Alterations of Glucose-Dependent and -Independent Bladder Smooth Muscle Contraction in Spontaneously Hypertensive and Hyperlipidemic Rat

2007 ◽  
Vol 324 (2) ◽  
pp. 631-642 ◽  
Author(s):  
Koji Nobe ◽  
Taigi Yamazaki ◽  
Toshio Kumai ◽  
Masako Okazaki ◽  
Shinichi Iwai ◽  
...  
2014 ◽  
Vol 593 (3) ◽  
pp. 681-700 ◽  
Author(s):  
Cai-Ping Chen ◽  
Xin Chen ◽  
Yan-Ning Qiao ◽  
Pei Wang ◽  
Wei-Qi He ◽  
...  

Planta Medica ◽  
2017 ◽  
Vol 84 (05) ◽  
pp. 296-303 ◽  
Author(s):  
Xiaojiang Qin ◽  
Xiaomin Hou ◽  
Kun Zhang ◽  
Qingshan Li

AbstractFarrerol, a typical natural flavanone and major active component in Rhododendron dauricum var. ciliatum, has been shown to possess vasoactive ability in vitro. The aim of this study was to investigate its effect on aorta gene expression in spontaneously hypertensive rats. Twelve-week-old male normotensive Wistar Kyoto rats and spontaneously hypertensive rats were treated with orally administered farrerol (50 mg/kg body weight) for 8 wk before they were sacrificed. We found that aorta samples showed 444 upregulated genes in control spontaneously hypertensive rats compared with the control Wistar Kyoto rats. Administration of farrerol in spontaneously hypertensive rats increased the expression of 2329 genes in the aorta compared with the control spontaneously hypertensive rats. Gene expression profiles performed on the aorta revealed that farrerol induced changes in vascular smooth muscle contraction, mitogen-activated protein kinase signaling pathway, regulation of actin cytoskeleton, vascular endothelial growth factor signaling pathway, calcium signaling pathway, and renin angiotensin system. Furthermore, 10 genes involved in the pathway of vascular smooth muscle contraction were verified using real-time polymerase chain reaction technique, and several novel potential target genes for the farrerol treatment of hypertension were identified. The findings of this study lend support to the potential use of farrerol as a novel therapeutic and antihypertensive candidate drug to prevent the development of hypertension.


2003 ◽  
Vol 170 (2) ◽  
pp. 634-637 ◽  
Author(s):  
KEN AIKAWA ◽  
TAKASHI SUGINO ◽  
SEIJI MATSUMOTO ◽  
PAUL CHICHESTER ◽  
CATHERINE WHITBECK ◽  
...  

2004 ◽  
Vol 287 (4) ◽  
pp. F690-F699 ◽  
Author(s):  
Xiaoling Su ◽  
Arun Changolkar ◽  
Samuel Chacko ◽  
Robert S. Moreland

The effect of diabetes mellitus on the regulation of urinary bladder smooth muscle contraction was studied. Diabetes was induced in the rabbit by alloxan injection followed by 16 wk of housing. The bladder was harvested and strips of wall devoid of both mucosa and serosa were examined. Intact strips of bladder smooth muscle from diabetic animals produced less stress in response to membrane depolarization than muscle from control animals; sensitivity to KCl was not changed. Carbachol responses were similar in muscle strips from the two animal groups. Basal myosin light chain (MLC) phosphorylation levels were significantly elevated in response to most stimuli in muscle strips from diabetic animals, although levels of stress were either unchanged or lower. α-Toxin-permeabilized strips that allow for control of the intracellular environment while maintaining excitation-contraction coupling showed increased levels of MLC phosphorylation but decreased sensitivity to activator Ca2+ in smooth muscle from diabetic animals. MLC phosphatase contents were similar in smooth muscle from the two animal groups; however, MLC phosphatase activity was greater in muscle from control compared with diabetic animals. These results suggest that diabetes mellitus uncouples basal MLC phosphorylation from force in the bladder smooth muscle cell.


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