动脉粥样硬化是心血管疾病重要的病理生理基础,延缓和防治动脉粥样硬化对于减少和降低心血管疾病的发病率及病死率具有重要意义。高密度脂蛋白(high density lipoprotein,HDL)通过参与介导胆固醇逆向转运(reverse cholesterol transport...动脉粥样硬化是心血管疾病重要的病理生理基础,延缓和防治动脉粥样硬化对于减少和降低心血管疾病的发病率及病死率具有重要意义。高密度脂蛋白(high density lipoprotein,HDL)通过参与介导胆固醇逆向转运(reverse cholesterol transport,RCT)在抗动脉粥样硬化的形成和进展中发挥了重要作用。Preβ-1高密度脂蛋白(prebeta-1 high density lipoprotein,Preβ-1HDL)作为HDL的一种亚类,是外周细胞移出胆固醇的最初接受体,直接参与了RCT的起始步骤,并在随后的胆固醇酯化及转运中起着重要作用。本文就Preβ-1HDL的结构、代谢及其与心血管疾病的关系作一简要综述。展开更多
This study investigated the modulatory effect of synthetic cannabinoids WIN55,212-2 on 5-HT3 receptor-activated currents (I5-HT3) in cultured rat trigeminal ganglion (TG) neurons using whole-cell patch clamp technique...This study investigated the modulatory effect of synthetic cannabinoids WIN55,212-2 on 5-HT3 receptor-activated currents (I5-HT3) in cultured rat trigeminal ganglion (TG) neurons using whole-cell patch clamp technique. The results showed that: (1) The majority of examined neurons (78.70%) were sensitive to 5-HT (3–300 μmol/L). 5-HT induced inward currents in a concentration-dependent manner and the currents were blocked by ICS 205-930 (1 μmol/L), a selective antagonist of the 5-HT3 receptor; (2) Pre-application of WIN55,212-2 (0.01–1 μmol/L) significantly inhibited I5-HT3 reversibly in concentration-dependent and voltage-independent manners. The concentra-tion-response curve of 5-HT3 receptor was shifted downward by WIN55,212-2 without any change of the threshold value. The EC50 values of two curves were very close (17.5±4.5) mmol/L vs. (15.2±4.5) mmol/L and WIN55,212-2 decreased the maximal amplitude of I5-HT3 by (48.65±4.15)%; (3) Neither AM281, a selective CB1 receptor antagonist, nor AM630, a selective CB2 receptor antagonist reversed the inhibition of I5-HT3 by WIN55,212-2; (4) When WIN55,212-2 was given from 15 to 120 s before 5-HT application, inhibitory effect was gradually increased and the maximal inhibition took place at 90 s, and the inhibition remained at the same level after 90 s. We are led to concluded that-WIN55,212-2 inhibited I5-HT3 significantly and neither CB1 receptor antagonist nor CB2 receptor antagonist could reverse the inhibition of I5-HT3 by WIN55,212-2. Moreover, WIN55,212-2 is not an open channel blocker (OCB) of 5-HT3 receptor. WIN55,212-2 significantly inhibited 5-HT-activated currents in a non-competitive manner. The inhibition of I5-HT3 by WIN55,212-2 is probably new one of peripheral analgesic mechanisms of WIN55,212-2, but the mechanism by which WIN55,212-2 inhibits I5-HT3 warrants further investigation.展开更多
Objectives To investigate effect of Angll, captopril on single guinea myocytes on L - type calcium current and sodium current. Methods Membrane patch clamp whole cell recording technique was used to investigate effect...Objectives To investigate effect of Angll, captopril on single guinea myocytes on L - type calcium current and sodium current. Methods Membrane patch clamp whole cell recording technique was used to investigate effect of angll, captopril on L - Ca maximum current density and sodium maximum current density. Resutls Angll increased the maximum current density compared with control after perfused 5 min, 357. 7 ±219. 7 Vs 279. 5± 240. 5 PA/PF, increase rate is 27. 9 %, the shape of current - voltage relationship curve was unchanged, peaked at + 10 mv, indicated that angll increased L - Ca current density in voltage - dependent. After perfused with captopril, captopril + angll 3, 5 min, L - Ca current was recorded, results suggest L - Ca maximum current density decreased significantly compared with control, in captopril group, 128. 4 ± 92. 6Vs286. 2 ± 89. 7, 66. 7±68. 3Vs 286. 2 ± 89. 7, respectively, rate of inhibition is 55. 1 %, 76. 6 %, respectively. L - Ca current further decreased in captopril perfused 5 min compared with 3 min, 66. 7 ± 68. 3 Vs 128. 4 ± 92. 6, in captopril + angll group, L - Ca current decreased greatly in 3, 5 min than control, 143. 4±117. 6Vs 267. 7±141. 4, 96. 4±82. 5 Vs 267. 7±141. 4, respectively, rate of inhibition is 46. 4 % , 63. 9 % respectively. We also investigated effect of captopril on Na current, which decreased significantly in 1 min and 3 min compared with control, 939. 1 ±319. 1 Vs 1398. 0±144. 6 PA/PF, 469. 95 ± 314. 9 Vs 1398. 0 ±144. 6 PA/PF, respectively, rate of inhibition is 32. 8 % , 66. 3 % , respectively. Na current density decreased significantly in 3 min compared with 1 min, 469. 9±314. 9 Vs 939. 1±319. 1PA/PF, rate of inhibition is 49. 9 % . Conclusions Angiotensin Ⅱexerts increased maximum current density of L - Ca in voltage dependent, captopril decreased maximum current density of L - Ca in voltage dependent, decreased sodium maximum current density, which is the prominently antiarrhythmia mechanisms through inhibition of angiotensin Ⅱ evoked calcium dependent transient inward current and calcium overload.展开更多
文摘动脉粥样硬化是心血管疾病重要的病理生理基础,延缓和防治动脉粥样硬化对于减少和降低心血管疾病的发病率及病死率具有重要意义。高密度脂蛋白(high density lipoprotein,HDL)通过参与介导胆固醇逆向转运(reverse cholesterol transport,RCT)在抗动脉粥样硬化的形成和进展中发挥了重要作用。Preβ-1高密度脂蛋白(prebeta-1 high density lipoprotein,Preβ-1HDL)作为HDL的一种亚类,是外周细胞移出胆固醇的最初接受体,直接参与了RCT的起始步骤,并在随后的胆固醇酯化及转运中起着重要作用。本文就Preβ-1HDL的结构、代谢及其与心血管疾病的关系作一简要综述。
基金supported by National Natural Science Foundation of China(No.30271500)Science and Tech-nology Research Project Fund from the Department of Edu-cation of Hubei Province of China(No.B20115101)
文摘This study investigated the modulatory effect of synthetic cannabinoids WIN55,212-2 on 5-HT3 receptor-activated currents (I5-HT3) in cultured rat trigeminal ganglion (TG) neurons using whole-cell patch clamp technique. The results showed that: (1) The majority of examined neurons (78.70%) were sensitive to 5-HT (3–300 μmol/L). 5-HT induced inward currents in a concentration-dependent manner and the currents were blocked by ICS 205-930 (1 μmol/L), a selective antagonist of the 5-HT3 receptor; (2) Pre-application of WIN55,212-2 (0.01–1 μmol/L) significantly inhibited I5-HT3 reversibly in concentration-dependent and voltage-independent manners. The concentra-tion-response curve of 5-HT3 receptor was shifted downward by WIN55,212-2 without any change of the threshold value. The EC50 values of two curves were very close (17.5±4.5) mmol/L vs. (15.2±4.5) mmol/L and WIN55,212-2 decreased the maximal amplitude of I5-HT3 by (48.65±4.15)%; (3) Neither AM281, a selective CB1 receptor antagonist, nor AM630, a selective CB2 receptor antagonist reversed the inhibition of I5-HT3 by WIN55,212-2; (4) When WIN55,212-2 was given from 15 to 120 s before 5-HT application, inhibitory effect was gradually increased and the maximal inhibition took place at 90 s, and the inhibition remained at the same level after 90 s. We are led to concluded that-WIN55,212-2 inhibited I5-HT3 significantly and neither CB1 receptor antagonist nor CB2 receptor antagonist could reverse the inhibition of I5-HT3 by WIN55,212-2. Moreover, WIN55,212-2 is not an open channel blocker (OCB) of 5-HT3 receptor. WIN55,212-2 significantly inhibited 5-HT-activated currents in a non-competitive manner. The inhibition of I5-HT3 by WIN55,212-2 is probably new one of peripheral analgesic mechanisms of WIN55,212-2, but the mechanism by which WIN55,212-2 inhibits I5-HT3 warrants further investigation.
文摘Objectives To investigate effect of Angll, captopril on single guinea myocytes on L - type calcium current and sodium current. Methods Membrane patch clamp whole cell recording technique was used to investigate effect of angll, captopril on L - Ca maximum current density and sodium maximum current density. Resutls Angll increased the maximum current density compared with control after perfused 5 min, 357. 7 ±219. 7 Vs 279. 5± 240. 5 PA/PF, increase rate is 27. 9 %, the shape of current - voltage relationship curve was unchanged, peaked at + 10 mv, indicated that angll increased L - Ca current density in voltage - dependent. After perfused with captopril, captopril + angll 3, 5 min, L - Ca current was recorded, results suggest L - Ca maximum current density decreased significantly compared with control, in captopril group, 128. 4 ± 92. 6Vs286. 2 ± 89. 7, 66. 7±68. 3Vs 286. 2 ± 89. 7, respectively, rate of inhibition is 55. 1 %, 76. 6 %, respectively. L - Ca current further decreased in captopril perfused 5 min compared with 3 min, 66. 7 ± 68. 3 Vs 128. 4 ± 92. 6, in captopril + angll group, L - Ca current decreased greatly in 3, 5 min than control, 143. 4±117. 6Vs 267. 7±141. 4, 96. 4±82. 5 Vs 267. 7±141. 4, respectively, rate of inhibition is 46. 4 % , 63. 9 % respectively. We also investigated effect of captopril on Na current, which decreased significantly in 1 min and 3 min compared with control, 939. 1 ±319. 1 Vs 1398. 0±144. 6 PA/PF, 469. 95 ± 314. 9 Vs 1398. 0 ±144. 6 PA/PF, respectively, rate of inhibition is 32. 8 % , 66. 3 % , respectively. Na current density decreased significantly in 3 min compared with 1 min, 469. 9±314. 9 Vs 939. 1±319. 1PA/PF, rate of inhibition is 49. 9 % . Conclusions Angiotensin Ⅱexerts increased maximum current density of L - Ca in voltage dependent, captopril decreased maximum current density of L - Ca in voltage dependent, decreased sodium maximum current density, which is the prominently antiarrhythmia mechanisms through inhibition of angiotensin Ⅱ evoked calcium dependent transient inward current and calcium overload.
