生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2003年
1期
96-100
,共5页
崔艺峰%李林%禹永春%金正元%李在琉%许文燮
崔藝峰%李林%禹永春%金正元%李在琉%許文燮
최예봉%리림%우영춘%금정원%리재류%허문섭
不饱和脂肪%毒蕈碱电流%低渗牵张%幽门窦%豚鼠
不飽和脂肪%毒蕈堿電流%低滲牽張%幽門竇%豚鼠
불포화지방%독심감전류%저삼견장%유문두%돈서
unsaturated fatty acids%muscarinic current%hyposmotic stretch%gastric antral myocytes%guinea pig
利用全细胞膜片钳技术在急性分离的胃窦平滑肌细胞上记录离子电流的方法, 探讨外源性不饱和脂肪酸是否参与低渗牵张加强毒蕈碱电流的过程.在豚鼠胃窦平滑肌细胞上膜电位被钳制在-20.0 mV等渗状态时, 50 μmol/L 卡巴胆碱(carbachol, CCh)引起的毒蕈碱电流(ICCh)作为对照, 发现低渗牵张可以使ICCh明显增加到对照的226.0±21.0%. 当用含5 μmol花生四烯酸(arachid acid, AA)、亚麻酸(linoleic acid, LA)或亚油酸(oleic acid, OA)细胞外液灌流时, ICCh 分别被抑制在对照的3.8±0.6%、 35.2±0.8%和66.6±0.6%.在这种情况下, 低渗牵张刺激可以使ICCh分别增加到106.0±2.5%、 173.2±6.8%和222.1±11.0%.5 μmol/L AA抑制低渗牵张增加的毒蕈碱电流51.2±3.8%, 而在等渗状态下抑制ICCh 为96.2±1.6%.上述结果提示, 不饱和脂肪酸中双键数目越多, 抑制效应越强; 但不饱和脂肪酸不参与低渗刺激加强毒蕈碱电流的过程.
利用全細胞膜片鉗技術在急性分離的胃竇平滑肌細胞上記錄離子電流的方法, 探討外源性不飽和脂肪痠是否參與低滲牽張加彊毒蕈堿電流的過程.在豚鼠胃竇平滑肌細胞上膜電位被鉗製在-20.0 mV等滲狀態時, 50 μmol/L 卡巴膽堿(carbachol, CCh)引起的毒蕈堿電流(ICCh)作為對照, 髮現低滲牽張可以使ICCh明顯增加到對照的226.0±21.0%. 噹用含5 μmol花生四烯痠(arachid acid, AA)、亞痳痠(linoleic acid, LA)或亞油痠(oleic acid, OA)細胞外液灌流時, ICCh 分彆被抑製在對照的3.8±0.6%、 35.2±0.8%和66.6±0.6%.在這種情況下, 低滲牽張刺激可以使ICCh分彆增加到106.0±2.5%、 173.2±6.8%和222.1±11.0%.5 μmol/L AA抑製低滲牽張增加的毒蕈堿電流51.2±3.8%, 而在等滲狀態下抑製ICCh 為96.2±1.6%.上述結果提示, 不飽和脂肪痠中雙鍵數目越多, 抑製效應越彊; 但不飽和脂肪痠不參與低滲刺激加彊毒蕈堿電流的過程.
이용전세포막편겸기술재급성분리적위두평활기세포상기록리자전류적방법, 탐토외원성불포화지방산시부삼여저삼견장가강독심감전류적과정.재돈서위두평활기세포상막전위피겸제재-20.0 mV등삼상태시, 50 μmol/L 잡파담감(carbachol, CCh)인기적독심감전류(ICCh)작위대조, 발현저삼견장가이사ICCh명현증가도대조적226.0±21.0%. 당용함5 μmol화생사희산(arachid acid, AA)、아마산(linoleic acid, LA)혹아유산(oleic acid, OA)세포외액관류시, ICCh 분별피억제재대조적3.8±0.6%、 35.2±0.8%화66.6±0.6%.재저충정황하, 저삼견장자격가이사ICCh분별증가도106.0±2.5%、 173.2±6.8%화222.1±11.0%.5 μmol/L AA억제저삼견장증가적독심감전류51.2±3.8%, 이재등삼상태하억제ICCh 위96.2±1.6%.상술결과제시, 불포화지방산중쌍건수목월다, 억제효응월강; 단불포화지방산불삼여저삼자격가강독심감전류적과정.
To investigate the function of exogenous unsaturated fatty acids in hyposmotic membrane stretch enhancement of muscarinic current (ICCh) in antral circular smooth muscle cells of guinea pig, we recorded the membrane current with the conventional whole cell patch-clamp technique. ICCh elicited by 50 μmol/L carbachol (CCh) at the holding potential of -20 mV under isosmotic condition was taken as control. Hyposmotic membrane stretch increased ICCh to 226.0±21.0%. When the cells were pretreated with 5 μmol/L arachidonic acid (AA), linoleic acid (LA) or oleic acid (OA), ICCh was inhibited to 3.8±0.6%, 35.2±0.8% and 66.6±0.6% respectively. Hyposmotic membrane stretch increased ICCh to 106.0±2.5%, 173.2±6.8% and 222.1±11.0% of the control respectively. Five μmol/L AA inhibited hyposmotic membrane stretch-enhanced ICCh by 51.2±3.8%, while the control ICCh under isosmotic condition was inhibited by 96.2±1.6%. The results suggest that unsaturated fatty acids inhibited ICCh and the inhibitory effect is more significant when the unsaturation degree is increased. However, the unsaturated fatty acids are not involved in the increase of ICCh induced by hyposmotic membrane stretch.