Smooth muscle membrane organization in the normal and dysfunctional human urinary bladder: A structural analysis

2005 ◽  
Vol 24 (2) ◽  
pp. 128-135 ◽  
Author(s):  
Fiona C. Burkhard ◽  
Katia Monastyrskaya ◽  
Urs E. Studer ◽  
Annette Draeger
Keyword(s):  
Smooth Muscle ◽  
Structural Analysis ◽  
Urinary Bladder ◽  
Muscle Membrane ◽  
Membrane Organization ◽  
Human Urinary Bladder ◽  
Smooth Muscle Membrane

Generation of a human urinary bladder smooth muscle cell line

2012 ◽  
Vol 48 (2) ◽  
pp. 84-96 ◽  
Author(s):  
Yongmu Zheng ◽  
Shaohua Chang ◽  
Ettickan Boopathi ◽  
Sandra Burkett ◽  
Mary John ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Smooth Muscle Cell ◽  
Cell Line ◽  
Muscle Cell ◽  
Bladder Smooth Muscle ◽  
Human Urinary Bladder ◽  
Urinary Bladder Smooth Muscle ◽  
Bladder Smooth Muscle Cell ◽  
Muscle Cell Line

Human urinary bladder smooth muscle is dependent on membrane cholesterol for cholinergic activation

2010 ◽  
Vol 634 (1-3) ◽  
pp. 142-148 ◽  
Author(s):  
Yulia Shakirova ◽  
Michiko Mori ◽  
Mari Ekman ◽  
Jonas Erjefält ◽  
Bengt Uvelius ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Membrane Cholesterol ◽  
Bladder Smooth Muscle ◽  
Human Urinary Bladder ◽  
Urinary Bladder Smooth Muscle ◽  
Cholinergic Activation

Endothelium-dependent hyperpolarization elicited by adenine compounds in rabbit carotid artery

1991 ◽  
Vol 260 (4) ◽  
pp. H1037-H1042 ◽  
Author(s):  
G. Chen ◽  
H. Suzuki
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Direct Action ◽  
Smooth Muscles ◽  
Muscle Membrane ◽  
Dependent Manner ◽  
Rabbit Carotid Artery ◽  
Mechanical Removal ◽  
Smooth Muscle Membrane ◽  
Adventitial Cells

Electrical responses of the membrane of intimal and adventitial smooth muscle cells of the rabbit carotid artery to ATP, ADP, AMP, and adenosine were recorded. In intimal cells, these compounds hyperpolarized the membrane. Mechanical removal of the endothelium altered the responses to ATP and ADP to one of a transient depolarization, with no alteration of the response to AMP and adenosine. In the adventitial cells, ATP and ADP produced a transient depolarization, whereas AMP and adenosine produced a sustained hyperpolarization, irrespective of the presence or absence of the endothelium. In tissues with an intact endothelium, 5'-adenylylimidodiphosphate tetralithium salt and alpha,beta-methylene ATP (mATP) transiently depolarized the membrane in these smooth muscles. In case of stabilization with mATP, only hyperpolarization was generated by ATP, in an endothelium-dependent manner. Our interpretation of these observations is that 1) ATP and ADP depolarize smooth muscle membrane by a direct action and hyperpolarize the membrane indirectly through the release of endothelium-derived hyperpolarizing factor, 2) AMP and adenosine hyperpolarize the membrane, independently of the endothelium, and 3) ATP receptors present on the endothelial cell membrane differ from those on smooth muscle membrane.

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat

1987 ◽  
Vol 252 (5) ◽  
pp. G654-G661
Author(s):  
W. J. Snape ◽  
S. T. Tan ◽  
H. W. Kao
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Wave Pattern ◽  
Isometric Tension ◽  
Muscle Membrane ◽  
Maximum Effect ◽  
Smooth Muscle Membrane

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

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