Canine intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors.
Canine intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors.
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参与心脏调节的犬固有心脏神经元拥有 NK1、NK2 和 NK3 受体。
DOI：
10.1152/ajpregu.1998.275.5.r1683
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Armour,JA
中科院分区：
文献类型：
--
作者：
Thompson,GW;Hoover,DB;Ardell,JL;Armour,JA
为了确定参与心脏调节的内在心脏神经元是否具有神经激肽 (NK) 受体亚型，我们将选择性 NK 受体激动剂单独（100 μM；0.1 ml）注入 18 只麻醉狗的右心房内在心脏神经元的冠状动脉血供中。选择性 NK1 受体激动剂 [Sar9,Met(O2)11]-P 物质抑制了 11 只狗的右心房神经元的自发活动（26.7 ± 6.7 至 13.0 ± 4.0 脉冲/分钟；P < 0.05），并增强了其他 5 只狗的自发活动（8.0 ± 3.1 至 27.8 ± 8.7 脉冲/分钟；P < 0.05）。局部给予选择性 NK2 受体激动剂 [β-Ala8]-NKA-(4-10) 会抑制右心房神经元活动（27.3 ± 6.4 至 14.7 ± 3.8 脉冲/分钟；P< 0.05），而选择性 NK3 受体激动剂 Senktide 会增强这种活动（18.9 ± 6.4 至 53.1 ± 12.0）脉冲/分钟；P<0.05）。当给予选择性 NK1 和 NK2 受体激动剂时，左心室压力下降。研究选择性 NK3 受体激动剂时，心率和右心室心肌内收缩压增加。施用选择性 NK1 或 NK2 受体拮抗剂会改变神经元活性，而施用其各自的受体激动剂后不会发生随后的活性变化。受体放射自显影显示速激肽受体与腹侧右心房内在心脏神经元相关。结论是，参与心脏调节的内在心脏神经元拥有 NK1、NK2 和 NK3 受体，并且一些内在心脏神经元通过内源释放的 NK 接收强直输入。
To determine whether intrinsic cardiac neurons involved in cardiac regulation possess neurokinin (NK) receptor subtypes, we administered selective NK receptor agonists individually (100 μM; 0.1 ml) into the coronary arterial blood supply of right atrial intrinsic cardiac neurons of 18 anesthetized dogs. The selective NK1receptor agonist [Sar9,Met(O2)11]-substance P depressed the spontaneous activity of right atrial neurons (26.7 ± 6.7 to 13.0 ± 4.0 impulses/min;P< 0.05) in 11 dogs and augmented such activity in the other 5 dogs (8.0 ± 3.1 to 27.8 ± 8.7 impulses/min;P< 0.05). Local administration of the selective NK2receptor agonist [β-Ala8]-NKA-(4—10) depressed right atrial neuronal activity (27.3 ± 6.4 to 14.7 ± 3.8 impulses/min;P< 0.05), whereas the selective NK3receptor agonist senktide augmented such activity (18.9 ± 6.4 to 53.1 ± 12.0 impulses/min;P< 0.05). Left ventricular chamber pressure fell when selective NK1and NK2receptor agonists were administered. Increases in heart rate and right ventricular intramyocardial systolic pressure occurred when the selective NK3receptor agonist was studied. Administration of a selective NK1or NK2receptor antagonist altered neuronal activity, with no subsequent change in activity occurring after administration of its respective receptor agonist. Receptor autoradiography demonstrated tachykinin receptors associated with ventral right atrial intrinsic cardiac neurons. It is concluded that intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3receptors and that some intrinsic cardiac neurons receive tonic input via endogenously released NKs.