Previous voltage clamp studies have demonstrated the modulation of sperm Ca 2+ activated K + (KCa) channels expressed in Xenopus oocytes by angiotensin II (Ang II) and extracellular ATP via AT 1 receptor and ...Previous voltage clamp studies have demonstrated the modulation of sperm Ca 2+ activated K + (KCa) channels expressed in Xenopus oocytes by angiotensin II (Ang II) and extracellular ATP via AT 1 receptor and P 2U receptor, respectively. In the present study, we investigated the involvement of KCa channels in receptor regulated sperm motility of the rat using a computer aided sperm analysis system, HTM IVOS, in conjunction with Ca 2+ mobilizing agents, receptor agonists/antagonists and KCa channels blockers. The percentage of motile sperm was increased by ionomycin (0.5 μmol/L), which could be inhibited by K + channel blockers, tetraethylammonium (TEA 1 μmol/L ) or charybdotoxin (ChTX, 300 nmol/L) indicating the presence of KCa channels. Ang II, at low concentration, 10 nmol/L, was found to increase motility, however, at higher concentration, 1 μmol/L, percentage of motility was found to be suppressed. Both stimulatory and inhibitory effects of Ang II could be reversed by losartan, a specific antagonist of AT 1 receptors, but not AT 2 antagonist PD123177, indicating the involvement of AT 1 but not AT2 receptor in mediating both effects. ChTX also abolished both stimulatory and inhibitory effects of Ang II, suggesting the involvement of KCa channels. The percentage of motility was also enhanced by extracellular ATP, a factor known to be involved in sperm activation. The ATP enhanced sperm motility was mimicked by UTP, and inhibited by ChTX and reactive blue, an antagonist of P 2 receptor, indicating the involvement of both P 2U and KCa channels. RT PCR study was also conducted to confirm the expression of KCa channels, AT 1 receptors and P 2U receptor, but not AT 2 receptor, in rat caudal epididymal sperm. The present findings suggest an important role of KCa channels in the regulation of sperm motility by AT 1 and P 2U receptors.展开更多
针对WES 2815:2014《Test method for brittle crack arrest toughness,Kca》和UR S33《Requirements for Use of Extremely Thick Steel Plates》中止裂韧性Kca的计算表达式和裂纹偏转时Kca的计算方法,利用有限元法计算了三种不同裂纹...针对WES 2815:2014《Test method for brittle crack arrest toughness,Kca》和UR S33《Requirements for Use of Extremely Thick Steel Plates》中止裂韧性Kca的计算表达式和裂纹偏转时Kca的计算方法,利用有限元法计算了三种不同裂纹形式的双重拉伸试样的止裂韧性Kca,基于计算结果指出了上述标准中止裂韧性Kca计算表达式缺少一系数项,并给出了正确的Kca计算表达式,同时提出裂纹偏转角度大时按照裂纹的直边投影计算Kca是不合理的。展开更多
Background Recent studies have showed that perivascular adipose tissue （PVAT） may secrete the adventitial-derived relaxing factor （ADRF） to affect vascular function.However,the functional change of ADRF in hyperte...Background Recent studies have showed that perivascular adipose tissue （PVAT） may secrete the adventitial-derived relaxing factor （ADRF） to affect vascular function.However,the functional change of ADRF in hypertensive status is seldom studied;and the mechanisms of ADRF remain unclear.Our study examined the ADRF secreted by perivascular adipose tissue of control rats with normal blood pressure （Wistar Kyoto rats,WKY） and discussed the mechanisms of ADRF;We observed the functional change in ADRF of perivascular adipose tissue in spontaneously hypertensive rats （SHRs）.Method The two adjacent thoracic aorta rings of SHR and WKY rats were divided into naked vessel subgroup and PVAT subgroup.The differences of vascular contractility between the two subgroups induced by 10-6 mmol/L phenylephrine were compared.The effect of PVAT culture medium of WKY on the vascular tension of Fat （-） vessels was observed by liquid transfer measure.The mechanism of ADRF was determined by tool drugs.Results In WKY group,vascular contractility of Fat （＋） subgroup was lower than that of the Fat （-） subgroup （P 0.05）;while in SHR group,there was no difference between the two subgroups （P 0.05）.Transferring the incubation solution of WKY Fat （＋） subgroup to the matched Fat （-） subgroup induced rapid vasodilation.When incubating blood vessels in calcium free PSS solution,there was no significant difference of phenylephrine-induced vasoconstriction between Fat （-） and Fat （＋） subgroup.Both glibenclamide,the blocker of ATP-sensitive potassium （KATP） channel and Tetraethy-lammonium chloride （TEA）,the inhibitor of calcium-dependent potassium （KCa） channel,effectively inhibited vasodilation function of ADRF.Conclusions Perivascular adipose tissue in WKY releases ADRF which can cause vasodilation,while this function was inhibited in SHR.ADRF acts through the activation of KCa and KATP channels and calcium ion is involved.展开更多
基金Direct Grant of the Chinese University of Hong Kong to Dr. HC Chan
文摘Previous voltage clamp studies have demonstrated the modulation of sperm Ca 2+ activated K + (KCa) channels expressed in Xenopus oocytes by angiotensin II (Ang II) and extracellular ATP via AT 1 receptor and P 2U receptor, respectively. In the present study, we investigated the involvement of KCa channels in receptor regulated sperm motility of the rat using a computer aided sperm analysis system, HTM IVOS, in conjunction with Ca 2+ mobilizing agents, receptor agonists/antagonists and KCa channels blockers. The percentage of motile sperm was increased by ionomycin (0.5 μmol/L), which could be inhibited by K + channel blockers, tetraethylammonium (TEA 1 μmol/L ) or charybdotoxin (ChTX, 300 nmol/L) indicating the presence of KCa channels. Ang II, at low concentration, 10 nmol/L, was found to increase motility, however, at higher concentration, 1 μmol/L, percentage of motility was found to be suppressed. Both stimulatory and inhibitory effects of Ang II could be reversed by losartan, a specific antagonist of AT 1 receptors, but not AT 2 antagonist PD123177, indicating the involvement of AT 1 but not AT2 receptor in mediating both effects. ChTX also abolished both stimulatory and inhibitory effects of Ang II, suggesting the involvement of KCa channels. The percentage of motility was also enhanced by extracellular ATP, a factor known to be involved in sperm activation. The ATP enhanced sperm motility was mimicked by UTP, and inhibited by ChTX and reactive blue, an antagonist of P 2 receptor, indicating the involvement of both P 2U and KCa channels. RT PCR study was also conducted to confirm the expression of KCa channels, AT 1 receptors and P 2U receptor, but not AT 2 receptor, in rat caudal epididymal sperm. The present findings suggest an important role of KCa channels in the regulation of sperm motility by AT 1 and P 2U receptors.
文摘针对WES 2815:2014《Test method for brittle crack arrest toughness,Kca》和UR S33《Requirements for Use of Extremely Thick Steel Plates》中止裂韧性Kca的计算表达式和裂纹偏转时Kca的计算方法,利用有限元法计算了三种不同裂纹形式的双重拉伸试样的止裂韧性Kca,基于计算结果指出了上述标准中止裂韧性Kca计算表达式缺少一系数项,并给出了正确的Kca计算表达式,同时提出裂纹偏转角度大时按照裂纹的直边投影计算Kca是不合理的。
文摘Background Recent studies have showed that perivascular adipose tissue （PVAT） may secrete the adventitial-derived relaxing factor （ADRF） to affect vascular function.However,the functional change of ADRF in hypertensive status is seldom studied;and the mechanisms of ADRF remain unclear.Our study examined the ADRF secreted by perivascular adipose tissue of control rats with normal blood pressure （Wistar Kyoto rats,WKY） and discussed the mechanisms of ADRF;We observed the functional change in ADRF of perivascular adipose tissue in spontaneously hypertensive rats （SHRs）.Method The two adjacent thoracic aorta rings of SHR and WKY rats were divided into naked vessel subgroup and PVAT subgroup.The differences of vascular contractility between the two subgroups induced by 10-6 mmol/L phenylephrine were compared.The effect of PVAT culture medium of WKY on the vascular tension of Fat （-） vessels was observed by liquid transfer measure.The mechanism of ADRF was determined by tool drugs.Results In WKY group,vascular contractility of Fat （＋） subgroup was lower than that of the Fat （-） subgroup （P 0.05）;while in SHR group,there was no difference between the two subgroups （P 0.05）.Transferring the incubation solution of WKY Fat （＋） subgroup to the matched Fat （-） subgroup induced rapid vasodilation.When incubating blood vessels in calcium free PSS solution,there was no significant difference of phenylephrine-induced vasoconstriction between Fat （-） and Fat （＋） subgroup.Both glibenclamide,the blocker of ATP-sensitive potassium （KATP） channel and Tetraethy-lammonium chloride （TEA）,the inhibitor of calcium-dependent potassium （KCa） channel,effectively inhibited vasodilation function of ADRF.Conclusions Perivascular adipose tissue in WKY releases ADRF which can cause vasodilation,while this function was inhibited in SHR.ADRF acts through the activation of KCa and KATP channels and calcium ion is involved.
