MECHANISMS OF ACTION OF HYDROGEN SULFIDE ON CONTRACTILE ACTIVITY VASCULAR SMOOTH MUSCLE

2011 ◽  
Vol 29 ◽  
pp. e335
Author(s):  
M. Baskakov ◽  
S. Gusakova ◽  
A. Zheludeva ◽  
L. Smagly ◽  
I. Kovalev ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Contractile Activity ◽  
Mechanisms Of Action

scholarly journals Effect of hydrogen sulfide on the contractile activity of smooth muscle cells from the rat aorta

2010 ◽  
Vol 9 (6) ◽  
pp. 12-17
Author(s):  
M. B. Baskakov ◽  
S. V. Gusakova ◽  
A. S. Zheludeva ◽  
L. V. Smagly ◽  
I. V. Kovalyov ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Activity ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Mechanisms Of Action ◽  
High K ◽  
Lower Amplitude

In preparations of rat aorta, used as a model of muscular type arteries, the method mehanografii studied the effect of hydrogen sulfide on the reduction of isolated of vascular smooth muscle. Found that hydrogen sulfide in concentrations 1—50 mmol increases the mechanical stress of smooth muscle in high-K + medium. At higher concentrations (300—1 000 mmol) H2S leads to lower amplitude giperkalievoy contraction in high-K + medium. Reduction of smooth muscle cells caused by phenylephrine inhibited the action of hydrogen sulfide in the whole range of concentrations. The causes of differences in data obtained with the results of studies in other laboratories, and possible mechanisms of action of hydrogen sulfide on the contractile activity of vascular smooth muscle.

Mechanisms of Hydrogen Sulfide Effects on Contractile Activity of Vascular Smooth Muscle in Rats

2012 ◽  
Vol 3 (2) ◽  
pp. 149-160
Author(s):  
Olena M. Semenykhina ◽  
Olga V. Bazilyuk ◽  
Yulia P. Korkach ◽  
Vadim F. Sagach
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Contractile Activity

scholarly journals Fundamental Roles of Axial Stretch in Isometric and Isobaric Evaluations of Vascular Contractility

2019 ◽  
Vol 141 (3) ◽  
Author(s):  
Alexander W. Caulk ◽  
Jay D. Humphrey ◽  
Sae-Il Murtada
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Function ◽  
Contractile Function ◽  
Contractile Activity ◽  
Comparison Of Methods ◽  
Axial Stretch ◽  
Smooth Muscle Function ◽  
In Vivo Loading

Vascular smooth muscle cells (VSMCs) can regulate arterial mechanics via contractile activity in response to changing mechanical and chemical signals. Contractility is traditionally evaluated via uniaxial isometric testing of isolated rings despite the in vivo environment being very different. Most blood vessels maintain a locally preferred value of in vivo axial stretch while subjected to changes in distending pressure, but both of these phenomena are obscured in uniaxial isometric testing. Few studies have rigorously analyzed the role of in vivo loading conditions in smooth muscle function. Thus, we evaluated effects of uniaxial versus biaxial deformations on smooth muscle contractility by stimulating two regions of the mouse aorta with different vasoconstrictors using one of three testing protocols: (i) uniaxial isometric testing, (ii) biaxial isometric testing, and (iii) axially isometric plus isobaric testing. Comparison of methods (i) and (ii) revealed increased sensitivity and contractile capacity to potassium chloride and phenylephrine (PE) with biaxial isometric testing, and comparison of methods (ii) and (iii) revealed a further increase in contractile capacity with isometric plus isobaric testing. Importantly, regional differences in estimated in vivo axial stretch suggest locally distinct optimal biaxial configurations for achieving maximal smooth muscle contraction, which can only be revealed with biaxial testing. Such differences highlight the importance of considering in vivo loading and geometric configurations when evaluating smooth muscle function. Given the physiologic relevance of axial extension and luminal pressurization, we submit that, when possible, axially isometric plus isobaric testing should be employed to evaluate vascular smooth muscle contractile function.

Mechanisms of Action of Adenosine on Vascular Smooth Muscle and Cardiac Cells

1983 ◽  
pp. 319-332 ◽  
Author(s):  
Rafael Rubio ◽  
Maureen T. Knabb ◽  
Tokumasa Tsukada ◽  
Robert M. Berne
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Mechanisms Of Action ◽  
Cardiac Cells

Interaction of Methylglyoxal and Hydrogen Sulfide in Rat Vascular Smooth Muscle Cells

2010 ◽  
Vol 12 (9) ◽  
pp. 1093-1100 ◽  
Author(s):  
Tuanjie Chang ◽  
Ashley Untereiner ◽  
Jianghai Liu ◽  
Lingyun Wu
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

Vasoconstrictive effect of hydrogen sulfide involves downregulation of cAMP in vascular smooth muscle cells

2008 ◽  
Vol 295 (5) ◽  
pp. C1261-C1270 ◽  
Author(s):  
Jia Jia Lim ◽  
Yi-Hong Liu ◽  
Ester Sandar Win Khin ◽  
Jin-Song Bian
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nitric Oxide Synthase Inhibitor ◽  
Vasorelaxant Effect ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Hydrogen sulfide (H2S), a new endogenous mediator, produces both vasorelaxation and vasoconstriction. This study was designed to examine whether cAMP mediates the vasoconstrictive effect of H2S. We found that NaHS at a concentration range of 10–100 μM (yields ∼3–30 μM H2S) concentration-dependently reversed the vasodilation caused by isoprenaline and salbutamol, two β-adrenoceptor agonists, and forskolin, a selective adenylyl cyclase activator, in phenylephrine-precontracted rat aortic rings. Pretreatment with NaHS (10–100 μM) for 5 min also significantly attenuated the vasorelaxant effect of salbutamol and forskolin. More importantly, NaHS (5–100 μM) significantly reversed forskolin-induced cAMP accumulation in vascular smooth muscle cells. However, NaHS produced significant, but weaker, vasoconstriction in the presence of NG-nitro-l-arginine methyl ester (100 μM), a nitric oxide synthase inhibitor, or in endothelium-denuded aortic rings. Blockade of ATP-sensitive potassium channels with glibenclamide (10 μM) failed to attenuate the vasoconstriction induced by H2S. Taken together, we demonstrated for the first time that the vasoconstrictive effect of H2S involves the adenyly cyclase/cAMP pathway.

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