Relevant bibliographies by topics / Renal nerves

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

Academic literature on the topic 'Renal nerves'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Renal nerves"

1

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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Kopp, Ulla C. "Renorenal reflexes: Interaction between efferent and afferent renal nerve activity." Canadian Journal of Physiology and Pharmacology 70, no. 5 (May 1, 1992): 750–58. http://dx.doi.org/10.1139/y92-099.

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In rats, stimulation of renal mechanoreceptors by increasing ureteral pressure results in a contralateral inhibitory renorenal reflex response consisting of increases in ipsilateral afferent renal nerve activity, decreases in contralateral efferent renal nerve activity, and increases in contralateral urine flow rate and urinary sodium excretion. Mean arterial pressure is unchanged. To study possible functional central interaction among the afferent renal nerves and the aortic and carotid sinus nerves, the responses to renal mechanoreceptor stimulation were compared in sinoaortic denervated rats and sham-denervated rats before and after vagotomy. In contrast to sham-denervated rats, there was an increase in mean arterial pressure in response to renal mechanoreceptor stimulation in sinoaortic-denervated rats. However, there were no differences in the renorenal reflex responses among the groups. Thus, our data failed to support a functional central interaction among the renal, carotid sinus, and aortic afferent nerves in the renorenal reflex response to renal mechanoreceptor stimulation. Studies to examine peripheral interaction between efferent and afferent renal nerves showed that marked reduction in efferent renal nerve activity produced by spinal cord section at T6, ganglionic blockade, volume expansion, or stretch of the junction of superior vena cava and right atrium abolished the responses in afferent renal nerve activity and contralateral renal function to renal mechanoreceptor stimulation. Conversely, increases in efferent renal nerve activity caused by thermal cutaneous stimulation increased basal afferent renal nerve activity and its responses to renal mechanoreceptor stimulation. These data suggest a facilitatory role of efferent renal nerves on renal sensory receptors.Key words: vagotomy, sinoaortic denervation, substance P, prostaglandins, mechanoreceptor stimulation.
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Kopp, Ulla C., Michael Z. Cicha, Lori A. Smith, Jan Mulder, and Tomas Hökfelt. "Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2-dependent activation of α1- and α2-adrenoceptors on renal sensory nerve fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 4 (October 2007): R1561—R1572. http://dx.doi.org/10.1152/ajpregu.00485.2007.

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Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA). To test whether the ERSNA-induced increases in ARNA involved norepinephrine activating α-adrenoceptors on the renal sensory nerves, we examined the effects of renal pelvic administration of the α1- and α2-adrenoceptor antagonists prazosin and rauwolscine on the ARNA responses to reflex increases in ERSNA (placing the rat's tail in 49°C water) and renal pelvic perfusion with norepinephrine in anesthetized rats. Hot tail increased ERSNA and ARNA, 6,930 ± 900 and 4,870 ± 670%·s (area under the curve ARNA vs. time). Renal pelvic perfusion with norepinephrine increased ARNA 1,870 ± 210%·s. Immunohistochemical studies showed that the sympathetic and sensory nerves were closely related in the pelvic wall. Renal pelvic perfusion with prazosin blocked and rauwolscine enhanced the ARNA responses to reflex increases in ERSNA and norepinephrine. Studies in a denervated renal pelvic wall preparation showed that norepinephrine increased substance P release, from 8 ± 1 to 16 ± 1 pg/min, and PGE2 release, from 77 ± 11 to 161 ± 23 pg/min, suggesting a role for PGE2 in the norepinephrine-induced activation of renal sensory nerves. Prazosin and indomethacin reduced and rauwolscine enhanced the norepinephrine-induced increases in substance P and PGE2. PGE2 enhanced the norepinephrine-induced activation of renal sensory nerves by stimulation of EP4 receptors. Interaction between ERSNA and ARNA is modulated by norepinephrine, which increases and decreases the activation of the renal sensory nerves by stimulating α1- and α2-adrenoceptors, respectively, on the renal pelvic sensory nerve fibers. Norepinephrine-induced activation of the sensory nerves is dependent on renal pelvic synthesis/release of PGE2.
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Foss, Jason D., Richard D. Wainford, William C. Engeland, Gregory D. Fink, and John W. Osborn. "A novel method of selective ablation of afferent renal nerves by periaxonal application of capsaicin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 2 (January 15, 2015): R112—R122. http://dx.doi.org/10.1152/ajpregu.00427.2014.

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Renal denervation has been shown to lower arterial pressure in some hypertensive patients, yet it remains unclear whether this is due to ablation of afferent or efferent renal nerves. To investigate the role of afferent renal nerves in arterial pressure regulation, previous studies have used methods that disrupt both renal and nonrenal afferent signaling. The present study was conducted to develop and validate a technique for selective ablation of afferent renal nerves that does not disrupt other afferent pathways. To do this, we adapted a technique for sensory denervation of the adrenal gland by topical application of capsaicin and tested the hypothesis that exposure of the renal nerves to capsaicin (renal-CAP) causes ablation of afferent but not efferent renal nerves. Renal-CAP had no effect on renal content of the efferent nerve markers tyrosine hydroxylase and norepinephrine; however, the afferent nerve marker, calcitonin gene-related peptide was largely depleted from the kidney 10 days after intervention, but returned to roughly half of control levels by 7 wk postintervention. Moreover, renal-CAP abolished the cardiovascular responses to acute pharmacological stimulation of afferent renal nerves. Renal-CAP rats showed normal weight gain, as well as cardiovascular and fluid balance regulation during dietary sodium loading. To some extent, renal-CAP did blunt the bradycardic response and increase the dipsogenic response to increased salt intake. Lastly, renal-CAP significantly attenuated the development of deoxycorticosterone acetate-salt hypertension. These results demonstrate that renal-CAP effectively causes selective ablation of afferent renal nerves in rats.
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Katsurada, Kenichi, Shyam S. Nandi, Neeru M. Sharma, Hong Zheng, Xuefei Liu, and Kaushik P. Patel. "Does glucagon-like peptide-1 induce diuresis and natriuresis by modulating afferent renal nerve activity?" American Journal of Physiology-Renal Physiology 317, no. 4 (October 1, 2019): F1010—F1021. http://dx.doi.org/10.1152/ajprenal.00028.2019.

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Glucagon-like peptide-1 (GLP-1), an incretin hormone, has diuretic and natriuretic effects. The present study was designed to explore the possible underlying mechanisms for the diuretic and natriuretic effects of GLP-1 via renal nerves in rats. Immunohistochemistry revealed that GLP-1 receptors were avidly expressed in the pelvic wall, the wall being adjacent to afferent renal nerves immunoreactive to calcitonin gene-related peptide, which is the dominant neurotransmitter for renal afferents. GLP-1 (3 μM) infused into the left renal pelvis increased ipsilateral afferent renal nerve activity (110.0 ± 15.6% of basal value). Intravenous infusion of GLP-1 (1 µg·kg−1·min−1) for 30 min increased renal sympathetic nerve activity (RSNA). After the distal end of the renal nerve was cut to eliminate the afferent signal, the increase in efferent renal nerve activity during intravenous infusion of GLP-1 was diminished compared with the increase in total RSNA (17.0 ± 9.0% vs. 68.1 ± 20.0% of the basal value). Diuretic and natriuretic responses to intravenous infusion of GLP-1 were enhanced by total renal denervation (T-RDN) with acute surgical cutting of the renal nerves. Selective afferent renal nerve denervation (A-RDN) was performed by bilateral perivascular application of capsaicin on the renal nerves. Similar to T-RDN, A-RDN enhanced diuretic and natriuretic responses to GLP-1. Urine flow and Na+ excretion responses to GLP-1 were not significantly different between T-RDN and A-RDN groups. These results indicate that the diuretic and natriuretic effects of GLP-1 are partly governed via activation of afferent renal nerves by GLP-1 acting on sensory nerve fibers within the pelvis of the kidney.
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Osborn, John W., Roman Tyshynsky, and Lucy Vulchanova. "Function of Renal Nerves in Kidney Physiology and Pathophysiology." Annual Review of Physiology 83, no. 1 (February 10, 2021): 429–50. http://dx.doi.org/10.1146/annurev-physiol-031620-091656.

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Renal sympathetic (efferent) nerves play an important role in the regulation of renal function, including glomerular filtration, sodium reabsorption, and renin release. The kidney is also innervated by sensory (afferent) nerves that relay information to the brain to modulate sympathetic outflow. Hypertension and other cardiometabolic diseases are linked to overactivity of renal sympathetic and sensory nerves, but our mechanistic understanding of these relationships is limited. Clinical trials of catheter-based renal nerve ablation to treat hypertension have yielded promising results. Therefore, a greater understanding of how renal nerves control the kidney under physiological and pathophysiological conditions is needed. In this review, we provide an overview of the current knowledge of the anatomy of efferent and afferent renal nerves and their functions in normal and pathophysiological conditions. We also suggest further avenues of research for development of novel therapies targeting the renal nerves.
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Vizzard, M. A., A. Standish, and W. S. Ammons. "Renal afferent input to the ventrolateral medulla of the cat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 2 (August 1, 1992): R412—R422. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r412.

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Experiments were performed to determine if information from the kidneys projects to the rostral ventrolateral medulla. Extracellular action potentials were recorded from 148 cells within the rostral ventrolateral medulla of alpha-chloralose-anesthetized cats. Cells within the rostral ventrolateral medulla were tested for responses to electrical stimulation of both left and right renal nerves. Electrical stimulation of renal nerves excited 144 cells (97.3%) and inhibited 4. The majority of cells received either bilateral or contralateral renal nerve input. Cells with bilateral renal nerve input responded to contralateral renal nerve stimulation with a significantly greater number of impulses compared with ipsilateral renal nerve stimulation (P less than 0.05). All cells but one responding to renal nerve stimulation had convergent somatic input. Comparisons between thresholds for cell responses and activation thresholds for the A and C volleys of the compound action potential recorded in the least splanchnic nerve revealed that 44 cells required activation of A delta-fibers, and 12 cells required activation of both A delta- and C-fibers. A conditioning stimulus applied to renal nerves on one side significantly decreased the response elicited by a test stimulus applied to the renal nerves on the opposite side for at least 300 ms (P less than 0.05). The demonstration that an afferent connection exists between the kidneys and the ventrolateral medulla suggests that the rostral ventrolateral medulla may play a role in mediating supraspinal reflexes of renal origin.
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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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Oparil, Suzanne, Wanida Sripairojthikoon, and J. Michael Wyss. "The renal afferent nerves in the pathogenesis of hypertension." Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1548–58. http://dx.doi.org/10.1139/y87-244.

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The renal nerves play a role in the pathogenesis of hypertension in a number of experimental models. In the deoxycorticosterone acetate – salt (DOCA–NaCl) hypertensive rat and the spontaneously hypertensive rat (SHR) of the Okamoto strain, total peripheral renal denervation delays the development and blunts the severity of hypertension and causes an increase in urinary sodium excretion, suggesting a renal efferent mechanism. Further, selective lesioning of the renal afferent nerves by dorsal rhizotomy reduces hypothalamic norepinephrine stores without altering the development of hypertension in the SHR, indicating that the renal afferent nerves do not play a major role in the development of hypertension in this genetic model. In contrast, the renal afferent nerves appear to be important in one-kidney, one-clip and two-kidney, one-clip Goldblatt hypertensive rats (1K, 1C and 2K, 1C, respectively) and in dogs with chronic coarctation hypertension. Total peripheral renal denervation attenuates the severity of hypertension in these models, mainly by interrupting renal afferent nerve activity, which by a direct feedback mechanism attenuates systemic sympathetic tone, thereby lowering blood pressure. Peripheral renal denervation has a peripheral sympatholytic effect and alters the level of activation of central noradrenergic pathways but does not alter sodium or water intake or excretion, plasma renin activity or creatinine clearance, suggesting that efferent renal nerve function does not play an important role in the maintenance of this form of hypertension. Selective lesioning of the renal afferent nerves attenuates the development of hypertension, thus giving direct evidence that the renal afferent nerves participate in the pathogenesis of renovascular hypertension.
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DiBona, GF. "Role of Renal Nerves in Edema Formation." Physiology 9, no. 4 (August 1, 1994): 183–88. http://dx.doi.org/10.1152/physiologyonline.1994.9.4.183.

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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.
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Dissertations / Theses on the topic "Renal nerves"

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Janssen, Bernardus Jacobus Agnes. "Sensory renal nerves and hypertension." Maastricht ; Rijksuniversiteit Limburg ; Maastricht : University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5589.

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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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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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Amaral, Nathalia Oda. "Dieta hiperlipídica e hipernatremia: alterações autonômicas e cardiovasculares." Universidade Federal de Goiás, 2018. http://repositorio.bc.ufg.br/tede/handle/tede/8192.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Hypertension is the most common pathologies which affect population. Of the factors that can promote hypertension, food behavior is highlighted in relation to unhealthy eating habits present in western diet. Thus, present study sought to evaluate some aspects of this pathology in several situations, and themes were discussed separately in two chapters. In the first moment, effect of maternal hyperlipidic diet on metabolic and autonomic parameters in offspring was evaluated. It is known which obesity induced by maternal diet can modify central regulatory pathways of the fetus, mainly long-term regulation of appetite, but no work sought to evaluate the influence of the maternal hyperlipidic diet (HD) on cardiovascular and autonomic parameters in the offspring . Female Holtzman rats (280-300 g) were divided into two groups. One group received standard diet (SD) and other HD. The animals had free access to SD or HD for 6 weeks prior and during gestation and lactation period. All pups were weaned after 21 days of life and had free access to SD. After one week some offspring and mothers were submitted to glycemic test and later euthanized for removal of adipose tissue and blood. Other offspring were submitted to in situ preparation. DH increased adipose tissue in all females, but was able to change only metabolic triacylglycerols concentration. Offspring of HFD dams (OffHFD) showed an increase in adipose tissue and total cholesterol and HDL levels. Offspring of SD dams (OffSD) showed decrease in sympathetic activity after pre-colicular transection. This effect was not observed in males offspring of mothers with HFD (OffHFD). KCN infusion caused similar increases in abdominal activity (ABD), in phrenic nerve frequency (PNA f) and sympathetic activity (SNA), but in OffHFD this increase in SNA was smaller. KCN caused increase in phrenic nerve amplitude (PNA) and was higher in OffHFD. Hypercapnia resulted in increase in SNA, ABD and PNA and decrease in PNA f in both groups. The decrease in PNA f was more pronounced in OffHFD and increased PNA was higher in OffHFD. Phenylephrine caused in both groups decrease in SNA, ABD and PNA, and generated an increase in PNA f. The reduction of SNA was higher in OffHFD. These results suggest that maternal HFD during fetal development alters central connections in offspring. In second moment oxytocin effects on vascular reactivity and its role in hypernatremia-induced responses were evaluated. Changes in volume and/or extracellular compartments composition are known to evoke various autonomic, cardiovascular and hormonal responses that to modulate renal excretion of water and sodium. The main vegetative adjustments are: renal vasodilation and oxytocin secretion. Regulation of osmolarity and volume is critical for survival. Despite knowledge, no study evaluated interaction between renal sympathetic activity and oxytocin secretion on renal and cardiovascular responses induced by sodium overload. Male Wistar rats (280–350 g) were anesthetized with sodium thiopental (40 mg/kg, i.v.). Animals were also instrumented for measurement of mean arterial pressure (MAP) and renal blood flow (RBF). Renal vascular conductance (RVC) was calculated as the ratio of RBF by MAP. In anesthetized rats (n = 6), OT infusion (0.03 μg/kg, i.v.) induced renal vasodilation. Ex vivo experiments demonstrated that OT caused renal artery relaxation. Blockade of OT receptors (OTR) reduced these responses to OT, indicating a direct effect of this peptide on OTR on this artery. Hypertonic saline (3 M NaCl, 1.8 ml/kg b.wt., i.v.) was infused over 60 s. In sham rats (n=6), hypertonic saline induced renal vasodilation. The OXTR antagonist (AT; n=7) and renal denervation (RX) reduced the renal vasodilation induced by hypernatremia. Atosiban with renal denervation (RX+AT; n=7) completely abolished renal vasodilation induced by sodium overload. Intact rats excreted 51% of the injected sodium within 90 min. Natriuresis was slightly blunted by atosiban and renal denervation (42% and 42% of load, respectively), whereas atosiban with renal denervation reduced sodium excretion to 16% of the load. These results suggest that OT and renal nerves are involved in renal vasodilation and natriuresis induced by acute plasma hypernatremia. The understanding of regulatory mechanisms activated both during obesity and during hyperosmolarity allows greater possibility development new therapeutic tools for hypertension prevention and treatment.
A hipertensão arterial é uma das patologias mais comuns que afetam a população. Dentre os fatores que podem propiciar a hipertensão o comportamento alimentar ganha destaque no que se referem aos hábitos alimentares não saudáveis presentes na dieta ocidental. Sendo assim, o presente trabalho procurou avaliar alguns aspectos dessa patologia em diversas situações, e os temas foram discutidos de forma separada em dois capítulos. No primeiro momento avaliou-se o efeito da dieta hiperlipídica materna sobre os parâmetros metabólicos e autonômicos na prole. Sabe-se que a obesidade induzida pela dieta materna pode modificar os caminhos regulatórios centrais do feto, principalmente a regulação em longo prazo do apetite, porém nenhum trabalho procurou avaliar a influência da dieta hiperlipídica (DH) materna sobre os parâmetros cardiovasculares e autonômicos na prole. Ratas Holtzman adultas (280 - 300 g) foram divididas em dois grupos. Um grupo recebeu dieta padrão (DP) e o outro grupo DH. Os animais tiveram acesso livre a DP ou DH durante 6 semanas prévias (período de pré-gestação) e durante período de gestação e lactação. Todos os filhotes foram desmamados após 21 dias de vida e tiveram livre acesso a DP. Após uma semana alguns filhotes e as mães foram submetidos ao teste glicêmico e posteriormente eutanasiadas para retirada de tecido adiposo e sangue. Os outros filhotes foram submetidos à preparação coração-bulbo-hipotálamo (in situ). A DH aumentou o tecido adiposo nas ratas, mas foi capaz de alterar apenas as concentrações metabólicas de triacilgliceróis nesses animais. Filhotes machos de mães com DH (FMDH) apresentaram aumento no tecido adiposo, aumento nos níveis de colesterol total e nos níveis de HDL. Filhotes machos de mães com DP (FMDP) apresentaram redução da atividade simpática após transecção pré-colicular. Esse efeito não foi observado nos FMDH. A infusão de KCN provocou aumentos similares entre FMDP e FMDH quanto à atividade abdominal (ABD), na frequência do nervo frênico (f PNA) e na atividade simpática torácica (SNA), porém, no grupo FMDH esse aumento na SNA foi menor. O KCN provocou um aumento na amplitude do nervo frênico (PNA) sendo maior em FMDH. A hipercapnia provocou nos filhotes um aumento na SNA, na ABD e na PNA e gerou uma diminuição na f PNA em ambos os grupos. A diminuição na f PNA foi mais acentuada em FMDH e o aumento da PNA foi maior em FMDH. A fenilefrina provocou nos dois grupos uma diminuição na SNA, na ABD e na PNA, e gerou um aumento na f PNA. A simpatoinibição foi maior em FMDH. Esses resultados sugerem que a DH materna durante desenvolvimento fetal provavelmente altera as conexões centrais na prole. No segundo momento avaliou-se os efeitos da ocitocina sobre a reatividade vascular e seu papel nas respostas induzidas pela hipernatremia. Sabe-se que alterações no volume e/ou na composição dos compartimentos extracelulares evocam várias respostas autonômicas, cardiovasculares e hormonais que atuam em conjunto para modular a excreção renal de água e sódio. Os principais ajustes vegetativos são: vasodilatação renal e secreção de ocitocina. A regulação da osmolaridade e do volume é fundamental para sobrevivência. Apesar do vasto conhecimento na área nenhum estudo avaliou a interação entre a atividade simpática renal e a secreção de ocitocina sobre as respostas renais e cardiovasculares induzidas pela sobrecarga de sódio. Ratos Wistar machos (280-350 g) foram anestesiados e instrumentalizados para implantação de cateteres na bexiga, na veia e na artéria femoral e também para medição da pressão arterial média (PAM) e fluxo sanguíneo renal (FSR). Em ratos anestesiados (n = 6), a infusão de OT (0,03 μg/kg, i.v.) induziu vasodilatação renal. Em experimentações ex vivo a OT causou relaxamento da artéria renal. O bloqueio dos receptores de OT (OTR) reduziu essas respostas à OT, indicando um efeito direto desse peptídeo em seu receptor nesta artéria. O bloqueio dos receptores de ocitocina e a desnervação renal reduziu a vasodilatação renal e natriurese induzida pela sobrecarga de sódio aguda e a combinação do antagonista de receptores de ocitocina e a desnervação renal aboliram completamente a vasodilatação renal e reduziram ainda mais a natriurese induzida pela hipernatremia. Estes resultados sugerem que a OT e os nervos renais estão envolvidos na vasodilatação renal e natriurese induzida por hipernatremia aguda. O amplo conhecimento na área e a compreensão dos mecanismos regulatórios ativados tanto durante a obesidade quanto durante hiperosmolaridade permite uma maior possibilidade de desenvolvimento de novas ferramentas terapêuticas para a prevenção e tratamento da hipertensão.
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Bertotti, Márcia Elaine Zeugner [UNESP]. "Alterações odontológicas em pacientes urêmicos em hemodiálise e suas possíveis correlações com neuropatias de nervos cranianos." Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/86335.

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Este trabalho analisa alterações odontológicas em pacientes com insuficiência renal crônica, em programa de hemodiálise. As alterações odontológicas estudadas foram índice de dentes cariados, perdidos e obturados (CPOD), presença ou ausência de doença periodontal, número de desdentados totais e parciais. Os pacientes foram submetidos a exame neurológico dos nervos cranianos. Foi determinado o pH da saliva antes e após diálise. Dentre os 44 pacientes estudados, foram encontrados 23 desdentados totais, 7 desdentados parciais e 14 dentados. Vários apresentaram cáries, sem diferenças estatisticamente significativas em relação ao grupo controle; 7 pacientes apresentaram doença periodontal. Alterações de nervos cranianos foram encontradas em 36 pacientes. Os nervos cranianos mais freqüentemente acometidos foram VIII - vestíbulo-coclear, II - óptico e V - trigêmio. Alterações trigeminais foram encontradas em 20 pacientes. É provável que as alterações trigeminais aferentes estejam relacionadas com as perdas dentárias, na insuficiência renal crônica.
This paper analyzes odontological alterations in hemodialysis patients with chronic renal failure. Odontological alterations were: index of decayed, lost, or filled teeth (DLFT); presence or absence of periodontal disease; and totally and partially toothless. Patients were submitted to neurological examination of the cranial nerves. Saliva pH was recorded before and after dialysis. Out of 44 patients, 23 were totally toothless, 7 partially toothless, and 14 dentate. Several had decay, but this was not statistically significant to controls; 7 had periodontal disease. Cranial nerve alterations were found in 36 patients. The most frequently compromised nerves were the VIII - vestibulocochlear, II - optic, and V - trigeminal. Trigeminal alterations were found in 20 patients. Probably afferent trigeminal alterations are related to tooth loss in chronic renal failure.
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7

Garcia, Domingo Monica. "Influencia de la diabetes experimental en respuertas serotonergicas a nivel cardiovascular y renal." Université Louis Pasteur (Strasbourg) (1971-2008), 2005. https://publication-theses.unistra.fr/public/theses_doctorat/2005/GARCIA_DOMINGO_Monica_2005.pdf.

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Le diabète sucré est une pathologie en progression constante dont la gravité tient à ses complications. Dans cette thèse, nous avons recherché si les réponses cardiovasculaires et rénales à la 5-HT sont altérées au cours d'un diabète sucré expérimental induit chez le rat (alloxan ou streptozotocine). Les effets de la 5-HT sur la neurotransmission sympathique (vasculaire) ou cholinergique (cardiaque), ainsi que sur l'hémodynamique rénale ont été analysés. Les résultats obtenus montrent que :1. Dans le diabète, la 5-HT inhibe la neurotransmission sympathique via des récepteurs 5-HT1A présynaptiques alors que cette inhibition met en jeu les récepteurs 5-HT1D chez le rat normoglycémique. Le monoxyde d'azote contribue à cet effet chez le rat diabétique contrairement aux dérivés de la cyclooxygenase chez le rat normal. 2. Dans le diabète, la neurotransmission cholinergique cardiaque est régulée via les récepteurs 5-HT1A/1B (potentialisation) et 5-HT1D (inhibition) pré- et postsynaptiques, alors que chez le rat normoglycémique, seuls les récepteurs présynaptiques 5-HT3 (potentialisation) et 5-HT2 (inhibition) sont impliqués. 3. Sur le rein isolé perfusé, la 5-HT induit essentiellement une vasoconstriction via l'activation des récepteurs 5-HT2A, qui est potentialisée dans le diabète. L'activation spécifique des récepteurs 5-HT1A, 5-HT1B et 5-HT2B produit cependant une vasodilatation, non modifiée dans le diabète. 4. Le diabète sucré ne modifie pas l'expression des récepteurs 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A et 5-HT2B (RT-PCR quantitative) dans les artérioles intrarénales et l'aorte. Ce travail apporte ainsi de nouvelles connaissances quant à la participation des divers récepteurs sérotonergiques dans la régulation des fonctions cardiovasculaires et rénales. Le diabète sucré expérimental modifie les mécanismes sérotonergiques cardiovasculaires et rénaux, en particulier en ce qui concerne les types de récepteurs impliqués, l'intensité des réponses et la participation du NO
Prevalence of diabetes mellitus is increasing throughout the world with high incidence of cardiovascular complications. In this thesis, we looked for the alterations in cardiovascular and renal responses to 5-HT elicited by induction of experimental diabetes mellitus in rats (alloxan or streptozotocin). The effects of 5-HT were analysed on sympathetic (vessels) or cholinergic (heart) neurotransmission, as well as on renal hemodynamic. Present results show that :1. Sympathetic neurotransmission is inhibited by 5-HT via 5-HT1A presynaptic receptors in diabetic rats, with a marked contribution of nitric oxide. In contrast, 5-HT1D receptors are responsible for the inhibition induced by 5-HT in normoglycemic rats and cyclooxygenase products are involved in this response. 2. Cholinergique neurotransmission in diabetic rats is potentiated via the activation of 5-HT1A/1B receptors and inhibited via 5-HT1D receptors, both pre- and postsynaptic. This regulation again differs from that found in normoglycemic rats, where potentiation and inhibition occurred via presynaptic 5-HT3 and 5-HT2 receptors, respectively. 3. On the isolated perfused kidney, 5-HT elicits vasoconstriction via the activation of 5-HT2A receptors, and this response is increased in diabetic rats. However, the specific activation of 5-HT1A, 5-HT1B and 5-HT2B receptors is also able to elicit renal vasodilatation which was unaffected by diabetes. 4. Diabetes mellitus did not change expression (mRNA, RT-PCR quantitative) of 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A et 5-HT2B receptors on intrarenal arterioles or aorta. This work therefore provides new data about the contribution of the different 5-HT receptors in the regulation of cardiovascular and renal functions. Moreover, diabetes mellitus modifies these serotonergic mechanisms, particularly in respect with subtypes of 5-HT receptors involved, the level of response and the contribution of NO
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Kannan, Arun, Raul Ivan Medina, Nagapradeep Nagajothi, and Saravanan Balamuthusamy. "Renal sympathetic nervous system and the effects of denervation on renal arteries." Baishedeng Publishing Group, 2014. http://hdl.handle.net/10150/621331.

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UA Open Access Publishing Fund
Resistant hypertension is associated with chronic activation of the sympathetic nervous system resulting in various comorbidities. The prevalence of resistant hypertension is often under estimated due to various reasons. Activation of sympathetic nervous system at the renal- as well as systemic- level contributes to the increased level of catecholamines and resulting increase in the blood pressure. This increased activity was demonstrated by increased muscle sympathetic nerve activity and renal and total body noradrenaline spillover. Apart from the hypertension, it is hypothesized to be associated with insulin resistance, congestive heart failure and obstructive sleep apnea. Renal denervation is a novel procedure where the sympathetic afferent and efferent activity is reduced by various techniques and has been used successfully to treat drug-resistant hypertension improvement of various metabolic derangements. Renal denervation has the unique advantage of offering the denervation at the renal level, thus mitigating the systemic side effects. Renal denervation can be done by various techniques including radiofrequency ablation, ultrasound guided ablation and chemical ablation. Various trials evaluated the role of renal denervation in the management of resistant hypertension and have found promising results. More studies are underway to evaluate the role of renal denervation in patients presenting with resistant hypertension in different scenarios. Appropriate patient selection might be the key in determining the effectiveness of the procedure.
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Bertotti, Márcia Elaine Zeugner. "Alterações odontológicas em pacientes urêmicos em hemodiálise e suas possíveis correlações com neuropatias de nervos cranianos /." Botucatu : [s.n.], 2006. http://hdl.handle.net/11449/86335.

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Orientador: Luiz Antônio de Lima Resende
Banca: Luiz Antônio de Lima Resende
Banca: Pasqual Barretti
Banca: Heloisa Almeida de Lima Castro
Resumo: Este trabalho analisa alterações odontológicas em pacientes com insuficiência renal crônica, em programa de hemodiálise. As alterações odontológicas estudadas foram índice de dentes cariados, perdidos e obturados (CPOD), presença ou ausência de doença periodontal, número de desdentados totais e parciais. Os pacientes foram submetidos a exame neurológico dos nervos cranianos. Foi determinado o pH da saliva antes e após diálise. Dentre os 44 pacientes estudados, foram encontrados 23 desdentados totais, 7 desdentados parciais e 14 dentados. Vários apresentaram cáries, sem diferenças estatisticamente significativas em relação ao grupo controle; 7 pacientes apresentaram doença periodontal. Alterações de nervos cranianos foram encontradas em 36 pacientes. Os nervos cranianos mais freqüentemente acometidos foram VIII - vestíbulo-coclear, II - óptico e V - trigêmio. Alterações trigeminais foram encontradas em 20 pacientes. É provável que as alterações trigeminais aferentes estejam relacionadas com as perdas dentárias, na insuficiência renal crônica.
Abstract: This paper analyzes odontological alterations in hemodialysis patients with chronic renal failure. Odontological alterations were: index of decayed, lost, or filled teeth (DLFT); presence or absence of periodontal disease; and totally and partially toothless. Patients were submitted to neurological examination of the cranial nerves. Saliva pH was recorded before and after dialysis. Out of 44 patients, 23 were totally toothless, 7 partially toothless, and 14 dentate. Several had decay, but this was not statistically significant to controls; 7 had periodontal disease. Cranial nerve alterations were found in 36 patients. The most frequently compromised nerves were the VIII - vestibulocochlear, II - optic, and V - trigeminal. Trigeminal alterations were found in 20 patients. Probably afferent trigeminal alterations are related to tooth loss in chronic renal failure.
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Bertoli, Patricia Ribeiro. "Efeito da estimulação elétrica nervosa transcutânea (TENS) no tratamento da dor e capacidade funcional do ombro de pacientes com doença renal crônica." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5163/tde-05032010-151851/.

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INTRODUÇÃO: A doença renal crônica (DRC) favorece o desenvolvimento de inúmeras complicações entre elas a amiloidose. Nos ombros os depósitos de amilóide desencadeiam reações inflamatórias e dor intensa o que compromete a qualidade de vida dos pacientes acometidos. As propostas terapêuticas para o tratamento dessa complicação são escassas. OBJETIVO: O objetivo do presente estudo foi avaliar o efeito da estimulação elétrica nervosa transcutânea (do inglês, TENS) no tratamento da dor e capacidade funcional do ombro e dos fatores relacionados à qualidade de vida em pacientes com DRC. MÉTODOS: Trinta pacientes foram avaliados 5 vezes num período de 6 semanas. Na 1ª semana, o aparelho foi programado para não transmitir a corrente elétrica (placebo) e nas 5 semanas subseqüentes, utilizamos corrente de baixa frequência (10Hz, 150 µs, 2xdia, 40 minutos). A dor (escala visual analógica), a funcionalidade do ombro (Escore de Constant e Escala da UCLA) e os fatores relacionados à qualidade de vida (SF-36) foram avaliados. RESULTADOS: Nossos resultados mostram que o tratamento com a TENS reduziu significativamente a dor (p<0,05), melhorou a funcionalidade do ombro (tanto pelo Escore de Constant quanto Escala da UCLA; p<0,05) já na primeira semana e estes benefícios permaneceram até o final do tratamento (5 semanas) quando comparado com o período placebo. Os domínios capacidade funcional, dor, vitalidade e aspectos sociais apresentam uma melhora após 5 semanas de tratamento quando comparado com o período placebo (p<0,05). Foi verificado ainda que este efeito foi observado mesmo com a redução da quantidade de medicação analgésica. CONCLUSÃO: Nossos resultados mostram que a TENS de baixa frequência reduz a dor e melhora a funcionalidade do ombro e os fatores relacionados à qualidade de vida de pacientes com DRC.
INTRODUCTION: Chronic kidney disease (CKD) favors the development of numerous complications such as amyloidosis. In the shoulders, amyloid deposits promote inflammatory reactions and severe pain, which compromises the quality of life of patients with this disease. There are few therapeutic options for the treatment of this complication. OBJECTIVE: The objective of the present study was to evaluate the effect of transcutaneous electrical nerve stimulation (TENS) in the treatment of pain and in shoulder functional capacity, as well as factors related to the quality of life in patients with CKD. METHODS: Thirty patients were evaluated 5 times over a period of 6 weeks. At week 1, the equipment was programmed to not transmit the electrical current (placebo) and in the 5 subsequent weeks we used low frequency current (10Hz, 150 µs, twice a day, 40 minutes). Pain (visual analog scale), shoulder functional capacity (Constant score and UCLA Shoulder Rating Scale) and factors related to the quality of life (SF-36) were evaluated. RESULTS: Our results show that the treatment with TENS significantly reduced pain (p<0.05), improved shoulder functional capacity (using both Constant score and UCLA Shoulder Rating Scale; p<0.05) at week 1 and these benefits remained until the end of the treatment (5 weeks) when compared with the placebo period. The domains of functional capacity, pain, vitality and social functioning present improvement after 5 weeks of treatment when compared with the placebo period (p<0.05). It was also found that this effect was observed even after the administration of analgesics was reduced. CONCLUSION: Our results show that low frequency TENS reduces pain and improves shoulder functional capacity and factors related to the quality of life of patients with CKD.
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Books on the topic "Renal nerves"

1

Shid-Moosavi, S. Mostafa. Effect of renal perfusion pressure and nerves on renal function, renin release and renin and angiotensinogen gene expression. Birmingham: University of Birmingham, 1998.

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Bolton, Charles Francis. Neurological complications of renal disease. Boston: Butterworths, 1990.

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Meisel, Abigail. Investigating eating disorders (anorexia, bulimia, and binge eating): Real facts for real lives. Berkeley Heights, NJ: Enslow Publishers, 2011.

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The life of a real girl. New York: St. Martin's Press, 1986.

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Garfield, Johanna. The life of a real girl: An autobiography of anorexia and madness. London: Sidgwick & Jackson, 1986.

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Dibona, Gerald F. Renal Nerves. S Karger AG, 1988.

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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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Gonzalez-Albarrán, Olga, and Luis M. Ruilope. The kidney and control of blood pressure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0210.

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The kidneys can be at the root of the development of arterial hypertension or they can participate in the maintenance of hypertension and its sequels. Renal alterations interfering with the regulation of sodium homeostasis or facilitating the generation of vasoconstrictors, particularly angiotensin II, are involved in the dysregulation of arterial blood pressure that underlies the development of arterial hypertension. The biology of angiotensin is described in detail.The kidneys are also the mediator of hypertension in such examples as renal ischaemia and hyperaldosteronism. The role of renal nerves, and renal depressor substances, are also described.Transplantation experiments in animals and observations in human transplantation, as well as some primary gene defects, show the importance of renal mechanisms in hypertension. Once kidneys have been damaged, they often contribute to an increase in arterial pressure. Salt sensitivity is probably a major part of the mechanism, but it is mediated by multiple pathways.
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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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Shaw, Pamela, and David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.

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Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.
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Book chapters on the topic "Renal nerves"

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Petersen, Jørgen S., Carmen Hinojosa-Laborde, Ulla C. Kopp, and Gerald F. DiBona. "Renal Nerves and Catecholamine Regulation of Renal Function." In International Yearbook of Nephrology 1993, 3–21. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-1948-7_1.

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Yoshimura, M., R. Takashina, H. Takahasi, and H. Ijichi. "Role of Renal Nerves and Dopamine on Prostaglandin E Release from the Kidney of Rats." In Vasodepressor Hormones in Hypertension: Prostaglandins and Kallikrein-Kinins, 93–100. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9299-5_10.

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Ito, T., H. Miura, T. Shiga, Mohamed O. Hashem, K. Kamiya, A. Yamada, Y. Tsuboko, et al. "Modeling of Signal Transmissions in Nerves in Vitro for the Development of a Renal Nerve Cooling Device for Hypertension Control." In IFMBE Proceedings, 448–51. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-02913-9_114.

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Tsioufis, Konstantinos, Panagiotis Iliakis, and Alexandros Kasiakogias. "Renal Nerve Ablation." In Updates in Hypertension and Cardiovascular Protection, 377–89. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-93320-7_24.

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Wholey, Mark H., Emily Stein, Michael Evans, and K. T. Venkateswara Rao. "Targeted Renal Nerve Deactivation by Neurotropic Agents." In Renal Denervation, 135–43. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-5223-1_16.

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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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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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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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Rakmanee, Sasipa, Supaporn Kulthinee, J. Michael Wyss, and Sanya Roysommuti. "Taurine Supplementation Reduces Renal Nerve Activity in Male Rats in which Renal Nerve Activity was Increased by a High Sugar Diet." In Advances in Experimental Medicine and Biology, 27–37. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1079-2_3.

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Loudyi, Aida, and Wolfram E. Samlowski. "Brain Metastasis in Renal Cell Carcinoma Patients." In Tumors of the Central Nervous system, Volume 3, 53–61. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1399-4_6.

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Conference papers on the topic "Renal nerves"

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Ye, Eunbi, Seung-Hyun Lee, Jinhwan Baik, Seon Young Ryu, Won Hoon Song, Eue-Keun Choi, Chang Wook Jeong, and Sung-Min Park. "Developing a Computational Model of Renal Nerves and Surgical System for Laparoscopic Renal Denervation." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513120.

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Celler, Stella, Golin, and Zanchetti. "Analysis Of The Time Course Of Renal Vascular And Excretory Responses To Electrical Stimulation Of The Renal Efferent Nerves." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.595861.

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Celler, Branko, Andrea Stella, Raffaello Golin, and Alberto Zanchetti. "Analysis of the time course of renal vascular and excretory responses to electrical stimulation of the renal efferent nerves." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761247.

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Jiman, Ahmad A., Kavaljit H. Chhabra, David C. Ratze, Alfor G. Lewis, Paul S. Cederna, Randy J. Seeley, Malcolm J. Low, and Tim M. Bruns. "Kilohertz Frequency Stimulation of Renal Nerves for Modulating Blood Glucose Concentration in Diabetic Rats." In 2019 9th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2019. http://dx.doi.org/10.1109/ner.2019.8717153.

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Pammi, SriLaxmi, Courtney Brown, Saurabh Datta, Goutham R. Kirikera, Mark J. Schulz, Payal Kaul, Peng He, Donglu Shi, F. James Boerio, and Mannur J. Sundaresan. "Building Artificial Nerves for Structures." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33475.

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Building artificial nerves for smart structures and for structural health monitoring is discussed. Structural Health Monitoring refers to using in-situ sensors to monitor the strains and strain waves and from these interpret the health of a structure in real-time. This will allow a structure to be operated at its maximum performance and efficiency while minimizing fatigue and other damage. To achieve this capability on a large structure, artificial nerves are used to mimic the biological nervous system. Two design concepts for nerve fibers are considered; piezoceramic active fibers and carbon nanotube conductive fibers. The piezoceramic fibers are self-powered and can sense acoustic emissions and dynamic strains due to damage. The carbon nanotube fibers change conductance when strained and can sense high strain due to damage. The processes being developed to fabricate the two types of nerves are discussed and some initial experimental results are presented.
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Iyengar, Satish G., Jayant Datta, and Laurel H. Carney. "A Fast Real-Time Auditory-Nerve Model." In 2007 IEEE International Conference on Acoustics, Speech, and Signal Processing. IEEE, 2007. http://dx.doi.org/10.1109/icassp.2007.366167.

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Neliubina, Anna Sergeevna. "Orthorexia Nervosa As A Cultural Phenomenon." In Psychology of Personality: Real and Virtual Context. European Publisher, 2020. http://dx.doi.org/10.15405/epsbs.2020.11.02.66.

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Hannawi, S., and I. AlSalmi. "SAT0131 Median nerve thickness related to renal impairment in rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1660.

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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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10

Lubba, Carl, Elie Mitrani, Jim Hokanson, Warren M. Grill, and Simon R. Schultz. "Real-time decoding of bladder pressure from pelvic nerve activity." In 2017 8th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2017. http://dx.doi.org/10.1109/ner.2017.8008427.

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