Selective, Direct Activation of High-Conductance, Calcium-Activated Potassium Channels Causes Smooth Muscle Relaxation

2012 ◽  
Vol 81 (4) ◽  
pp. 567-577 ◽  
Author(s):  
Cristiano G. Ponte ◽  
Owen B. McManus ◽  
William A. Schmalhofer ◽  
Dong-Ming Shen ◽  
Ge Dai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Potassium Channels ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Direct Activation ◽  
Calcium Activated Potassium Channels ◽  
High Conductance

Tremorgenic Indole Alkaloids Potently Inhibit Smooth Muscle High-Conductance Calcium-Activated Potassium Channels

Biochemistry ◽  
1994 ◽  
Vol 33 (19) ◽  
pp. 5819-5828 ◽  
Author(s):  
Hans-Guenther Knaus ◽  
Owen B. McManus ◽  
Seok H. Lee ◽  
William A. Schmalhofer ◽  
Margarita Garcia-Calvo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Potassium Channels ◽  
Indole Alkaloids ◽  
Calcium Activated Potassium Channels ◽  
High Conductance

scholarly journals A.122 Vascular effects of propofol: smooth muscle relaxation in human isolated veins and arteries

1996 ◽  
Vol 76 ◽  
pp. 38-39
Author(s):  
Eric Le Pelley ◽  
Pierre Corbi ◽  
Thierry Chataigneau ◽  
Robert Tricoche ◽  
Jacques Fusciardi
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Vascular Effects

[125I]Iberiotoxin-D19Y/Y36F, the First Selective, High Specific Activity Radioligand for High-Conductance Calcium-Activated Potassium Channels

Biochemistry ◽  
1997 ◽  
Vol 36 (7) ◽  
pp. 1943-1952 ◽  
Author(s):  
Alexandra Koschak ◽  
Robert O. Koch ◽  
Jessica Liu ◽  
Gregory J. Kaczorowski ◽  
Peter H. Reinhart ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Specific Activity ◽  
High Specific Activity ◽  
Calcium Activated Potassium Channels ◽  
High Conductance

216Acute administration of estradiol induces bladder smooth muscle relaxation through non-genomic pathways

2005 ◽  
Vol 4 (3) ◽  
pp. 56
Author(s):  
M. Dambros ◽  
P. Palma ◽  
C. Riccetto ◽  
R. Fraga ◽  
M. Thiel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Bladder Smooth Muscle

Role of cGMP in relaxation of vascular and other smooth muscle

1989 ◽  
Vol 67 (4) ◽  
pp. 251-262 ◽  
Author(s):  
Kanji Nakatsu ◽  
Jack Diamond
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscles ◽  
Phosphodiesterase Inhibitors ◽  
Current Evidence ◽  
Smooth Muscle Relaxation ◽  
Drug Induced ◽  
Intracellular Cgmp ◽  
Tissue Content

The hypothesis that the relaxant action of many drugs on vascular and other smooth muscle is mediated by increases in intracellular cGMP, the "cGMP hypothesis," is gaining wide acceptance. While much information supporting this idea can be found in the literature, there is also a significant amount of information indicating that an elevation in the tissue content of cGMP is by itself insufficient to cause smooth muscle relaxation. The literature is reviewed with reference to the criteria that need to be fulfilled to consider cGMP as the second messenger mediating relaxation of smooth muscle by a drug; i.e., activation of guanylate cyclase, elevation of tissue content of cGMP, potentiation by phosphodiesterase inhibitors, antagonism by inhibitors of cGMP synthesis, and production of relaxation by cGMP analogues. For each criterion, key observations supporting the hypothesis are considered, followed by examples of important observations not consistent with the hypothesis. It is concluded that in some smooth muscles, for example, rat myometrium and vas deferens, cGMP is not a mediator of drug-induced relaxation. In other smooth muscles, including vascular smooth muscle, cGMP appears to play an important role in the relaxation process; but current evidence suggests that other factors are also important and that the cGMP hypothesis may need to be modified.Key words: cGMP, vascular relaxation, smooth muscle relaxation, vasodilators.

scholarly journals Arteriolar vasodilation involves actin depolymerization

2018 ◽  
Vol 315 (2) ◽  
pp. H423-H428
Author(s):  
Philip S. Clifford ◽  
Brian S. Ferguson ◽  
Jeffrey L. Jasperse ◽  
Michael A. Hill
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Muscle Relaxation ◽  
Nitric Oxide Donor ◽  
Smooth Muscle Relaxation ◽  
Myosin Light Chain Phosphorylation ◽  
Actin Depolymerization

It is generally assumed that relaxation of arteriolar vascular smooth muscle occurs through hyperpolarization of the cell membrane, reduction in intracellular Ca2+ concentration, and activation of myosin light chain phosphatase/inactivation of myosin light chain kinase. We hypothesized that vasodilation is related to depolymerization of F-actin. Cremaster muscles were dissected in rats under pentobarbital sodium anesthesia (50 mg/kg). First-order arterioles were dissected, cannulated on glass micropipettes, pressurized, and warmed to 34°C. Internal diameter was monitored with an electronic video caliper. The concentration of G-actin was determined in flash-frozen intact segments of arterioles by ultracentrifugation and Western blot analyses. Arterioles dilated by ~40% of initial diameter in response to pinacidil (1 × 10−6 mM) and sodium nitroprusside (5 × 10−5 mM). The G-actin-to-smooth muscle 22α ratio was 0.67 ± 0.09 in arterioles with myogenic tone and increased significantly to 1.32 ± 0.34 ( P < 0.01) when arterioles were dilated with pinacidil and 1.14 ± 0.18 ( P < 0.01) with sodium nitroprusside, indicating actin depolymerization. Compared with control vessels (49 ± 5%), the percentage of phosphorylated myosin light chain was significantly reduced by pinacidil (24 ± 2%, P < 0.01) but not sodium nitroprusside (42 ± 4%). These findings suggest that actin depolymerization is an important mechanism for vasodilation of resistance arterioles to external agonists. Furthermore, pinacidil produces smooth muscle relaxation via both decreases in myosin light chain phosphorylation and actin depolymerization, whereas sodium nitroprusside produces smooth muscle relaxation primarily via actin depolymerization. NEW & NOTEWORTHY This article adds to the accumulating evidence on the contribution of the actin cytoskeleton to the regulation of vascular smooth muscle tone in resistance arterioles. Actin depolymerization appears to be an important mechanism for vasodilation of resistance arterioles to pharmacological agonists. Dilation to the K+ channel opener pinacidil is produced by decreases in myosin light chain phosphorylation and actin depolymerization, whereas dilation to the nitric oxide donor sodium nitroprusside occurs primarily via actin depolymerization. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/vascular-smooth-muscle-actin-depolymerization/ .

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