scholarly journals Role of BKCa Channels in Mesenteric Artery Vascular Smooth Muscle Tone of Diabetic Rats

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
ANA PATRICIA HERNÁNDEZ‐GARCIA ◽  
AURELIO HERNÁNDEZ‐MÉNDEZ ◽  
ERIKA GUADALUPE CHI‐AHUMADA ◽  
PAOLA ALGARA‐SUÁREZ ◽  
RICARDO ESPINOSA‐TANGUMA
2005 ◽  
Vol 201 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Elisabeth C. McLemore ◽  
Deron J. Tessier ◽  
Jeffrey Thresher ◽  
Padmini Komalavilas ◽  
Colleen M. Brophy

1989 ◽  
Vol 27 (3-4) ◽  
pp. 414-417 ◽  
Author(s):  
R. J. Sturm ◽  
D. A. Holloway ◽  
S. Buckley ◽  
M. C. Osborne ◽  
D. Grimes ◽  
...  

1989 ◽  
Vol 257 (4) ◽  
pp. H1315-H1320
Author(s):  
J. L. Mehta ◽  
D. L. Lawson ◽  
W. W. Nichols ◽  
P. Mehta

To determine the influence of polymorphonuclear leukocytes (PMNLs) on vascular smooth muscle tone, isolated human PMNLs (10(4)–10(7) cells/ml) were suspended in a tissue bath with precontracted rat aortic rings with or without endothelium. PMNLs in low concentrations (10(4) and 10(5) cells/ml) caused a mild contraction, and in higher concentrations (10(6) and 10(7) cells/ml) caused a modest relaxation of aortic rings with intact endothelium. In contrast, PMNLs caused a potent concentration-dependent relaxation of deendothelialized rings (P less than 0.01 compared with rings with intact endothelium). The PMNL-induced vascular smooth muscle relaxation was abolished by both hemoglobin and methylene blue and potentiated by both superoxide dismutase and captopril. Although suspension of PMNLs caused release of eicosanoids, thromboxane A2 and prostacyclin, from rings with intact endothelium, neither indomethacin nor the TxA2-endoperoxide receptor antagonist SQ 29548 modified the effects of PMNLs on vascular smooth muscle tone. These observations suggest that unstimulated PMNLs generate a smooth muscle relaxant, which has biological characteristics similar to the endothelium-derived relaxing factor. Since the activity of this PMNL-derived smooth muscle relaxant is more pronounced in deendothelialized vascular segments, it appears that endothelium provides a barrier against vasorelaxation by high concentrations of PMNLs.


2001 ◽  
Vol 91 (4) ◽  
pp. 1819-1827 ◽  
Author(s):  
Padmini Komalavilas ◽  
Shyamal Mehta ◽  
Christopher J. Wingard ◽  
Daniel T. Dransfield ◽  
Jyoti Bhalla ◽  
...  

Phosphatidylinositol 3-kinase (PI3-kinase) activates protein kinase B (also known as Akt), which phosphorylates and activates a cyclic nucleotide phosphodiesterase 3B. Increases in cyclic nucleotide concentrations inhibit agonist-induced contraction of vascular smooth muscle. Thus we hypothesized that the PI3-kinase/Akt pathway may regulate vascular smooth muscle tone. In unstimulated, intact bovine carotid artery smooth muscle, the basal phosphorylation of Akt was higher than that in cultured smooth muscle cells. The phosphorylation of Akt decreases in a time-dependent manner when incubated with the PI3-kinase inhibitor, LY-294002. Agonist (serotonin)-, phorbol ester (phorbol 12,13-dibutyrate; PDBu)-, and depolarization (KCl)-induced contractions of vascular smooth muscles were all inhibited in a dose-dependent fashion by LY-294002. However, LY-294002 did not inhibit serotonin- or PDBu-induced increases in myosin light chain phosphorylation or total O2 consumption, suggesting that inhibition of contraction was not mediated by reversal or inhibition of the pathways that lead to smooth muscle activation and contraction. Treatment of vascular smooth muscle with LY-294002 increased the activity of cAMP-dependent protein kinase and increased the phosphorylation of the cAMP-dependent protein kinase substrate heat shock protein 20 (HSP20). These data suggest that activation of the PI3-kinase/Akt pathway in unstimulated smooth muscle may modulate vascular smooth muscle tone (allow agonist-induced contraction) through inhibition of the cyclic nucleotide/HSP20 pathway and suggest that cyclic nucleotide-dependent inhibition of contraction is dissociated from the myosin light chain contractile regulatory pathways.


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