aldosterone system, antidiuretic hormone, nitric oxide, endothelin, and the natriuretic peptides. The role of renal sympathetic efferent and afferent sensory nerves in modulating renal and cardiac function are of particular importance. Stimulation of the renal sympathetic efferent nerves causes renin release, sodium retention, and reduced renal blood flow, all hallmarks of the renal manifestations of heart failure and the cardiorenal syndrome. Elevated afferent renal sensory nerve signalling increases sympathetic drive via central integration in the hypothalamic region, thereby mediating an increase in sympathetic outflow directed to various regions including the skeletal muscle vasculature, the kidneys, and the heart, which contributes substantially to elevated peripheral vascular resistance, vascular remodelling, and left ventricular hypertrophy as well as accelerating the decline of left ventricular function.
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Cheshire, William P. "Autonomic Physiology." In Clinical Neurophysiology, 617–28. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780195385113.003.0035.

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The autonomic nervous system consists of three divisions: the sympathetic (thoracolumbar), parasympathetic (craniosacral), and enteric nervous systems. The sympathetic and parasympathetic autonomic outflows involve a two-neuron pathway with a synapse in an autonomic ganglion. Preganglionic sympathetic neurons are organized into various functional units that control specific targets and include skin vasomotor, muscle vasomotor, visceromotor, pilomotor, and sudomotor units. Microneurographic techniques allow recording of postganglionic sympathetic nerve activity in humans. Skin sympathetic activity is a mixture of sudomotor and vasoconstrictor impulses and is regulated mainly by environmental temperature and emotional influences. Muscle sympathetic activity is composed of vasoconstrictor impulses that are strongly modulated by arterial baroreceptors. Heart rate is controlled by vagal parasympathetic and thoracic sympathetic inputs. Vagal influence on the heart rate is strongly modulated by respiration; it is more marked during expiration and is absent during inspiration. This is the basis for the so-called respiratory sinus arrhythmia, which is an important index of vagal innervation of the heart. Power spectral analysis of heart rate fluctuations allows noninvasive assessment of beat-to-beat modulation of neuronal activity affecting the heart. Arterial baroreflex, cardiopulmonary reflexes, venoarteriolar reflex, and ergoreflexes control sympathetic and parasympathetic influences on cardiovascular effectors. The main regulatory mechanism that prevents orthostatic hypotension is reflex arterial vasoconstriction in the splanchnic, renal, and muscular beds triggered by a decrease in transmural pressure at the level of carotid sinus baroreceptors.
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Kulenthiran, Saarraaken, Sebastian Ewen, and Felix Mahfoud. "Device-based treatment for hypertension." In ESC CardioMed, edited by Bryan Williams, 2458–65. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0570.

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Autonomic imbalance is thought to play an important role in the pathophysiology of hypertension. Despite the availability of diverse pharmacological options, non-adherence to medication or inability to tolerate current pharmacological therapies has led to the development of various device-based therapy options. Inhibiting components of the sympathetic nervous system offers a unique opportunity to target the ‘neural’ component of the neurohormonal axis. Combining novel drug-, device-, and procedure-based strategies with improved utilization of existing therapies (including appropriate attention to diet, exercise, and weight control) may result in improved outcomes. This chapter discusses the rationale and current experimental and clinical data of several novel device-based treatment options—renal nerve ablation, carotid body ablation, carotid baroreceptor stimulation, and central arteriovenous anastomosis.
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Kulenthiran, Saarraaken, Sebastian Ewen, and Felix Mahfoud. "Device-based treatment for hypertension." In ESC CardioMed, edited by Bryan Williams, 2458–65. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0570_update_001.

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Abstract:
Autonomic imbalance is thought to play an important role in the pathophysiology of hypertension. Despite the availability of diverse pharmacological options, non-adherence to medication or inability to tolerate current pharmacological therapies has led to the development of various device-based therapy options. Inhibiting components of the sympathetic nervous system offers a unique opportunity to target the ‘neural’ component of the neurohormonal axis. Combining novel drug-, device-, and procedure-based strategies with improved utilization of existing therapies (including appropriate attention to diet, exercise, and weight control) may result in improved outcomes. This chapter discusses the rationale and current experimental and clinical data of several novel device-based treatment options—renal nerve ablation, carotid body ablation, carotid baroreceptor stimulation, and central arteriovenous anastomosis.
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8

Schlaich, Markus, and Murray Esler. "Device-based approaches to target renal sympathetic nerves for hypertension." In Surgery of the Autonomic Nervous System, 73–94. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199686407.003.0005.

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9

A. Gomez, Jose. "Renin Angiotensin Aldosterone System Functions in Renovascular Hypertension." In Renin-Angiotensin Aldosterone System [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97491.

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The renin angiotensin aldosterone system (RAAS) plays a key function in renovascular hypertension induced by renal artery stenosis (RAS). RAS causes a decrease in renal perfusion in the stenosed kidney which in turn stimulates renin the rate limiting enzyme in RAAS. This stimulation triggers a series of events starting with renin release leading to Ang II production, decrease in sodium excretion, increase sympathetic tone; all contributing to the development of renovascular hypertension. In RAS increase of superoxide reduce nitric oxide in the afferent arteriole increasing vasoconstriction and a marked decrease in glomerular filtration rate. In renovascular hypertension prostaglandins mediate renin release in the stenosed kidney. Targeting different RAAS components is part of the therapy for renovascular hypertension, with other options including renal nerves denervation and revascularization. Different clinical studies had explored revascularization, RAAS blocking and renal nerves denervation as a therapy. We will discuss organ, cellular and molecular components of this disease.
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Emmett, Stevan R., Nicola Hill, and Federico Dajas-Bailador. "Cardiovascular medicine." In Clinical Pharmacology for Prescribing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780199694938.003.0010.

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Hypertension (HTN) is the most common condition man¬aged in primary care and a major risk factor for cardio-vascular disease. Numerous randomized controlled trials have demonstrated that the use of antihypertensives to manage blood pressure (BP) helps reduce cardiovascular disease risk. Prevalence of HTN increases with age so that around 33% of men and 25% of women aged 45– 54 years have a clinical diagnosis. It is generally defined as a raised blood pressure exceeding 140/ 90 mmHg, divided into two types: ● Essential (or primary) hypertension: accounts for 95% of cases and is where no secondary cause is identified. ● Secondary hypertension: the result of an underlying disease (e.g. renal, pulmonary, endocrine, or drug/ toxin). Pre- HTN is defined as systolic BP (SBP) 120– 139 mmHg and diastolic BP (DBP) 80– 89 mmHg. BP is the product of cardiac output (heart stroke volume and heart rate) and the total peripheral resistance of ves­sels supplied by the heart. Thus, three main systems are responsible for generating BP: the heart (pumping pres­sure), vessel tone (being the systemic resistance), and the kidney (regulating intravascular volume). Three main physiological systems regulate heart, ves­sels, and kidney with respect to blood pressure: 1. The sympathetic nervous system: changes in BP are sensed by a feedback mechanism mediated by baro­receptors in the walls of the aortic arch and carotid sinuses. Increasing BP causes firing of glossopha­ryngeal and vagus nerves, inhibiting sympathetic outflow via the medulla (tractus solitarius). This, in turn, leads to parasympathetic dominance and a reduction in peripheral resistance (vasodilation through β1- adrenoceptors) and cardiac output (by reduced heart rate and reduced contractility through α1- adrenoceptors). Centrally acting antihypertensive drugs act at the nucleus tractus solitarius (e.g. clonidine/ methyldopa) or ventrolateral medulla (e.g. moxonidine). 2. The renin- angiotensin- aldosterone system: this system regulates blood volume and systemic vascular resistance, thus influencing cardiac output and arterial pressure. This feedback mechanism starts in the kidney with the release of renin into the peripheral circula­tion. Renin release, from juxtaglomerular cells (JC), is stimulated by sympathetic mechanisms (involving α1- receptors on JC themselves), decreased afferent ar­teriole pressure (from systemic hypotension or renal artery stenosis) or declining Na<sup>+</sup> levels in the distal tu­bules of the kidney. Prostaglandins, such as PGE2 and PGI2 (prostacyclin), also cause release of renin sec­ondary to reduced NaCl transport in the macular densa (see Topic 5.2 ‘Acute kidney injury’).
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Conference papers on the topic "Renal sympathetic nerve"

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Roth, Austin, Leslie Coleman, Kenichi Sakakura, Elena Ladich, and Renu Virmani. "Circumferential targeted renal sympathetic nerve denervation with preservation of the renal arterial wall using intra-luminal ultrasound." In SPIE BiOS, edited by Thomas P. Ryan. SPIE, 2015. http://dx.doi.org/10.1117/12.2080260.

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Karaaslan, Fatih. "Analysis of Effect of Increased and Reduced Renal Sympathetic Nerve Activity on Arterial Blood Pressure by Using a Mathematical Model." In 2021 Medical Technologies Congress (TIPTEKNO). IEEE, 2021. http://dx.doi.org/10.1109/tiptekno53239.2021.9632977.

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