scholarly journals Prenatal hypoxia inhibited propionate‐evoked BK channels of mesenteric artery smooth muscle cells in offspring

2020 ◽  
Vol 24 (5) ◽  
pp. 3192-3202 ◽  
Author(s):  
Wenna Zhang ◽  
Xueqin Feng ◽  
Yumeng Zhang ◽  
Miao Sun ◽  
Lingjun Li ◽  
...  
2018 ◽  
Vol 45 (4) ◽  
pp. 1603-1616 ◽  
Author(s):  
Bailin Liu ◽  
Yanping Liu ◽  
Ruixiu Shi ◽  
Xueqin Feng ◽  
Xiang Li ◽  
...  

Background/Aims: Chronic hypoxia in utero could impair vascular functions in the offspring, underlying mechanisms are unclear. This study investigated functional alteration in large-conductance Ca2+-activated K+ (BK) channels in offspring mesenteric arteries following prenatal hypoxia. Methods: Pregnant rats were exposed to normoxic control (21% O2, Con) or hypoxic (10.5% O2, Hy) conditions from gestational day 5 to 21, their 7-month-old adult male offspring were tested for blood pressure, vascular BK channel functions and expression using patch clamp and wire myograh technique, western blotting, and qRT-PCR. Results: Prenatal hypoxia increased pressor responses and vasoconstrictions to phenylephrine in the offspring. Whole-cell currents density of BK channels and amplitude of spontaneous transient outward currents (STOCs), not the frequency, were significantly reduced in Hy vascular myocytes. The sensitivity of BK channels to voltage, Ca2+, and tamoxifen were reduced in Hy myocytes, whereas the number of channels per patch and the single-channel conductance were unchanged. Prenatal hypoxia impaired NS1102- and tamoxifen-mediated relaxation in mesenteric arteries precontracted with phenylephrine in the presence of Nω-nitro-L-arginine methyl ester. The mRNA and protein expression of BK channel β1, not the α-subunit, was decreased in Hy mesenteric arteries. Conclusions: Impaired BK channel β1-subunits in vascular smooth muscle cells contributed to vascular dysfunction in the offspring exposed to prenatal hypoxia.


Life Sciences ◽  
2007 ◽  
Vol 80 (22) ◽  
pp. 2060-2066 ◽  
Author(s):  
Benzhi Cai ◽  
Dongmei Gong ◽  
Zhenwei Pan ◽  
Yu Liu ◽  
Hong Qian ◽  
...  

2001 ◽  
Vol 534 (2) ◽  
pp. 313-326 ◽  
Author(s):  
Yoshiaki Ohi ◽  
Hisao Yamamura ◽  
Norihiro Nagano ◽  
Susumu Ohya ◽  
Katsuhiko Muraki ◽  
...  

1993 ◽  
Vol 29 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Paul G. McGuire ◽  
Helen M. Walker-Caprioglio ◽  
Sally A. Little ◽  
Linda J. McGuffee

2004 ◽  
Vol 287 (6) ◽  
pp. C1577-C1588 ◽  
Author(s):  
Ronghua ZhuGe ◽  
Kevin E. Fogarty ◽  
Stephen P. Baker ◽  
John G. McCarron ◽  
Richard A. Tuft ◽  
...  

Ca2+ sparks are highly localized Ca2+ transients caused by Ca2+ release from sarcoplasmic reticulum through ryanodine receptors (RyR). In smooth muscle, Ca2+ sparks activate nearby large-conductance, Ca2+-sensitive K+ (BK) channels to generate spontaneous transient outward currents (STOC). The properties of individual sites that give rise to Ca2+ sparks have not been examined systematically. We have characterized individual sites in amphibian gastric smooth muscle cells with simultaneous high-speed imaging of Ca2+ sparks using wide-field digital microscopy and patch-clamp recording of STOC in whole cell mode. We used a signal mass approach to measure the total Ca2+ released at a site and to estimate the Ca2+ current flowing through RyR [ ICa(spark)]. The variance between spark sites was significantly greater than the intrasite variance for the following parameters: Ca2+ signal mass, ICa(spark), STOC amplitude, and 5-ms isochronic STOC amplitude. Sites that failed to generate STOC did so consistently, while those at the remaining sites generated STOC without failure, allowing the sites to be divided into STOC-generating and STOC-less sites. We also determined the average number of spark sites, which was 42/cell at a minimum and more likely on the order of at least 400/cell. We conclude that 1) spark sites differ in the number of RyR, BK channels, and coupling ratio of RyR-BK channels, and 2) there are numerous Ca2+ spark-generating sites in smooth muscle cells. The implications of these findings for the organization of the spark microdomain are explored.


1983 ◽  
Vol 33 ◽  
pp. 216
Author(s):  
Toshiro Inoue ◽  
Kazuo Takeda ◽  
Shiro Ishikawa ◽  
Yushi Ito ◽  
Hirosi Kuriyama

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