scholarly journals Mechanisms of BK Channel Activation by Docosahexaenoic Acid in Rat Coronary Arterial Smooth Muscle Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Ling-Ling Qian ◽  
Man-Qing Sun ◽  
Ru-Xing Wang ◽  
Tong Lu ◽  
Ying Wu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Docosahexaenoic Acid ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bk Channel ◽  
Arterial Smooth Muscle ◽  
Channel Activation ◽  
Arterial Smooth Muscle Cells

scholarly journals Type 1 IP3 receptors activate BKCa channels via local molecular coupling in arterial smooth muscle cells

2010 ◽  
Vol 136 (3) ◽  
pp. 283-291 ◽  
Author(s):  
Guiling Zhao ◽  
Zachary P. Neeb ◽  
M. Dennis Leo ◽  
Judith Pachuau ◽  
Adebowale Adebiyi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bkca Channel ◽  
Ip3 Receptors ◽  
Arterial Smooth Muscle ◽  
Bkca Channels ◽  
Channel Activation ◽  
Arterial Smooth Muscle Cells

Plasma membrane large-conductance Ca2+-activated K+ (BKCa) channels and sarcoplasmic reticulum inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are expressed in a wide variety of cell types, including arterial smooth muscle cells. Here, we studied BKCa channel regulation by IP3 and IP3Rs in rat and mouse cerebral artery smooth muscle cells. IP3 activated BKCa channels both in intact cells and in excised inside-out membrane patches. IP3 caused concentration-dependent BKCa channel activation with an apparent dissociation constant (Kd) of ∼4 µM at physiological voltage (−40 mV) and intracellular Ca2+ concentration ([Ca2+]i; 10 µM). IP3 also caused a leftward-shift in BKCa channel apparent Ca2+ sensitivity and reduced the Kd for free [Ca2+]i from ∼20 to 12 µM, but did not alter the slope or maximal Po. BAPTA, a fast Ca2+ buffer, or an elevation in extracellular Ca2+ concentration did not alter IP3-induced BKCa channel activation. Heparin, an IP3R inhibitor, and a monoclonal type 1 IP3R (IP3R1) antibody blocked IP3-induced BKCa channel activation. Adenophostin A, an IP3R agonist, also activated BKCa channels. IP3 activated BKCa channels in inside-out patches from wild-type (IP3R1+/+) mouse arterial smooth muscle cells, but had no effect on BKCa channels of IP3R1-deficient (IP3R1−/−) mice. Immunofluorescence resonance energy transfer microscopy indicated that IP3R1 is located in close spatial proximity to BKCa α subunits. The IP3R1 monoclonal antibody coimmunoprecipitated IP3R1 and BKCa channel α and β1 subunits from cerebral arteries. In summary, data indicate that IP3R1 activation elevates BKCa channel apparent Ca2+ sensitivity through local molecular coupling in arterial smooth muscle cells.

scholarly journals Angiotensin II Effects on BK Channel in Mesenteric Arterial Smooth Muscle Cells of SS, BN, and Congenic Renin+ and Renin- Rats

2010 ◽  
Vol 98 (3) ◽  
pp. 124a
Author(s):  
Anna Stadnicka ◽  
Stephen J. Contney ◽  
Carol Moreno ◽  
Richard J. Roman ◽  
Thomas A. Stekiel
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bk Channel ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells

scholarly journals LRRC26 Is a Functional BK Channel Auxiliary γ Subunit in Arterial Smooth Muscle Cells

2014 ◽  
Vol 115 (4) ◽  
pp. 423-431 ◽  
Author(s):  
Kirk W. Evanson ◽  
John P. Bannister ◽  
M. Dennis Leo ◽  
Jonathan H. Jaggar
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bk Channel ◽  
Arterial Smooth Muscle ◽  
Γ Subunit ◽  
Arterial Smooth Muscle Cells

β1-subunit of BK channels regulates arterial wall [Ca2+] and diameter in mouse cerebral arteries

2001 ◽  
Vol 91 (3) ◽  
pp. 1350-1354 ◽  
Author(s):  
Matthias Löhn ◽  
Birgit Lauterbach ◽  
Hermann Haller ◽  
Olaf Pongs ◽  
Friedrich C. Luft ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Bk Channels ◽  
Bk Channel ◽  
Systemic Hypertension ◽  
Myogenic Tone ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells

Mice with a disrupted β1(BKβ1)-subunit of the large-conductance Ca2+-activated K+ (BK) channel gene develop systemic hypertension and cardiac hypertrophy, which is likely caused by uncoupling of Ca2+ sparks to BK channels in arterial smooth muscle cells. However, little is known about the physiological levels of global intracellular Ca2+ concentration ([Ca2+]i) and its regulation by Ca2+ sparks and BK channel subunits. We utilized a BKβ1 knockout C57BL/6 mouse model and studied the effects of inhibitors of ryanodine receptor and BK channels on the global [Ca2+]i and diameter of small cerebral arteries pressurized to 60 mmHg. Ryanodine (10 μM) or iberiotoxin (100 nM) increased [Ca2+]i by ∼75 nM and constricted +/+ BKβ1 wild-type arteries (pressurized to 60 mmHg) with myogenic tone by ∼10 μm. In contrast, ryanodine (10 μM) or iberiotoxin (100 nM) had no significant effect on [Ca2+]i and diameter of −/− BKβ1-pressurized (60 mmHg) arteries. These results are consistent with the idea that Ca2+ sparks in arterial smooth muscle cells limit myogenic tone through activation of BK channels. The activation of BK channels by Ca2+ sparks reduces the voltage-dependent Ca2+ influx and [Ca2+]i through tonic hyperpolarization. Deletion of BKβ1 disrupts this negative feedback mechanism, leading to increased arterial tone through an increase in global [Ca2+]i.

Sign in / Sign up

Export Citation Format

Share Document