Effects of procainamide (PA) on human platelet aggregation and the cytosolic free-Ca2+ concentration ([Ca2+]) were investigated in vitro. PA at doses of 8.5 , 34 and 136 μmol·L-1 could inhibit the human platelet...Effects of procainamide (PA) on human platelet aggregation and the cytosolic free-Ca2+ concentration ([Ca2+]) were investigated in vitro. PA at doses of 8.5 , 34 and 136 μmol·L-1 could inhibit the human platelet aggregation induced by 0. 5 μmol · L-1 A23187 with a good concentration -effect relationship. One min and maximal aggregation rates were also inhibited ( P<0. 01 ,vs control). The [Ca2+], was decreased in the presence of PA ,and the changes of [Ca2+], showed a significant linear correlation with 1 min or maximal aggregation rate (P<0.05). These results suggest that the mechanisms of PA inhibiting platelet aggregation relate to the decrease of [Ca2+].展开更多
There is now growing evidence that membrane vesicle trafficking proteins, especially of the superfamily of SNAREs, are critical for cellular signalling in plants. Work from this laboratory first demonstrated that a so...There is now growing evidence that membrane vesicle trafficking proteins, especially of the superfamily of SNAREs, are critical for cellular signalling in plants. Work from this laboratory first demonstrated that a soluble, inhibitory （dominant-negative） fragment of the SNARE NtSyp121 blocked K^＋ and CI^- channel responses to the stress-related hormone abscisic acid （ABA）, but left open a question about functional impacts on signal intermediates, especially on Ca^2＋-mediated signalling events. Here, we report one mode of action for the SNARE mediated directly through alterations in Ca^2＋ channel gating and its consequent effects on cytosolic-free [Ca^2＋] （[Ca^2＋]i） elevation. We find that expressing the same inhibitory fragment of NtSyp121 blocks ABA-evoked stomatal closure, but only partially suppresses stomatal closure in the presence of the NO donor, SNAP, which promotes [Ca^2＋]i elevation independently of the plasma membrane Ca^2＋ channels. Consistent with these observations, Ca^2＋ channel gating at the plasma membrane is altered by the SNARE fragment in a manner effective in reducing the potential for triggering a rise in [Ca^2＋]i, and we show directly that its expression in vivo leads to a pronounced suppression of evoked [Ca^2＋]i transients. These observations offer primary evidence for the functional coupling of the SNARE with Ca^2＋ channels at the plant cell plasma membrane and, because [Ca^2＋]i plays a key role in the control of K^＋ and CI^- channel currents in guard cells, they underscore an important mechanism for SNARE integration with ion channel regulation during stomatal closure.展开更多
文摘Effects of procainamide (PA) on human platelet aggregation and the cytosolic free-Ca2+ concentration ([Ca2+]) were investigated in vitro. PA at doses of 8.5 , 34 and 136 μmol·L-1 could inhibit the human platelet aggregation induced by 0. 5 μmol · L-1 A23187 with a good concentration -effect relationship. One min and maximal aggregation rates were also inhibited ( P<0. 01 ,vs control). The [Ca2+], was decreased in the presence of PA ,and the changes of [Ca2+], showed a significant linear correlation with 1 min or maximal aggregation rate (P<0.05). These results suggest that the mechanisms of PA inhibiting platelet aggregation relate to the decrease of [Ca2+].
文摘There is now growing evidence that membrane vesicle trafficking proteins, especially of the superfamily of SNAREs, are critical for cellular signalling in plants. Work from this laboratory first demonstrated that a soluble, inhibitory （dominant-negative） fragment of the SNARE NtSyp121 blocked K^＋ and CI^- channel responses to the stress-related hormone abscisic acid （ABA）, but left open a question about functional impacts on signal intermediates, especially on Ca^2＋-mediated signalling events. Here, we report one mode of action for the SNARE mediated directly through alterations in Ca^2＋ channel gating and its consequent effects on cytosolic-free [Ca^2＋] （[Ca^2＋]i） elevation. We find that expressing the same inhibitory fragment of NtSyp121 blocks ABA-evoked stomatal closure, but only partially suppresses stomatal closure in the presence of the NO donor, SNAP, which promotes [Ca^2＋]i elevation independently of the plasma membrane Ca^2＋ channels. Consistent with these observations, Ca^2＋ channel gating at the plasma membrane is altered by the SNARE fragment in a manner effective in reducing the potential for triggering a rise in [Ca^2＋]i, and we show directly that its expression in vivo leads to a pronounced suppression of evoked [Ca^2＋]i transients. These observations offer primary evidence for the functional coupling of the SNARE with Ca^2＋ channels at the plant cell plasma membrane and, because [Ca^2＋]i plays a key role in the control of K^＋ and CI^- channel currents in guard cells, they underscore an important mechanism for SNARE integration with ion channel regulation during stomatal closure.
