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Journal articles on the topic 'Rats – Nervous system'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Levine, Seymour, Arthur Saltzman, and Alden Loud. "Inflammatory Siderosis of the Nervous System in Rats." Journal of Neuropathology and Experimental Neurology 48, no. 4 (July 1989): 391–98. http://dx.doi.org/10.1097/00005072-198907000-00001.

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2

Kuzmenko, N. V., M. G. Pliss, N. S. Rubanova, and V. A. Tsyrlin. "SPECULATIONS ОN BLOOD PRESSURE INCREASE MECHANISMS IN RENAL ARTERY CLIPPED WISTAR RATS." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 3 (June 28, 2013): 221–26. http://dx.doi.org/10.18705/1607-419x-2013-19-3-221-226.

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Objective.To examine the mechanisms underlying the activation of the sympathetic nervous system and blood pressure elevation in vasorenal hypertension in the male Wistar rats weighing 250–300 g.Design and methods.We observed the development of renovascular hypertension, beat-to-beat interval and heart rate variability in animals with intact renal nerves and denervated ischemic kidney for 8 weeks after renal artery clamping. Eight weeks later after renal artery clamping in hypertensive rats with denervated ischemic kidney, both-sided renal denervation was performed, and blood pressure was monitored for 6 weeks.Results.Although the ischemic kidney denervation reduces the activity of the sympathetic nervous system, it does not prevent renovascular hypertension development. However, both-sided renal denervation leads to the normalization of blood pressure in the rats with stable renovascular hypertension.Conclusion.We suggest that increased afferent fl ow from structural formations of the ischemic kidney plays an important role for the increased sympathetic nervous system activity.

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3

Arieli, R., and G. Hershko. "Prediction of central nervous system oxygen toxicity in rats." Journal of Applied Physiology 77, no. 4 (October 1, 1994): 1903–6. http://dx.doi.org/10.1152/jappl.1994.77.4.1903.

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Cumulative O2 toxicity (K) can be calculated using the expression K = t2 x PO2c, where t is exposure time and the power c is to be determined; the phenomenon is liable to occur when K reaches Kc, the threshold value of K at which a symptom is manifested. Six rats were each exposed six times to 6 ATA O2 at 2-day intervals until the first electrical discharge (FED) was noted in an electroencephalogram. There was no difference in latency to FED in the series of six exposures. Thirteen rats were exposed to O2 until FED was noted in an electroencephalogram. They were exposed to four constant PO2's of 5, 6, 7, and 8 ATA and to two combined profiles of 1) 5 min at 7 ATA followed by 5 ATA and 2) 15 min at 5 ATA followed by 7 ATA. The solution of the equation for each rat was used to predict its latency to FED on the combined profile. The correlation of predicted to measured latency was significant (P < 0.0001), and the slope was not different from 1. Solving for these parameters using the combination of all the data, we obtained Kc = 5.71 x 10(6) and c = 5.39, which correctly predicted the mean latency but failed to predict individual latency. It is preferable to use each rat as its own control. The significance of the correlation supports the validity of the power equation for calculating K.

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4

Giuliano, Francois, Jacques Bernabe, Alain Jardin, and Jean Paul Rousseau. "Antierectile Role of the Sympathetic Nervous System in Rats." Journal of Urology 150, no. 2 Part 1 (August 1993): 519–24. http://dx.doi.org/10.1016/s0022-5347(17)35539-8.

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5

Hamidi, Mehrdad. "Central nervous system distribution kinetics of indinavir in rats." Journal of Pharmacy and Pharmacology 59, no. 8 (August 2007): 1077–85. http://dx.doi.org/10.1211/jpp.59.8.0004.

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6

Parham, D., A. Tereba, P. J. Talbot, D. P. Jackson, and V. L. Morris. "Analysis of JHM Central Nervous System Infections in Rats." Archives of Neurology 43, no. 7 (July 1, 1986): 702–8. http://dx.doi.org/10.1001/archneur.1986.00520070058019.

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7

Bamshad, Maryam, Victor T. Aoki, M. Gregory Adkison, Wade S. Warren, and Timothy J. Bartness. "Central nervous system origins of the sympathetic nervous system outflow to white adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 1 (July 1, 1998): R291—R299. http://dx.doi.org/10.1152/ajpregu.1998.275.1.r291.

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White adipose tissue (WAT) is innervated by postganglionic sympathetic nervous system (SNS) neurons, suggesting that lipid mobilization could be regulated by the SNS [T. G. Youngstrom and T. J. Bartness. Am. J. Physiol. 268 ( Regulatory Integrative Comp. Physiol. 37): R744–R751, 1995]. A viral transsynaptic retrograde tract tracer, the pseudorabies virus (PRV), was used to identify the origins of the SNS outflow from the brain to WAT neuroanatomically. PRV was injected into epididymal or inguinal WAT (EWAT and IWAT, respectively) of Siberian hamsters and IWAT of rats. PRV-infected neurons were visualized by immunocytochemistry and found in the spinal cord, brain stem (medulla, nucleus of the solitary tract, caudal raphe nucleus, C1 and A5 regions), midbrain (central gray), and several areas within the forebrain. The general pattern of infection of WAT in both species was more similar than different and resembled that seen after PRV injections into the adrenal medulla in rats (A. M. Strack, W. B. Sawyer, J. H. Hughes, K. B. Platt, and A. D. Loewy. Brain Res. 491: 156–162, 1989). EWAT versus IWAT injected hamsters had relatively less labeling in the suprachiasmatic, dorsomedial, and arcuate nuclei. Overall, it appeared that the SNS innervation of WAT originates from the general SNS outflow of the central nervous system and therefore may play a significant role in lipid mobilization.

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8

Song, Jian-gang, Hong-hai Li, Yun-fei Cao, Xin Lv, Ping Zhang, Ye-sheng Li, Yong-jun Zheng, et al. "Electroacupuncture Improves Survival in Rats with Lethal Endotoxemia via the Autonomic Nervous System." Anesthesiology 116, no. 2 (February 1, 2012): 406–14. http://dx.doi.org/10.1097/aln.0b013e3182426ebd.

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Background Recent advances have indicated a complex interplay between the autonomic nervous system and the innate immune system. Targeting neural networks for the treatment of sepsis is being developed as a therapeutic strategy. Because electroacupuncture at select acupoints can modulate activities of the autonomic nervous system, we tested the hypothesis that electroacupuncture at specific acupoints could modulate systemic inflammatory responses and improve survival via its impact on the autonomic nervous system in a rat model of sepsis. Methods Sprague-Dawley male rats received electroacupuncture for 45 min before and at 1, 2, or 4 h after a lethal dose of intraperitoneal lipopolysaccharide injection (6 mg/kg). Outcomes included survival and systemic cytokine responses. Also, the possible roles of neural circuitry, including the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, were evaluated. Results Electroacupuncture pretreatment at the Hegu acupoints significantly attenuate systemic inflammatory responses and improve survival rate from 20% to 80% in rats with lethal endotoxemia. Such a site-specific effect requires the activation of muscarinic receptors in the central nervous system, but not increasing central sympathetic tone. In the periphery synergistic, rather than independent, action of the sympathetic and parasympathetic systems is also necessary. Conclusions Electroacupuncture pretreatment has a dramatic survival-enhancing effect in rats with lethal endotoxemia, which involves the activation of efferent neural circuits of the autonomic nervous system (e.g., cholinergic antiinflammatory pathway). This approach could be developed as a prophylactic treatment for sepsis or perioperative conditions related to excessive inflammation.

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9

Huang, Zhihui, Yiqiao Wang, Meiling Chen, and Prof Lei Sha. "ODP228 Obesity Induced a Down-Regulation of nNOS in Intrapancreatic Nervous System." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A327—A328. http://dx.doi.org/10.1210/jendso/bvac150.679.

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Abstract Objective Obesity has become a serious global public health problem. Obesity is frequently preceding and the most important risk factor of type 2 diabetes. Pancreas regulates glucose metabolism and glucose homeostasis, and abnormality of pancreas play an important role in insulin resistance and diabetes. Intrapancreatic nerve innervation modulates insulin release and is tightly linked to the onset and development of diabetes. However, it is not known whether the activity of the intrapancreatic nervous system has been altered before the onset of diabetes. In this study, we examined the intrapancreatic nervous system in rats with obesity looking for the changes induced by obesity. Methods Obese Sprague-Dawley rats were developed with feeding high fat diet for 10 weeks. Using Immunofluorescence method, choline acetyl transferase (ChAT) and nNOS positive neurons in intrapancreatic ganglia were counted. ChAT and nNOS expression in pancreas were also measured with western blot method. Results (1) There was no significant difference in fasting blood glucose between obese rats and normal rats, but oral glucose tolerance test showed that the oral glucose tolerance was impaired in obese rats. (2) In rats fed with normal diet, 80.2%±1.5 neurons in intrapancreatic ganglia were ChAT positive, and in the obese rats, 79.3%±1.8 neurons were ChAT positive. There was no significant difference between the two groups (p>0. 05, n=5). In intrapancreatic ganglia of obese rats, 40%±1.4 neurons were nNOS positive, which was significantly lower than that (60.5%±1.2) of rats fed with normal diet (p<0. 01,n=5). (3) In pancreatic tissue, the relative expression level of ChAT protein was 1. 02±0. 03 in rats fed with normal diet and 0.98±0. 05 in obese rats (p>0. 05, n=5). The relative expression level of nNOS protein was 1.70±0. 08 in normal rats and 1.10±0. 05 in obese rats (p>0. 01, n=5). Conclusion The cholinergic nerves in intrapancreatic nervous system was not altered in obese rats, however, nNOS nerves was down-regulated in obese rats. The down-regulation of nNOS would induce a hyperactivity in intrapancreatic nervous system and this would cause an enhancement of insulin release, which has been observed in obese individuals. Presentation: No date and time listed

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10

Fisher, L. A., C. R. Cave, and M. R. Brown. "Central nervous system cardiovascular effects of bombesin in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (April 1, 1985): H425—H431. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h425.

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The effects of intracerebroventricular administration of bombesin on mean arterial pressure and heart rate were studied in conscious, freely moving rats. Injection of bombesin produced dose-dependent elevations of mean arterial pressure and reductions of heart rate. These effects were not caused by leakage of bombesin into the peripheral circulation. Adrenalectomy abolished the pressor action of bombesin but did not alter bombesin-induced bradycardia. Systemic phentolamine pretreatment prevented bombesin-induced changes of mean arterial pressure, whereas rats treated intravenously with captopril or a vasopressin antagonist still exhibited pressor responses to bombesin administration. Bombesin-induced bradycardia was partially antagonized by intravenous atropine methyl nitrate administration, whereas systemic injections of propranolol did not modify this response. It is concluded that bombesin acts within the central nervous system to elevate mean arterial pressure through an adrenal-dependent mechanism involving alpha-adrenergic receptors and to reduce heart rate through an adrenal-independent mechanism involving, at least in part, cardiac parasympathetic nervous activation.

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11

Mizuno, Masaki, Toru Kawada, Atsunori Kamiya, Tadayoshi Miyamoto, Shuji Shimizu, Toshiaki Shishido, Scott A. Smith, and Masaru Sugimachi. "Dynamic characteristics of heart rate control by the autonomic nervous system in rats." Experimental Physiology 95, no. 9 (June 18, 2010): 919–25. http://dx.doi.org/10.1113/expphysiol.2010.053090.

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12

Anini, Youn??s, Claire Jarrousse, Jacques Chariot, Claire Nagain, Noboru Yanaihara, Kazuyuki Sasaki, Nicole Bernad, Dung Le Nguyen, Dominique Bataille, and Claude Roz?? "Oxyntomodulin Inhibits Pancreatic Secretion Through the Nervous System in Rats." Pancreas 20, no. 4 (May 2000): 348–60. http://dx.doi.org/10.1097/00006676-200005000-00003.

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13

Szenohradszky, János, Anthony J. Trevor, Philip Bickler, James E. Caldwell, Manohar L. Sharma, Ira J. Rampil, and Ronald D. Miller. "Central Nervous System Effects of Intrathecal Muscle Relaxants in Rats." Anesthesia & Analgesia 76, no. 6 (June 1993): 1304–9. http://dx.doi.org/10.1213/00000539-199306000-00020.

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14

Szenohradszky, János, Anthony J. Trevor, Philip Bickler, James E. Caldwell, Manohar L. Sharma, Ira J. Rampil, and Ronald D. Miller. "Central Nervous System Effects of Intrathecal Muscle Relaxants in Rats." Anesthesia & Analgesia 76, no. 6 (June 1993): 1304–9. http://dx.doi.org/10.1213/00000539-199376060-00020.

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15

Albertini, R., L. Vargas, P. Oliveri, F. Pardo, and M. C. Paredes. "SYMPATHETIC NERVOUS SYSTEM MEDIATES URINARY KALLIKREIN EXCRETION IN CONSCIOUS RATS." Clinical and Experimental Pharmacology and Physiology 14, no. 4 (April 1987): 291–301. http://dx.doi.org/10.1111/j.1440-1681.1987.tb00974.x.

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16

Lee, Tai-Hee, Kunihiro Doi, Muneyoshi Yoshida, and Shigeaki Baba. "Morphological study of nervous system in vacor-induced diabetic rats." Diabetes Research and Clinical Practice 4, no. 4 (April 1988): 275–79. http://dx.doi.org/10.1016/s0168-8227(88)80029-9.

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17

Rykaczewska-Czerwińska, Monika, Piotr Oleś, Michał Oleś, Mariola Kuczer, Danuta Konopińska, and Andrzej Plech. "Effect of alloferon 1 on central nervous system in rats." Pharmacological Reports 62 (September 2010): 62–63. http://dx.doi.org/10.1016/s1734-1140(10)71168-3.

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18

Hosoda, Hiroshi, and Kenji Kangawa. "The autonomic nervous system regulates gastric ghrelin secretion in rats." Regulatory Peptides 146, no. 1-3 (February 2008): 12–18. http://dx.doi.org/10.1016/j.regpep.2007.07.005.

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19

Crabb, David W., Sandra L. Morzorati, Jay R. Simon, and Ting-Kai Li. "Central nervous system control of alcohol dehydrogenase activity in rats." Life Sciences 37, no. 25 (December 1985): 2381–87. http://dx.doi.org/10.1016/0024-3205(85)90105-5.

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20

Glišić, Radmila, Maja Čakić-Milošević, and Mirela Ukropina. "Immunohistochemical study of enteric nervous system in dexamethasone-treated rats." Kragujevac Journal of Science, no. 40 (2018): 163–73. http://dx.doi.org/10.5937/kgjsci1840163g.

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21

Miyaguchi, Hideki, Ineko Kato, Tadashi Sano, Hisanori Sobajima, Shinji Fujimoto, and Hajime Togari. "Dopamine penetrates to the central nervous system in developing rats." Pediatrics International 41, no. 4 (August 1999): 363–68. http://dx.doi.org/10.1046/j.1442-200x.1999.01084.x.

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22

Lee, Jong S., Don Morrow, Michael C. Andresen, and Kyoung S. K. Chang. "Isoflurane Depresses Baroreflex Control of Heart Rate in Decerebrate Rats." Anesthesiology 96, no. 5 (May 1, 2002): 1214–22. http://dx.doi.org/10.1097/00000542-200205000-00026.

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Background Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.

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23

Williams, J. L., and M. D. Johnson. "Sympathetic nervous system and blood pressure maintenance in the Brattleboro DI rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 5 (May 1, 1986): R770—R775. http://dx.doi.org/10.1152/ajpregu.1986.250.5.r770.

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Experiments were performed to determine the functional role of the sympathetic nervous system (SNS) in blood pressure regulation in Brattleboro diabetes insipidus (DI) rats and to determine the effects of synthetic arginine vasopressin (AVP) on sympathetic function in DI rats. The experiments were conducted in male age-matched Long-Evans (LE) and DI rats in the conscious unstressed state. Mean arterial pressure (MAP) and heart rate were similar in conscious unstressed LE and DI rats, but basal plasma concentrations of norepinephrine (NE) and epinephrine (E) were elevated in DI rats compared with LE rats. An intra-arterial bolus injection of hexamethonium (30 mg/kg) resulted in greater reductions of MAP in DI rats (-62 +/- 5 mmHg) than in LE rats (-42 +/- 7 mmHg; P less than 0.05). Administration of AVP to DI rats by osmotic minipump reduced plasma NE concentration in DI rats to a level not different from that in LE rats, but E concentration remained elevated. AVP administration to DI rats also reduced the hexamethonium-induced fall in MAP in these animals (-47 +/- 7 mmHg) to a level not different from that in LE rats. We conclude that the SNS plays a greater role in blood pressure maintenance in conscious DI rats than in LE rats and that AVP administration can normalize plasma NE concentration and the contribution of the SNS to blood pressure maintenance in these animals.

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24

Overton, J. M., G. Davis-Gorman, and L. A. Fisher. "Central nervous system cardiovascular actions of CRF in sinoaortic-denervated rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 3 (March 1, 1990): R596—R601. http://dx.doi.org/10.1152/ajpregu.1990.258.3.r596.

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Studies were performed in unrestrained conscious Sprague-Dawley rats to examine the central nervous system (CNS) mechanism by which corticotropin-releasing factor (CRF) produces simultaneous elevations of arterial pressure and heart rate. To test the hypothesis that CRF inhibits ongoing impulse transmission through and/or transmitter release from the CNS terminations of baroreceptor afferents, the cardiovascular effects of intracerebroventricular administration of CRF were compared in rats subjected to prior sham surgery (Sham) or sinoaortic denervation (SAD). Resting levels of arterial pressure and heart rate were elevated after SAD. In addition, SAD resulted in greater chronotropic sympathetic tone and reduced chronotropic parasympathetic tone as assessed by intravenous injections of atropine methyl nitrate and DL-propranolol. Intracerebroventricular administration of CRF in both surgical groups elicited significant increases in arterial pressure and heart rate, although a tendency for reduced tachycardic responses after SAD was apparent. Pretreatment with atropine or propranolol revealed that both the parasympathetic and sympathetic nervous systems contribute to CRF-induced heart rate responses in both surgical groups. These results suggest that ongoing baroreceptor afferent transmission is not requisite for the expression of CRF-induced cardiovascular changes. Thus it is unlikely that CRF elevates arterial pressure and heart rate through an exclusive action at the CNS terminations of baroreceptor sensory fibers.

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25

Cerutti, C., M. P. Gustin, C. Z. Paultre, M. Lo, C. Julien, M. Vincent, and J. Sassard. "Autonomic nervous system and cardiovascular variability in rats: a spectral analysis approach." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1292—H1299. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1292.

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Mechanisms underlying systolic (SBP) and diastolic (DBP) blood pressure and heart rate (HR) beat-to-beat variability were investigated using spectral analysis in conscious genetically normotensive (LN) and hypertensive (LH) adult rats from the Lyon strains. In LN rats, basal SBP, DBP, and HR spectra exhibited peaks in low (LF: 0.38-0.45 Hz) and high (HF: 1.04-1.13 Hz) frequencies. The LF peak of SBP, and even more of DBP, could be attributed to the influence of the sympathetic nervous system as it disappeared after destruction of the sympathetic nerves or a combined alpha- and beta-adrenoceptor blockade, whereas it was higher after blockade of the parasympathetic system. The HF peak of HR, linked to the respiratory rate, was abolished by the parasympathetic system blockade, whereas those of SBP and DBP were enhanced. In LH rats, which exhibit a lower sympathetic activity, the LF peaks of SBP and DBP were less distinct compared with LN controls. We conclude that the LF peak of DBP and the HF peak of HR are likely to represent useful estimates of the sympathetic vascular control and of the parasympathetic cardiac control, respectively.

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26

Glac, W., P. Badtke, A. Dzialoszewski, K. Krajewska, K. Ptaszek, and G. Kloss. "Sympathetic nervous system mediates amphetamine-induced effects on the immune system in rats." European Neuropsychopharmacology 26 (October 2016): S212—S213. http://dx.doi.org/10.1016/s0924-977x(16)31062-8.

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27

MADDEN, KELLEY S., SUZANNE Y. FELTEN, DAVID L. FELTEN, and DENISE L. BELLINGER. "Sympathetic Nervous System-Immune System Interactions in Young and Old Fischer 344 Rats." Annals of the New York Academy of Sciences 771, no. 1 Stress (December 1995): 523–34. http://dx.doi.org/10.1111/j.1749-6632.1995.tb44707.x.

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28

Bruinstroop, Eveline, Susanne E. la Fleur, Mariette T. Ackermans, Ewout Foppen, Joke Wortel, Sander Kooijman, Jimmy F. P. Berbée, Patrick C. N. Rensen, Eric Fliers, and Andries Kalsbeek. "The autonomic nervous system regulates postprandial hepatic lipid metabolism." American Journal of Physiology-Endocrinology and Metabolism 304, no. 10 (May 15, 2013): E1089—E1096. http://dx.doi.org/10.1152/ajpendo.00614.2012.

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The liver is a key organ in controlling glucose and lipid metabolism during feeding and fasting. In addition to hormones and nutrients, inputs from the autonomic nervous system are also involved in fine-tuning hepatic metabolic regulation. Previously, we have shown in rats that during fasting an intact sympathetic innervation of the liver is essential to maintain the secretion of triglycerides by the liver. In the current study, we hypothesized that in the postprandial condition the parasympathetic input to the liver inhibits hepatic VLDL-TG secretion. To test our hypothesis, we determined the effect of selective surgical hepatic denervations on triglyceride metabolism after a meal in male Wistar rats. We report that postprandial plasma triglyceride concentrations were significantly elevated in parasympathetically denervated rats compared with control rats ( P = 0.008), and VLDL-TG production tended to be increased ( P = 0.066). Sympathetically denervated rats also showed a small rise in postprandial triglyceride concentrations ( P = 0.045). On the other hand, in rats fed on a six-meals-a-day schedule for several weeks, a parasympathetic denervation resulted in >70% higher plasma triglycerides during the day ( P = 0.001), whereas a sympathetic denervation had no effect. Our results show that abolishing the parasympathetic input to the liver results in increased plasma triglyceride levels during postprandial conditions.

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29

Held, Heather E., Raffaele Pilla, Geoffrey E. Ciarlone, Carol S. Landon, and Jay B. Dean. "Female rats are more susceptible to central nervous system oxygen toxicity than male rats." Physiological Reports 2, no. 4 (April 2014): e00282. http://dx.doi.org/10.14814/phy2.282.

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30

Carlson, Scott H., and J. Michael Wyss. "Hepatic denervation does not affect plasma vasopressin response to intragastric hypertonic saline in conscious rats." American Journal of Physiology-Endocrinology and Metabolism 277, no. 1 (July 1, 1999): E161—E167. http://dx.doi.org/10.1152/ajpendo.1999.277.1.e161.

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Peripheral osmoreceptors monitor dietary NaCl and modify central nervous system and renal sympathetic nervous system activity accordingly. Experimental evidence suggests that these responses are dependent on the hepatic nerves. Peripheral osmoreceptors also modify arginine vasopressin (AVP) secretion. However, although hepatic denervation reportedly blunts activation of both supraoptic and paraventricular hypothalamic neurons after intraportal NaCl infusion, the role of the hepatic nerves in the AVP release has not been directly examined. The present study tests the hypothesis that the hepatic nerves modify AVP release in response to intragastric NaCl infusion. Wistar-Kyoto rats (WKY) received either hepatic denervation or a sham operation. Intragastric NaCl infusion significantly elevated plasma AVP in both sham-operated WKY and hepatic-denervated WKY, and the responses were not different between these groups. Second, previous studies suggest that both AVP secretion and baroreflexes are blunted in spontaneously hypertensive rats (SHR), deficits that contribute to the observed hypertension in SHR. We hypothesized that SHR also have a blunted peripheral osmoreceptor reflex and that this contributes to NaCl-sensitive hypertension. In contrast to our prediction, in SHR intragastric NaCl infusion induced an increase in plasma AVP that was similar to that in the WKY groups. Thus, although hepatic osmoreceptors are important for chronic regulation of arterial pressure, renal sympathetic nervous system activity, and the activity of hypothalamic neurons, they do not appear to influence plasma AVP concentration in response to intragastric NaCl.

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31

Wyss, J. Michael, Suzanne Oparil, and Wanida Sripairojthikoon. "Neuronal control of the kidney: Contribution to hypertension." Canadian Journal of Physiology and Pharmacology 70, no. 5 (May 1, 1992): 759–70. http://dx.doi.org/10.1139/y92-100.

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The renal nerves contribute to hypertension in experimental models of the disease, and appear to play a role in human hypertension. Several lines of evidence indicate that both in spontaneously hypertensive rats and in deoxycorticosterone acetate–NaCl rats, the full development of hypertension is dependent on renal efferent nerves and their induction of excess sodium retention. Renal sensory (afferent nerve) feedback to the central nervous system does not contribute to either of these forms of hypertension. In contrast, renovascular hypertension in rats and aortic coarctation hypertension in dogs are mediated, at least in part, by overactivity of renal afferent nerves and a resultant increase in systemic sympathetic nervous system activity. These forms of hypertension are not associated with sodium retention, and selective sensory denervation of renal afferent nerves by dorsal rhizotomy and total renal denervation result in similar reductions in hypertension. Surprisingly, the renal nerves do not contribute to dietary NaCl exacerbated hypertension in the spontaneously hypertensive rat, dietary NaCl-induced hypertension in the Dahl NaCl-sensitive rat, or the chronic hypertensive and nephrotoxic effects of cyclosporine A therapy in the rat, despite the finding that in all three forms of hypertension, overactivity of the sympathetic nervous system is prominent. Clinical studies indicate that the renal afferent and efferent nerves contribute to hypertension of different etiologies. Together these data point to the complex role that the renal nerves likely play in human essential hypertension.Key words: kidney, cyclosporine, spontaneously hypertensive rat, renal deafferentation, renal denervation.

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32

Levin, E. R., M. A. Weber, and S. Mills. "Atrial natriuretic factor-induced vasodepression occurs through central nervous system." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (September 1, 1988): H616—H622. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h616.

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To characterize the blood pressure and heart rate effects of atrial natriuretic peptide (ANP) in the brain, we administered 20 micrograms/kg of atriopeptin III in 5 microliters of 0.9 normal saline into the fourth ventricle of awake, freely moving, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. ANP produced a 13 +/- 1 mmHg decrease in mean arterial blood pressure (MAP) in the SHR (P less than 0.001 vs. base line or saline control, n = 10) and a 9 +/- 2 mmHg decrease in the WKY (P less than 0.02). Heart rate did not change significantly in response to ANP. To determine whether an interaction with the adrenergic nervous system played a role in the effects of ANP, we administered 100 ng yohimbine HCL, an alpha 2-antagonist, by intracerebroventricular injection, 45 min before ANP and completely prevented the ANP-induced decrease in MAP. In contrast, 100 ng intracerebroventricular prazosin, an alpha 1-adrenergic antagonist, had no significant influence on the MAP effect induced by ANP. A third group of SHR was pretreated with intracerebroventricular 6-OH dopamine to deplete central catecholamines or with saline. The rats pretreated with 6-OH dopamine (n = 6) had no significant response to ANP, which was administered 9 days later. This was significantly different from the saline-pretreated control group (n = 6), which responded with a 19 +/- 3 mmHg decrease in MAP (P less than 0.025). These studies indicate that the administration of ANP into the fourth ventricle of the brain decreases the MAP of rats through an interaction with the central alpha 2-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

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33

Silva, Glasiella Gonzalez Perez da. "Neuroprotective action ofGinkgo bilobaon the enteric nervous system of diabetic rats." World Journal of Gastroenterology 17, no. 7 (2011): 898. http://dx.doi.org/10.3748/wjg.v17.i7.898.

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34

Stauss, H. M., P. B. Persson, A. K. Johnson, and K. C. Kregel. "Frequency-response characteristics of autonomic nervous system function in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H786—H795. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h786.

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To characterize the efferent pathway from the hypothalamic paraventricular nucleus (PVN) to peripheral autonomic neurons and finally to selected effector organs, we stimulated the PVN in 10 conscious rats at frequencies ranging from 0.05 to 2.0 Hz. Simultaneously, blood pressure, heart rate, splanchnic sympathetic nerve activity, and mesenteric artery blood flow were measured. The sinus node of the heart responded to PVN stimulation via the parasympathetic pathway (during beta 1-adrenergic blockade) up to a stimulation frequency of 2.0 Hz, whereas the sympathetically mediated response (during muscarinic blockade) was limited to stimulation frequencies < 0.5 Hz. The splanchnic nerve responded to PVN stimulation with synchronous discharges up to stimulation frequencies of 2.0 Hz, whereas the oscillatory component of the vasoconstrictor response of the mesenteric artery was negligible beyond stimulation frequencies of 1.0 Hz. We conclude that sympathetic transmission to the heart is at least four times slower than parasympathetic transmission. In addition, the time-limiting step in sympathetic transmission from the hypothalamus to vascular smooth muscle contraction and pacemaker activity of the sinus node may be located at the site of synaptic transmission to the adrenergic receptors.

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35

YATOMI, A., A. IGUCHI, S. YANAGISAWA, H. MATSUNAGA, I. NIKI, and N. SAKAMOTO. "Prostaglandins Affect the Central Nervous System to Produce Hyperglycemia in Rats*." Endocrinology 121, no. 1 (July 1987): 36–41. http://dx.doi.org/10.1210/endo-121-1-36.

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36

Cano, Georgina, J. Patrick Card, Linda Rinaman, and Alan F. Sved. "Connections of Barrington’s nucleus to the sympathetic nervous system in rats." Journal of the Autonomic Nervous System 79, no. 2-3 (March 2000): 117–28. http://dx.doi.org/10.1016/s0165-1838(99)00101-0.

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37

Naseem, Syed M. "Toxicokinetics of [3H]saxitoxinol in peripheraland central nervous system of rats." Toxicology and Applied Pharmacology 141, no. 1 (November 1996): 49–58. http://dx.doi.org/10.1016/s0041-008x(96)80008-1.

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38

Inagaki, N., A. Yamatodani, T. Watanabe, M. Tohyama, K. Sinoda, and H. Wada. "Distribution of histaminergic terminals in the central nervous system of rats." Japanese Journal of Pharmacology 43 (1987): 262. http://dx.doi.org/10.1016/s0021-5198(19)58590-0.

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39

Ates, Ozkan, Suleyman R. Cayli, Neslihan Yucel, Eyup Altinoz, Ayhan Kocak, M. Akif Durak, Yusuf Turkoz, and Saim Yologlu. "Central nervous system protection by resveratrol in streptozotocin-induced diabetic rats." Journal of Clinical Neuroscience 14, no. 3 (March 2007): 256–60. http://dx.doi.org/10.1016/j.jocn.2005.12.010.

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40

Asakawa, Akihiro, Akira Niijima, Naoki Fujitsuka, Tomohisa Hattori, Marie Sameshima, Haruka Amitani, and Akio Inui. "T1752 Gastric Ghrelin Signaling and Autonomic Nervous System Activity in Rats." Gastroenterology 138, no. 5 (May 2010): S—571. http://dx.doi.org/10.1016/s0016-5085(10)62630-3.

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41

Bourjeili, Nabil, Monte Turner, Jerry Stinner, and Daniel Ely. "Sympathetic nervous system influences salt appetite in four strains of rats." Physiology & Behavior 58, no. 3 (September 1995): 437–43. http://dx.doi.org/10.1016/0031-9384(95)00077-v.

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42

Karavelioglu, Ergun, Yucel Gonul, Hasan Aksit, Mehmet Gazi Boyaci, Mustafa Karademir, Nejdet Simsek, Mustafa Guven, Tugay Atalay, and Usame Rakip. "Cabazitaxel causes a dose-dependent central nervous system toxicity in rats." Journal of the Neurological Sciences 360 (January 2016): 66–71. http://dx.doi.org/10.1016/j.jns.2015.11.033.

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43

Zakaria, Mohamed Naguib, Hany M. El-Bassossy, and Waleed Barakat. "Targeting AGEs Signaling Ameliorates Central Nervous System Diabetic Complications in Rats." Advances in Pharmacological Sciences 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/346259.

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Diabetes is a chronic endocrine disorder associated with several complications as hypertension, advanced brain aging, and cognitive decline. Accumulation of advanced glycation end products (AGEs) is an important mechanism that mediates diabetic complications. Upon binding to their receptor (RAGE), AGEs mediate oxidative stress and/or cause cross-linking with proteins in blood vessels and brain tissues. The current investigation was designed to investigate the effect of agents that decrease AGEs signaling, perindopril which increases soluble RAGE (sRAGE) and alagebrium which cleaves AGEs cross-links, compared to the standard antidiabetic drug, gliclazide, on the vascular andcentral nervous system(CNS) complications in STZ-induced (50 mg/kg, IP) diabetes in rats. Perindopril ameliorated the elevation in blood pressure seen in diabetic animals. In addition, both perindopril and alagebrium significantly inhibited memory decline (performance in the Y-maze), neuronal degeneration (Fluoro-Jade staining), AGEs accumulation in serum and brain, and brain oxidative stress (level of reduced glutathione and activities of catalase and malondialdehyde). These results suggest that blockade of AGEs signaling after diabetes induction in rats is effective in reducing diabetic CNS complications.

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44

Křeček, J., S. Doležel, H. Dlouhá, and J. Zicha. "Sympathetic Nervous System and Age-Dependent Salt Hypertension in Brattleboro Rats." Clinical and Experimental Hypertension. Part A: Theory and Practice 9, sup1 (January 1987): 2075–93. http://dx.doi.org/10.3109/10641968709159076.

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45

Bennett, T. "Sympathetic nervous system and blood pressure maintenance in Brattleboro DI rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 5 (November 1, 1986): R1009—R1010. http://dx.doi.org/10.1152/ajpregu.1986.251.5.r1009.

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46

Mercer, L. Preston, Danita S. Kelley, Holly M. Bundrant, Akram-Ul Haq, and Laurie L. Humphries. "Gender Affects Rats' Central Nervous System Histaminergic Responses to Dietary Manipulation." Journal of Nutrition 126, no. 12 (December 1, 1996): 3128–35. http://dx.doi.org/10.1093/jn/126.12.3128.

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47

Krinke, Georg J., Wolfgang Kaufmann, Ahmed T. Mahrous, and Philippe Schaetti. "Morphologic Characterization of Spontaneous Nervous System Tumors in Mice and Rats." Toxicologic Pathology 28, no. 1 (January 2000): 178–92. http://dx.doi.org/10.1177/019262330002800123.

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48

Křeček, J., S. Doležel, H. Dlouhá, and J. Zicha. "Sympathetic Nervous System and Age-Dependent Salt Hypertension in Brattleboro Rats." Clinical and Experimental Hypertension. Part A: Theory and Practice 9, no. 12 (January 1987): 2075–93. http://dx.doi.org/10.1080/07300077.1987.11978716.

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49

Yanai, Akira, and M. Takeuchi. "Nervous System. Vascular changes of expanded neurovascular bundles in rats. (Japanese)." Plastic and Reconstructive Surgery 95, no. 2 (February 1995): 431. http://dx.doi.org/10.1097/00006534-199502000-00061.

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50

Arvidson, B., and H. Tj�lve. "Distribution of109Cd in the nervous system of rats after intravenous injection." Acta Neuropathologica 69, no. 1-2 (1986): 111–16. http://dx.doi.org/10.1007/bf00687046.

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