nerve inhibition
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2019 ◽  
Vol 21 (5) ◽  
pp. 426-433 ◽  
Author(s):  
S. Ahmed Ali ◽  
John E. Hanks ◽  
Aaron W. Stebbins ◽  
Samantha T. Cohen ◽  
Daniel A. Hunter ◽  
...  

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Yosuke Matsuta ◽  
Zeyad Schwen ◽  
Abhijith Mally ◽  
Bing Shen ◽  
Jicheng Wang ◽  
...  

2012 ◽  
Vol 302 (9) ◽  
pp. F1090-F1097 ◽  
Author(s):  
Changfeng Tai ◽  
Jeffrey A. Larson ◽  
P. Dafe Ogagan ◽  
Guoqing Chen ◽  
Bing Shen ◽  
...  

Naloxone (an opioid receptor antagonist) was used to examine the role of opioid mechanisms in bladder reflexes and in somatic afferent inhibition of these reflexes by tibial nerve stimulation (TNS). Experiments were conducted in α-chloralose-anesthetized cats when the bladder was infused with saline or 0.25% acetic acid (AA). The bladder volume was measured at the first large-amplitude (>30 cmH2O) contraction during a cystometrogram and termed “estimated bladder capacity” (EBC). AA irritated the bladder, induced bladder overactivity, and significantly ( P < 0.0001) reduced EBC to 14.3 ± 1.9% of the saline control. TNS (5 Hz, 0.2 ms) at 4 and 8 times the threshold (T) intensity for inducing an observable toe movement suppressed AA-induced bladder overactivity and significantly increased EBC to 41.5 ± 9.9% (4T, P < 0.05) and 46.1 ± 7.9% (8T, P < 0.01) of the saline control. Naloxone (1 mg/kg iv) completely eliminated TNS inhibition of bladder overactivity. Naloxone (0.001–1 mg/kg iv) did not change EBC during AA irritation. However, during saline infusion naloxone (1 mg/kg iv) significantly ( P < 0.01) reduced EBC to 66.5 ± 8.1% of the control EBC. During saline infusion, TNS induced an acute increase in EBC and an increase that persisted following the stimulation. Naloxone (1 mg/kg) did not alter either type of inhibition. However, naloxone administered during the poststimulation inhibition decreased EBC. These results indicate that opioid receptors have different roles in modulation of nociceptive and nonnociceptive bladder reflexes and in somatic afferent inhibition of these reflexes, raising the possibility that opioid receptors may be a target for pharmacological treatment of lower urinary tract disorders.


2012 ◽  
Vol 187 (4S) ◽  
Author(s):  
Abhijith Mally ◽  
Jeffrey Larson ◽  
P. Dafe Ogagan ◽  
Changfeng Tai ◽  
Bing Shen ◽  
...  

2012 ◽  
Vol 119 (4) ◽  
pp. 359-367 ◽  
Author(s):  
Bai Lei ◽  
Daisuke Nakano ◽  
Yoshihide Fujisawa ◽  
Ya Liu ◽  
Hirofumi Hitomi ◽  
...  

2000 ◽  
Vol 279 (5) ◽  
pp. R1827-R1833 ◽  
Author(s):  
C. N. May ◽  
R. M. McAllen ◽  
M. J. McKinley

The lamina terminalis is situated in the anterior wall of the third ventricle and plays a major role in fluid and electrolyte homeostasis and cardiovascular regulation. The present study examined whether the effects of intracerebroventricular infusion of hypertonic saline and ANG II on renal sympathetic nerve activity (RSNA) were mediated by the lamina terminalis. In control, conscious sheep ( n = 5), intracerebroventricular infusions of 0.6 M NaCl (1 ml/h for 20 min) and ANG II (10 nmol/h for 30 min) increased mean arterial pressure (MAP) by 6 ± 1 ( P < 0.001) and 14 ± 3 mmHg ( P < 0.001) and inhibited RSNA by 80 ± 6 ( P < 0.001) and 89 ± 7% ( P < 0.001), respectively. Both treatments reduced plasma renin concentration (PRC). Intracerebroventricular infusion of artificial cerebrospinal fluid (1 ml/h for 30 min) had no effect. In conscious sheep with lesions of the lamina terminalis ( n = 6), all of the responses to intracerebroventricular hypertonic saline and ANG II were abolished. In conclusion, the effects of intracerebroventricular hypertonic saline and ANG II on RSNA, PRC, and MAP depend on the integrity of the lamina terminalis, indicating that this site plays an essential role in coordinating the homeostatic responses to changes in brain Na+ concentration.


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