Neural and hormonal control mechanisms in excitatory cardiac regulation of the hermit crabs

我们研究了一种甲壳类心包肽--直肠肽对肛门螺心的影响。通过记录心肌细胞的收缩力、细胞内膜电位和心肌神经节细胞的细胞外电位来研究这些效应。我们使用了半完整的心脏，与背部、甲壳一起隔离，以及完全隔离的心脏。正性变力作用和正性变力作用的阈值浓度分别约为10^~(-13)M和10^~(-10)M。在10^&lt；-7&gt；M时，变力作用达到正常搏动幅度的150%以上。在直肠降压素(10^&lt；-6&gt；M-10^&lt；-5&gt；M)灌流期间，最初的正性变时性效应之后是负性效应。变力作用主要是由于心脏神经节细胞爆发期内脉冲率的增加。正变时性效应(&lt；50%)反映了神经节爆裂率的增加。在应用原胆碱的过程中，复合动作电位的幅度和肌肉动作电位的幅度增大，而心肌细胞膜的电导没有改变。甚至在含有河豚毒素的生理盐水中也观察到了正性变力作用。在含有蛋白激酶抑制剂H-7的生理盐水中，这种痉挛被解除。H-7对心肌膜电位无影响，但对神经节细胞活性略有增强。腺苷环化酶激活剂Forsklin和G蛋白激活剂霍乱毒素可增强神经节活性，但不能促进肌挛缩。在A1F4^-存在的情况下，直肠素效应不增强。某些磷酸二酯酶抑制剂咖啡因、茶碱、3-甲基黄嘌呤和IBMX影响神经节，但不影响心肌活动本身。也就是说，在抑制剂的存在下，原胆碱对心脏神经节的作用显著增强，但对心肌细胞的作用不明显。不是二丁酰cGMP，而是

We studied the effects, on the A.aniculus heart, of a crustacean pericardial peptide, proctolin. Those effects were investigated by means of recording contractile force, intracellular membrane potential of the myocardium and extracellular potential from cardiac ganglionic cells. We used semi-intact hearts, isolated together with the dorsal, carapace, as well as totally isolated hearts. Threshold concentrations for positively inotropic and positively tonotropic effects were approximately 10^<-13> M and 10^<-10> M, respectively. At 10^<-7> M, inotropic effects amounted to more than 150% of the normal beat amplitude. Initially positive chronotropic effects were followed by negative effects during a period of perfusion with proctolin (10^<-6> M - 10^<-5> M). The inotropic effects resulted mainly from augmentation of the intra-burst impulse rate of cardiac ganglionic cells. The positively chronotropic effects (<50%) reflected increases in burst rate of the ganglion. The amplitude of the compound EJPs and that of the muscle action potentials were augmented, while conductance of the myocardial cell membrane was not changed, during proctolin application. Positively tonotropic effects were observed as contracture even in TTX-containing saline. The contracture was abolished in saline containing a protein kinase inhibitor, H-7. H-7 did not affect myocardial membrane potential but slightly enhanced ganglionic activity. An adenylate cyclase activator, forskolin, and a G-protein activator, cholera toxin, enhanced ganglionic activity but not contracture. In the presence of A1F_4^-, proctolin effects were not augmented. Certain phosphodiesterase inhibitors, caffeine, theophylline, 3-methylxanthine and IBMX affected the ganglion but not myocardial activity itself. That is, in the presence of the inhibitors, proctolin actions on the cardiac ganglion, but not on the myocardial cells, were significantly augmented. Not dibutyryl cGMP, but instead