scholarly journals Direct Effect of Carbon Monoxide on Relaxation Induced by Electrical Field Stimulation in Rat Corpus Cavernosum

2010 ◽  
Vol 51 (8) ◽  
pp. 572 ◽  
Author(s):  
Dae Woong Kim ◽  
Chen Zhao ◽  
Myung Ki Kim ◽  
Jong Kwan Park
1994 ◽  
Vol 22 (5) ◽  
pp. 291-293 ◽  
Author(s):  
Y. C. Kim ◽  
M. G. Davies ◽  
L. Marson ◽  
P. -O. Hagen ◽  
C. C. Carson

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Inger S Stallmann-Jorgensen ◽  
R. Clinton Webb

Hypertension (HTN) and diabetes (DM) are comorbid conditions, each associated with inflammation. Lipopolysaccharide (LPS) is elevated in the serum of patients with DM and capable of robustly activating the immune system. Risk of erectile dysfunction (ED) is increased in both HTN and DM. Vascular relaxation is needed to regulate vascular tone and erectile function. Our previous studies showed that corpus cavernosum (CC) nitrergic relaxation to electrical field stimulation (EFS) was reduced after LPS exposure. It is not known whether LPS-induced inflammation plays a role in DM-associated ED. Our study aim was to examine vascular function of rat CC under high glucose conditions in the presence of LPS. We hypothesized that high glucose would exacerbate the LPS-induced decrease in EFS relaxation. Isolated rat CC strips incubated with control (5mM) or high glucose (HG, 25 mM) media with or without LPS (1 ug/mL) for 6 h. CC strips were mounted in a myograph and pre-contracted with phenylephrine (PE, 10 -5 M) before eliciting relaxation responses using 20-volt stimuli of 1, 2, 4, 8, and 16 Hz. Four Hz produced the half maximal response (%PE contraction) and was used to compare treatment effects. LPS-treated CC (7.13±1.53%) relaxed less than Control CC (19.1±2.67%). The decrease in relaxation was greatest in HG+LPS-treated CC (-3.58±1.43%), Fig. 1. Thus, we show that the LPS-induced reduction in relaxation is exacerbated in the HG+LPS condition, suggesting that elevated LPS and hyperglycemia act synergistically in the promotion of vascular dysfunction and ED.


1990 ◽  
Vol 170 (2) ◽  
pp. 843-850 ◽  
Author(s):  
Louis J. Ignarro ◽  
Peggy A. Bush ◽  
Georgette M. Buga ◽  
Keith S. Wood ◽  
Jon M. Fukuto ◽  
...  

2002 ◽  
Vol 282 (6) ◽  
pp. R1730-R1738 ◽  
Author(s):  
Hitoshi Masuda ◽  
Toshihiko Tsujii ◽  
Tetsuo Okuno ◽  
Kazunori Kihara ◽  
Moritaka Goto ◽  
...  

We examined whether endogenous inhibitors of nitric oxide (NO) synthesis are involved in the impaired cavernosal relaxation with ischemia in rabbits. Two weeks after cavernosal ischemia caused by partial vessel occlusion, endothelium-dependent and electrical field stimulation (EFS)-induced neurogenic NO-mediated relaxations, but not sodium nitroprusside (SNP)-induced relaxation, were significantly impaired in the isolated corpus cavernosum. The Ca2+-dependent NO synthase (NOS) activity and the basal and stimulated cGMP productions with carbachol or EFS were significantly decreased after ischemia. Supplementation of excessl-arginine partially recovered both of the impaired relaxations. The contents of N G-monomethyl-l-arginine (l-NMMA) and asymmetric N G, N G-dimethyl-l-arginine (ADMA) but not l-arginine and symmetric N G, N′G-dimethyl-l-arginine (SDMA) were increased in the cavernosal tissues after ischemia. Authentic l-NMMA and ADMA but not SDMA concentration dependently inhibited both relaxations without affecting the relaxation produced by SNP in the control. Excess l-arginine abolished the inhibition with l-NMMA and ADMA. These results suggest that the impaired NO-mediated cavernosal relaxations after ischemia are closely related to the decreased NOS activity and the increased accumulation of l-NMMA and ADMA.


PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183766 ◽  
Author(s):  
Rafael Campos ◽  
Fabíola Z. Mónica ◽  
Renata Lopes Rodrigues ◽  
Julio Alejandro Rojas-Moscoso ◽  
Ronilson Agnaldo Moreno ◽  
...  

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