Stretch-activated channel blockers modulate cell volume in cardiac ventricular myocytes.
Stretch-activated channel blockers modulate cell volume in cardiac ventricular myocytes.
复制标题
牵张激活通道阻滞剂调节心室肌细胞的细胞体积。
DOI：
10.1016/s0022-2828(08)80062-4
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发表时间：
1995
影响因子：
5
通讯作者：
Baumgarten,CM
中科院分区：
文献类型：
--
作者：
Suleymanian,MA;Clemo,HF;Cohen,NM;Baumgarten,CM
Stretch-activated channels (SAC) are postulated to regulate cell volume. While this hypothesis is appealing, direct evidence is lacking. Using digital video microscopy, we found that pharmacological blockade of SACs alters the cell volume of isolated rabbit ventricular myocytes during hypoosmotic stress. Under control conditions, relative cell volume increased from 1.0 to 1.311±0.019 after 10 min in 195 mosmol/l solution. The cation SAC blocker gadolinium (Gd3+10 μM) reduced the amount of swelling in hypoosmotic solution by 24% and induced a regulatory volume decrease otherwise not observed. In contrast, the anion SAC blocker 9-anthracene carboxylic acid (9-AC; 1 mm) increased swelling by 44% under the same conditions. Based on the direction of SAC currents, Gd3+and 9-AC are expected to have opposite effects on cell volume. Furthermore, Gd3+ and 9-AC changed cell volume by only ~ 2% in isosmotic solutions when SACs are expected to be closed. This supports the idea that Gd3+and 9-AC affect stretch-activated transport processes. In contrast, omitting bath Ca2+did not alter cell volume under iso- or hypoosmotic conditions suggesting stretch-activated Ca2+influx is not important in setting cell volume. Not all channels can affect cell volume. Opening ATP-sensitive K+channels with aprikalim (100 μM) or blocking them with glibenclamide (1 μM) did not alter cell volume under isosmotic or hypoosmotic conditions. These data support the idea that SACs are involved in cardiac cell volume regulation.
