Objective To study the action of brain angiotensin Ⅱ(Ang Ⅱ) receptors and underlying intracellular mechanism in the catecholaminergic system Methods Action potentials (APs) of the primary co cultured catecholamin...Objective To study the action of brain angiotensin Ⅱ(Ang Ⅱ) receptors and underlying intracellular mechanism in the catecholaminergic system Methods Action potentials (APs) of the primary co cultured catecholaminergic tumor (CATH.a) cells were recorded with the whole cell patch clamp configuration in current clamp mode. Expression of Ang Ⅱ receptors subtypes (AT 1 and AT 2 ) was detected by RT PCR technique. Results The differentiated CATH.a cells represented a neuron like characterization. All CATH.a cells expressed mRNA encoding both Ang Ⅱ AT 1 and AT 2 receptor subtypes. Ang Ⅱ increased the firing rate in the CATH.a cells, which was inhibited completely by addition administration of the AT 1 but not AT 2 receptor antagonist, and partially by using the inhibitors of signal molecules, U73122 (10 μmol·L -1 ), or KN 93 (10 μmol·L -1 ), or calphostin C (10 μmol·L -1 ). Conclusion Ang Ⅱ increases firing rate in CATH.a cells via AT 1 receptor. The CATH.a cells expressing functional AT 1 and AT 2 receptor subtypes may be of general utility for the study of the Ang Ⅱ receptor induced modulation of brain catecholaminergic system.展开更多
文摘Objective To study the action of brain angiotensin Ⅱ(Ang Ⅱ) receptors and underlying intracellular mechanism in the catecholaminergic system Methods Action potentials (APs) of the primary co cultured catecholaminergic tumor (CATH.a) cells were recorded with the whole cell patch clamp configuration in current clamp mode. Expression of Ang Ⅱ receptors subtypes (AT 1 and AT 2 ) was detected by RT PCR technique. Results The differentiated CATH.a cells represented a neuron like characterization. All CATH.a cells expressed mRNA encoding both Ang Ⅱ AT 1 and AT 2 receptor subtypes. Ang Ⅱ increased the firing rate in the CATH.a cells, which was inhibited completely by addition administration of the AT 1 but not AT 2 receptor antagonist, and partially by using the inhibitors of signal molecules, U73122 (10 μmol·L -1 ), or KN 93 (10 μmol·L -1 ), or calphostin C (10 μmol·L -1 ). Conclusion Ang Ⅱ increases firing rate in CATH.a cells via AT 1 receptor. The CATH.a cells expressing functional AT 1 and AT 2 receptor subtypes may be of general utility for the study of the Ang Ⅱ receptor induced modulation of brain catecholaminergic system.
