Role of intracellular and extracellular calcium in activation of serotonin-induced contraction of pulmonary arterial smooth muscle

1988 ◽  
Vol 106 (3) ◽  
pp. 1211-1214
Author(s):  
V. A. Buryi ◽  
A. V. Gurkovskaya ◽  
N. I. Gokina ◽  
M. F. Shuba

2010 ◽  
Vol 31 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Jing Jiang ◽  
Shuang Wang ◽  
Zhigang Wang ◽  
Jun Ma ◽  
Shulin Liu ◽  
...  


2013 ◽  
Vol 46 (6) ◽  
pp. 654-664 ◽  
Author(s):  
Q. Yang ◽  
M. J. Dahl ◽  
K. H. Albertine ◽  
R. Ramchandran ◽  
M. Sun ◽  
...  


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Micheal Munson ◽  
Xin Yun ◽  
Haiyang Jiang ◽  
Nicolas Philip ◽  
John Huetsch ◽  
...  




2001 ◽  
Vol 281 (1) ◽  
pp. L1-L12 ◽  
Author(s):  
Elizabeth A. Coppock ◽  
Jeffrey R. Martens ◽  
Michael M. Tamkun

The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of vascular smooth muscle cell voltage-gated K+(KV) channels open at the resting membrane potential. Pulmonary arterial smooth muscle cell KV channel expression, antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, and the O2 sensitivity of cloned KV channels expressed in heterologous expression systems have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive KV current. Likely components include Kv2.1/Kv9.3 and Kv1.2/Kv1.5 heteromeric channels and the Kv3.1b α-subunit. Although the mechanism of KV channel inhibition by hypoxia is unknown, it appears that KV α-subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or β-subunit. This review summarizes the role of KV channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of KV channel subunits involved in this response, and the possible mechanisms of KV channel regulation by hypoxia.



1996 ◽  
Vol 80 (2) ◽  
pp. 496-505 ◽  
Author(s):  
I. S. Farrukh ◽  
J. R. Hoidal ◽  
W. H. Barry

In this study, we investigated the role of Na+/H+ antiport in regulating cytosolic (intracellular) pH (pHi) in isolated and cultured ferret pulmonary arterial smooth muscle cells (PSMC). We also studied the effects of modulating pHi on the cytosolic (intracellular) calcium concentration ([Ca2+]i) in the PSMC and on the pulmonary arterial pressure (Ppa) of isolated ferret lungs. pHi was modulated by the NH4Cl washout method. To eliminate the contribution of Cl-/HCO3- exchangers, the PSMC and isolated lungs were perfused in HCO3- free buffer. Blocking the Na+/H+ antiporter decreased baseline pHi and prevented the recovery from NH4Cl washout-induced intracellular acidosis. Intracellular alkalinization caused an initial transient increase in both [Ca2+]i and Ppa that were dependent on extracellular Ca2+ entry. Maintaining cytosolic alkalinization caused another increase in Ppa that was not associated with an increase in [Ca2+]i. Intracellular acidosis also caused an increase in [Ca2+]i and Ppa. The cytosolic acidosis-induced increase in [Ca2+]i and Ppa were mediated by both extracellular Ca2+ influx and release of stored intracellular Ca2+. Cytosolic acidosis also appears to have a direct effect on the smooth muscle contractile elements. Both cytosolic alkalosis and acidosis increased vascular reactivity.



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